What is COPD? How is it diagnosed & treated?

"Chronic obstructive pulmonary disease (COPD)is a term referring to two lung diseases, chronic bronchitis and emphysema, that are characterized by obstruction to airflow that interferes with normal breathing. Both of these conditions frequently co-exist, hence physicians prefer the term COPD. It does not include other obstructive diseases such as asthma."
American Lung Association, Chronic Obstructive Pulmonary Disease (COPD) Fact Sheet (Chronic Bronchitis and Emphysema) July 2005 http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=35020

Air is conducted from the trachea to the periphery of the lungs through an airway tree that branches out following rules of irregular dichotomy, i.e., one branch gives rise to daughter branches that may differ greatly in length and width. It is estimated that individual paths from the trachea to the lung periphery range from 11 to 30 generations, and average about 24-25 generations.

The system of airways in the lungs can be subdivided into 3 zones, a conducting zone that only conducts air, a purely gas exchanging zone, and a transitional zone.

The conducting zone includes the trachea, bronchi, bronchioles and terminal bronchioles. These are purely air-conducting structures that lies on average between the trachea and the 16th generation of airway branches (counting the trachea as generation zero.) These structures are lined with typical epithelial tissue lined with ciliated cells (which look something like brush bristles). There are also mucous-producing goblet cells in the proximal part of the conducting zone (closest to the trachea). In the bronchioles (5th to 16th generation on average) the goblet cells are replaced by another type of fluid- secreting cell called the Clara Cell.

The function of the conducting zone is to moisten, warm, and filter the air that it conducts to the gas exchanging and transitional zones. The epithelium is covered by a layer of low-viscosity fluid that intercepts particles which the ciliated cells sweep outwards. There is also a layer of high-viscosity mucous in the larger airways which is swept outward by the ciliated cells to the pharynx, where it is swallowed.

The transitional zone consists of structures called respiratory bronchioles with cup-like out-pouchings called alveoli, that become more densely packed as you proceed toward the end of the airway path. The alveoli are tiny air sacs with very thin walls where gas exchange takes place between the lungs and bloodstream.

The purely gas exchanging zone begins with branches where the alveoli become so densely packed that an air wall proper is missing. These structures called alveolar ducts. The airway paths ends in a cluster of alveolar sacs (which look something like a bunch of grapes).

"COPD is defined as a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema: the airflow obstruction is generally progressive, may be accompanied by airway reactivity, and may be partially reversible.

"In the past, asthma -- viewed as a condition in which increased responsiveness of the tracheobronchial tree was the most prominent feature -- was generally subsumed under COPD. Now, inflammation with participation of complex cellular and chemical mediators is considered the salient characteristic of asthma. It therefore seems prudent and practical to separate these conditions…

"Chronic Bronchitis is defined as the presence of a productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded.

"Emphysema is defined as abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Destruction is defined as lack of uniformity in the pattern of respiratory airspace enlargement; the orderly appearance of the acinus* and its components is disturbed and may be lost" [*acinus is a primary respiratory lobule, consisting of a bronchiole and its branches]

Source: American Thoracic Society
Medical Section of the American Lung Association, Standards for the Diagnosis and Care of Patients with Chronic Obstructive Pulmonary Disease (COPD) 1995, Page 578 http://www.thoracic.org/statements

Most cases of COPD are believed to be primarily the result of a combination of genetic and environmental factors. Exposure to cigarette smoke is known to be the leading environmental cause. Other lung irritants, allergens, and respiratory infections also play a role in triggering inflammatory responses and producing permanent changes in lung structures.

1.1 The diagnosis of COPD depends on thinking of it as a cause of breathlessness or cough. The diagnosis is suspected on the basis of symptoms and signs and supported by spirometry.

[Spirometry is the measurement of Forced Expiratory Volume (FEV). The procedure involves having the patient inhale as deeply as possible, then exhale as quickly and completely as possible into a hand held device. The results are usually expressed as FVC (Forced Vital Capacity), which is the total volume exhaled, or FEV in 6 seconds (FEV6), and FEV in 1 second (FEV), and an FEV1 / FVC ratio. The results are compared to expected results for FVC, FEV1 and an FEV1/FVC ratio according to sex, height, and age. A note of caution: The expected results are based on a statistical average and should be considered a rough guide. There are large variations from the norm unrelated to any lung disease, such as individual differences in body type, etc.]

