Marcelo Figueroa Casas
Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease characterized by airflow obstruction that is not completely reversible.
Airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily cigarette smoke. Even though the
COPD mainly affects the lungs and also produces important systemic consequences.
Chronic Bronchitis : It is clinically defined as a chronic productive cough for 3 months in 2 successive years in patients in whom other causes of chronic productive cough have been excluded.
Emphysema : It is defined by pathological anatomy as the abnormal and permanent enlargement of the air spaces beyond the terminal bronchiole, accompanied by destruction of the walls and without evident fibrosis.
In COPD patients, either of these two conditions may be present. However, the relative contribution of each of these disease processes is difficult to differentiate.
The Asthma differs from COPD pathogenesis and therapeutic response, and therefore should be considered a distinct clinical entity. However, some patients with asthma develop poorly reversible airflow limitation. These patients are indistinguishable from COPD patients, but in practice they are treated as asthma. The high prevalence of these two diseases in the population results in the coexistence of the two diseases in many individuals.
COPD is one of the main causes of mortality and morbidity in the world with a huge economic and social impact. It is the 4th leading cause of death in the US and Europe. Risk factors can be divided into two Host groups: genetic (α-1 antitrypsin deficiency), bronchial hyper-reactivity and asthma, elevated immunoglobulin E, and female sex; and Exposure: smoking, occupation, socioeconomic status, environmental pollution, diet, and recurrent bronchopulmonary infections. Tobacco smoke is by far the main cause.
Natural history of disease
COPD has a variable course and not all individuals have the same clinical course. The statistic that 15-20% of smokers develop COPD is equivocal and clearly underestimates the prevalence of the disease. An accelerated decline in lung function is the hallmark of the disease in susceptible smokers, which may decrease or even stop in those who quit.
The diagnosis of COPD should be considered in anyone with the following symptoms:
- Sputum production
- History of exposure to risk factors for the disease
Diagnosis requires Spirometry: post-bronchodilator FEV1 / Forced Vital Capacity ratio less than 0.7. The study should be requested from all patients with a history of smoking or exposure to pollution, a family history of respiratory diseases and symptoms such as: cough, expectoration and dyspnea.
|Table 1. Classification according to spirometry
|FEV 1 % predicted
|> 80 %
|50 - 80
|30 - 50
|Very severe COPD
FEV1: Forced expiratory volume (1st second)
FVC: Forced vital capacity
Assessment of severity
It is accepted that a single measurement of FEV1 is an incomplete representation of the complex clinical consequences of COPD because: 1- many patients are practically asymptomatic. 2 - cough and expectoration generally precede the development of airflow obstruction and 3 - in the course of the disease systemic consequences can develop such as weight loss and peripheral muscle dysfunction.
Together with FEV1, dyspnea, and body mass index (BMI) they have proven useful in. a prediction of morbidity and mortality and its measurement is recommended in these patients
The cough may be intermittent at the beginning, and progressively occurs throughout the day, rarely it is only nocturnal. Usually productive, with thin and thick mucous expectoration. Change in sputum volume or color may indicate the presence of an infectious exacerbation. Dyspnea initially occurs during exercise, progresses and in advanced cases it may be during rest.
The clinical history of bronchial asthma, recurrent infections, tuberculosis, family history and exposure to cigarette smoke are key data to think about this diagnosis.
Physical examination is usually normal in the early forms of the disease. Examination of the patient should look for a barrel chest, narrow lip breathing, use of accessory muscles, and abnormal diaphragm movements. All the latter denote airflow obstruction and hyperinflation. Percussion can detect a decrease in diaphragm excursion and bloating due to bullae or hyperinflation. On auscultation, the vesicular murmur is diminished with rhonchi, wheezing, and prolonged expiration. Distension of the neck veins, peripheral edema, and hepatomegaly alert to the presence of cor-pulmonale. Loss of muscle mass are indicators of malnutrition and systemic inflammation. Cyanosis of the mucous membranes and skin indicate the presence of hypoxemia.
Spirometry necessary for diagnosis, assessment of severity and monitoring of evolution should be performed in all patients; the bronchodilator reversibility test is performed at least once to exclude asthma and to determine the best lung function of the patient. Rx should also be performed. of the thorax (fyp), which is not sensitive for its diagnosis, but it is sensitive to exclude other diseases (pneumonia, CHF, pneumothorax, neoplasms, pneumothorax and pleural effusion). Common but nonspecific signs are flattened diaphragms, hyper clarity in upper fields, increased retro-cardiac and retrosternal clear space, and reduced vasculature.
In selected patients, the following may be requested: α-1 antitrypsin, arterial blood gases, chest CT, pulmonary diffusion of CO and lung volumes, 6-minute walk test and Doppler echocardiogram.
|Table 2. BODE Index
|FEV1 (% of predicted)
|50 - 64
|36 - 49
|Walking distance in 6 min (m)
|249 - 350
|150 - 249
|MMRC dyspnea scale
|0 - 1
|Body mass index
|Total possible values are 0-10
|Table 3. Differential diagnostics