Emphysema and chronic bronchitis are airflow-limited states contained within the disease state known as chronic obstructive pulmonary disease (COPD). [1] Just as asthma is no longer grouped with COPD, the current definition of COPD put forth by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) also no longer distinguishes between emphysema and chronic bronchitis. [2]
Emphysema is pathologically defined as an abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of alveolar walls and without obvious fibrosis. [1] This process leads to reduced gas exchange, changes in airway dynamics that impair expiratory airflow, and progressive air trapping. [3] Clinically, the term emphysema is used interchangeably with chronic obstructive pulmonary disease, or COPD.
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The theory surrounding this definition has been around since the 1950s, with a key concept of irreversibility and/or permanent acinar damage. However, new data posit that increased collagen deposition leads to active fibrosis, which inevitably is associated with breakdown of the lung’s elastic framework. An entity known as combined pulmonary fibrosis and emphysema (CPFE) has been shown to exist in a subset of emphysematous patients. [4] This implies an association between fibrosis and the permanence of alveolar damage. The complex mechanism thought to be responsible is the interplay between Notch and Wnt, two signaling pathways playing critical roles in epithelial and mesenchymal precursor cell maintenance and differentiation. [5]
Discussions on how obstructive diseases share similar phenotypes have been emerging and evolving within the literature. Asthma and chronic obstructive pulmonary disease overlap syndrome (ACOS) is a term that has been used to describe patients who have severe COPD and/or severe asthma who find themselves with frequent exacerbations/hospitalizations and difficult-to-control or refractory symptoms. In its 2017 guidelines update the Global Initiative for Asthma (GINA)-Global Initiative for Chronic Obstructive Lung Diseases (GOLD) explained that it no longer used the term asthma-COPD overlap syndrome (ASCO) because asthma-COPD overlap does not describe a single disease entity. Presentations with combined features of both disorders more likely have several different phenotypes of airway disease caused by a variety of mechanisms. [6]
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Chronic lower respiratory disease, primarily COPD, is the third leading cause of death in the United States and the fourth leading cause of death worldwide, although it may become the fourth global cause of death in 2020. [1] Almost 15.7 million Americans (6.4%) in 2014 reported that they were diagnosed with COPD, however the actual number is likely much higer. More than 50% of adults with low pulmonary function were not aware that they had COPD. The following groups were more likely to report COPD in 2013 [7] :
The risk factors thought to be responsible for the development of COPD are all associated with an accelerated decline in FEV1 over time. Tobacco smoke is a key factor in the development and progression of COPD, although exposure to air pollutants in the home and workplace, genetic factors, and respiratory infections also play a role. Women in developing countries who are exposed to biomass cooking of liquids and fuels, including wood, crops, animal dung, and coal, are at increased risk of developing COPD. Add to that poor ventilation of the home and dependent family members’ (children and elderly persons) risk also increases. Globally, COPD is a disease of occupation and environmental pollutants too, including but not limited to organic and inorganic dusts, isocyanates, and phosgenes. [8]
The latest systematic review looked at the impact of air pollution on COPD sufferers (inclusive of articles prior to 1990); the investigators concluded that the need to continue to improve air quality guidelines is more important than ever as biomass cooking in low-income nations was clearly associated with COPD mortality in adult female nonsmokers [9] .
However, the evolution of disease based on smoke exposure differs widely among people, suggesting genetic factors to be involved. It is not truly known why certain people with a positive smoke exposure develop injury patterns, symptoms, and disease. For instance, the Lung Health Study from 2002 showed that a third of smokers never developed impaired lung function after 11 years despite a baseline study of airway obstruction. [10]
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Genetic risk factors for the development of COPD include alpha-1-antitrypsin (AAT) deficiency (also known as alpha-1 antiprotease deficiency). AAT is a glycoprotein member of the serine protease inhibitor family that is synthesized in the liver and is secreted into the blood stream. The main purpose of this 394-amino acid, single-chain protein is to neutralize neutrophil elastase in the lung interstitium and to protect the lung parenchyma from elastolytic breakdown. If not inactivated by AAT, neutrophil elastase destroys lung connective tissue leading to emphysema. Therefore, severe AAT deficiency predisposes to unopposed elastolysis with the clinical sequela of an early onset of panacinar emphysema.
Deficiency of AAT is inherited as an autosomal codominant condition. The gene, located on the long arm of chromosome 14, expresses different phenotypes (serum protease inhibitor phenotype notated Pi type). The most common type of severe AAT phenotype (more than 90%) occurs in individuals who are homozygous for the Z allele. Homozygous individuals (Pi ZZ), usually of northern European descent, have serum levels well below the reference range levels at about 20% of the normal level (2.5 to 7 mmol/L). The normal M allele phenotype is Pi MM, with levels of 20-48 mmol/L. [11] Lifetime nonsmokers who are homozygous for the Z allele rarely develop emphysema. Hence, cigarette smoking is the most important risk factor for emphysema development in individuals with AATD.
The hallmark physical examination finding of emphysema is the limitation of expiratory flow with relative preservation of inspiratory flow. A forced expiratory time more than 6 seconds indicates severe expiratory airflow obstruction. The forced expiratory volume in one second (FEV1) and the forced vital capacity (FVC) are used in determining flows. The ratio of the two (FEV1/FVC) results as a percentage on spirometry and is used to confirm the diagnosis of obstructive airway disease and assess responses to treatment and disease progression.
The goal of therapy is to relieve symptoms, prevent disease progression, improve exercise tolerance and health status, prevent and treat complications and exacerbations, and reduce mortality. [12] Treatments should be added in a stepwise fashion to reach these goals.
Once the diagnosis of chronic obstructive pulmonary disease (COPD) is established, the patient should be educated about the disease and should be encouraged to participate actively in therapy. For patient education resources, visit the Lung Disease and Respiratory Health Center.
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