1.1.1.1 The diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with one or more of the following symptoms:

Quotations from: National Institute for Clinical Excellence, Chronic obstructive pulmonary disease Clinical guideline 12, February 2004, pages 8-12
http://www.nice.org.uk/page.aspx?o=104441

The goals of COPD treatment are to improve lung function and to stop or slow down the progression of the disease, and to reduce the intensity, length and number of exacerbations. The earlier the diagnosis and the start of appropriate treatment, the more promising the outlook. Reduced exposure to environmental triggers of the inflammatory process, such as cigarette smoke and allergens, is important.

The cornerstone of medical therapy is intermittent-to-chronic use of bronchodilators, most often Beta-agonists (e.g., Albuterol), anticholinergics (e.g., Atrovent) or a combination of the two. [Spiriva, a long-acting anticholinergic, usually taken once per day, is frequently prescribed.] These medications dilate air passages and have other properties that create less favorable conditions for bacterial growth. One of the longer acting beta-agonists is also believed to have direct anti-inflammatory effects. Theophyline (similar to caffeine) and other drugs in the same class are not often used due to their side effects and narrow margin of safety between theraputic and toxic levels. Theophyline is used mainly to treat patients in advanced stages of COPD. The bronchodilator(s) of choice should be based on a careful evaluation of the disease.

As COPD progresses, the lungs become increasingly bacteria-friendly: Air passages are obstructed to varying degrees, scar tissue replaces normal epithelial tissue, mucous production increases, and the cilia which lines bronchial tubes is less able to sweep mucous and other debris out of the lungs.

In documents cited in this article, the American Lung Association, the Centers for Disease Control and the National Institute for Clinical Excellence recommend antibiotics for COPD exacerbations where there are signs of a possible bacterial infection, such as purulent sputum, which is usually yellow, green or dark grey in color.

"Among otherwise healthy individuals, antibiotics have not demonstrated any consistent benefit in the symptomatology or natural history of acute bronchitis. Antibiotics are recommended to patients with bronchiectasis or COPD exacerbation or if purulent sputum production has lasted beyond 7 days without evidence of improvement to other conventional therapy." -- "Bronchitis" Article by Samer Qarah, MD, Pulmonary Critical Care Consultant, Department of Internal Medicine, Division of Pulmonary and Critical Care, The Brooklyn Hospital Center and Cornell University.
http://www.emedicine.com/med/topic247.htm

It is estimated that about 80% of COPD exacerbations are caused primarily by bacteria and / or viruses. Viral infections and other non-bacterial causes of COPD are believed to frequently set the stage for bacterial infections that will respond favorably to treatment with antibiotics (if the right antibiotic is chosen).

In one study of Emergency room patients who were experiencing a severe COPD exacerbation, 19% of those who received antibiotic treatment returned to the ER due to persistent or worsening symptoms within 14 days, compared to 32% of those received a placebo (a fake antibiotic). Relapse rates for those who received amoxicillin were higher than for those who received a placebo.

"Corticosteroids reduce, reverse, and in some cases prevent irritation, swelling and mucus build-up in breathing tubes…Non-corticosteroids [Anti-Inflammatories and Anti-Leukotrienes] prevent swelling and mucus build up when you come in contact with an irritating substance." - COPD Self-management guide, Health Partners Carespan program

In clinical practice I have generally seen doctors prescribe non-steroidal anti-inflammatory drugs (such as ibuprofen) or corticosteroids on a short term basis for COPD exacerbations.

NICE guidelines state "None of the inhaled corticosteroids currently available are licensed for use alone in the treatment of COPD." Oral or inhaled corticosteroids are widely used for treatment of COPD exacerbations, usually in combination with a bronchodilator and antibiotics, and are generally approved for up to 14 days.

Longer term corticosteroid treatment should generally be reserved for patients who are in the "severe" to "very severe" stages of COPD or asthmatics who cannot adequately control their symptoms with bronchodilators alone.

None of the inhaled corticosteroids currently available are licensed for use alone in the treatment of COPD. The following recommendations therefore include usage outside licensed indications, and prescribers need to remember that responsibility for such prescribing lies with them.

Grade A - Oral corticosteroid reversibility tests do not predict response to inhaled corticosteroid therapy and should not be used to identify which patients should be prescribed inhaled corticosteroids.

Grade B - Inhaled corticosteroids should be prescribed for patients with an FEV1 less than or equal to 50% predicted, who are having two or more exacerbations requiring treatment with antibiotics or oral corticosteroids in a 12-month period. The aim of treatment is to reduce exacerbation rates and slow the decline in health status and not to improve lung function per se.

Grade D - Clinicians should be aware of the potential risk of developing osteoporosis and other side effects in patients treated with high-dose inhaled corticosteroids (especially in the presence of other risk factors), and should discuss the risk with patients.
http://www.guideline.gov/summary/summary.aspx?doc_id=5061


				*Doug Mann LPN, LNC* *What is COPD? How is it diagnosed & treated?*



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		What is Chronic Obstructive Pulmonary Disease (COPD)? How is it diagnosed and treated?



		WHAT IS COPD? "Chronic obstructive pulmonary disease (COPD)is a term referring to two lung diseases, chronic bronchitis and emphysema, that are characterized by obstruction to airflow that interferes with normal breathing. Both of these conditions frequently co-exist, hence physicians prefer the term COPD. It does not include other obstructive diseases such as asthma." American Lung Association, Chronic Obstructive Pulmonary Disease (COPD) Fact Sheet (Chronic Bronchitis and Emphysema) July 2005 http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=35020 LUNG STRUCTURE AND FUNCTION (See end note for the text under this heading for the information source) Air is conducted from the trachea to the periphery of the lungs through an airway tree that branches out following rules of irregular dichotomy, i.e., one branch gives rise to daughter branches that may differ greatly in length and width. It is estimated that individual paths from the trachea to the lung periphery range from 11 to 30 generations, and average about 24-25 generations. The system of airways in the lungs can be subdivided into 3 zones, a conducting zone that only conducts air, a purely gas exchanging zone, and a transitional zone. The conducting zone includes the trachea, bronchi, bronchioles and terminal bronchioles. These are purely air-conducting structures that lies on average between the trachea and the 16th generation of airway branches (counting the trachea as generation zero.) These structures are lined with typical epithelial tissue lined with ciliated cells (which look something like brush bristles). There are also mucous-producing goblet cells in the proximal part of the conducting zone (closest to the trachea). In the bronchioles (5th to 16th generation on average) the goblet cells are replaced by another type of fluid- secreting cell called the Clara Cell. The function of the conducting zone is to moisten, warm, and filter the air that it conducts to the gas exchanging and transitional zones. The epithelium is covered by a layer of low-viscosity fluid that intercepts particles which the ciliated cells sweep outwards. There is also a layer of high-viscosity mucous in the larger airways which is swept outward by the ciliated cells to the pharynx, where it is swallowed. The transitional zone consists of structures called respiratory bronchioles with cup-like out-pouchings called alveoli, that become more densely packed as you proceed toward the end of the airway path. The alveoli are tiny air sacs with very thin walls where gas exchange takes place between the lungs and bloodstream. The purely gas exchanging zone begins with branches where the alveoli become so densely packed that an air wall proper is missing. These structures called alveolar ducts. The airway paths ends in a cluster of alveolar sacs (which look something like a bunch of grapes). Source: Respiration and Respiratory Systems, subheading: Structural design of the airway tree. The New Encyclopedia Britannica, 15th Edition, (1989) vol. 26, page 781 A CLINICAL DEFINITION OF COPD American Thoracic society "COPD is defined as a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema: the airflow obstruction is generally progressive, may be accompanied by airway reactivity, and may be partially reversible. "In the past, asthma -- viewed as a condition in which increased responsiveness of the tracheobronchial tree was the most prominent feature -- was generally subsumed under COPD. Now, inflammation with participation of complex cellular and chemical mediators is considered the salient characteristic of asthma. It therefore seems prudent and practical to separate these conditions… "Chronic Bronchitis is defined as the presence of a productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded. "Emphysema is defined as abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Destruction is defined as lack of uniformity in the pattern of respiratory airspace enlargement; the orderly appearance of the acinus* and its components is disturbed and may be lost" [acinus is a primary respiratory lobule, consisting of a bronchiole and its branches] Source: American Thoracic Society Medical Section of the American Lung Association, Standards for the Diagnosis and Care of Patients with Chronic Obstructive Pulmonary Disease (COPD) 1995, Page 578 http://www.thoracic.org/statements WHAT CAUSES COPD? Most cases of COPD are believed to be primarily the result of a combination of genetic and environmental factors. Exposure to cigarette smoke is known to be the leading environmental cause. Other lung irritants, allergens, and respiratory infections also play a role in triggering inflammatory responses and producing permanent changes in lung structures. HOW IS COPD DIAGNOSED? (quotation of excerpts from NICE guidelines) 1.1 The diagnosis of COPD depends on thinking of it as a cause of breathlessness or cough. The diagnosis is suspected on the basis of symptoms and signs and supported by spirometry. [Spirometry is the measurement of Forced Expiratory Volume (FEV). The procedure involves having the patient inhale as deeply as possible, then exhale as quickly and completely as possible into a hand held device. The results are usually expressed as FVC (Forced Vital Capacity), which is the total volume exhaled, or FEV in 6 seconds (FEV6), and FEV in 1 second (FEV), and an FEV1 / FVC ratio. The results are compared to expected results for FVC, FEV1 and an FEV1/FVC ratio according to sex, height, and age. A note of caution: The expected results are based on a statistical average and should be considered a rough guide. There are large variations from the norm unrelated to any lung disease, such as individual differences in body type, etc.] 1.1.1.1 The diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with one or more of the following symptoms: Exertional breathlessness Chronic cough Regular sputum production Frequent winter ‘bronchitis’ wheeze 1.1.2.1 Spirometry should be performed at time of diagnosis to reconsider the diagnosis, if the patients show an exceptionally good response to the treatment. Table 3: Differences between COPD and asthma COPD Asthma Smoker or ex-smoker Nearly all Possibly Symptoms under age 35 Rare Common Chronic productive cough Common Uncommon Breathlessness Persistent and Variable progressive Night time waking with Uncommon Common breathlessness or wheeze Significant diurnal or day Uncommon Common to day variability of symptoms 1.1.4.4 To help resolve cases where diagnostic doubt remains, or, both COPD and asthma are present, the following findings should be used to help identify asthma A large (greater than 400 ml) response to bronchodilators A large (greater than 400 ml) response to 30 mg oral prednisolone daily for 2 weeks Serial peak flow measurements showing 20% or greater diurnal or day-to-day variability. Clinically significant COPD is not present if the FEV1 and FEV1/FVC ratio return to normal with drug therapy. Quotations from: National Institute for Clinical Excellence, Chronic obstructive pulmonary disease Clinical guideline 12, February 2004, pages 8-12 http://www.nice.org.uk/page.aspx?o=104441 STANDARDS FOR TREATMENT The goals of COPD treatment are to improve lung function and to stop or slow down the progression of the disease, and to reduce the intensity, length and number of exacerbations. The earlier the diagnosis and the start of appropriate treatment, the more promising the outlook. Reduced exposure to environmental triggers of the inflammatory process, such as cigarette smoke and allergens, is important. The cornerstone of medical therapy is intermittent-to-chronic use of bronchodilators, most often Beta-agonists (e.g., Albuterol), anticholinergics (e.g., Atrovent) or a combination of the two. [Spiriva, a long-acting anticholinergic, usually taken once per day, is frequently prescribed.] These medications dilate air passages and have other properties that create less favorable conditions for bacterial growth. One of the longer acting beta-agonists is also believed to have direct anti-inflammatory effects. Theophyline (similar to caffeine) and other drugs in the same class are not often used due to their side effects and narrow margin of safety between theraputic and toxic levels. Theophyline is used mainly to treat patients in advanced stages of COPD. The bronchodilator(s) of choice should be based on a careful evaluation of the disease. DIFFERENCES BETWEEN ACUTE & CHRONIC BRONCHITIS EXACERBATIONS As COPD progresses, the lungs become increasingly bacteria-friendly: Air passages are obstructed to varying degrees, scar tissue replaces normal epithelial tissue, mucous production increases, and the cilia which lines bronchial tubes is less able to sweep mucous and other debris out of the lungs. In documents cited in this article, the American Lung Association, the Centers for Disease Control and the National Institute for Clinical Excellence recommend antibiotics for COPD exacerbations where there are signs of a possible bacterial infection, such as purulent sputum, which is usually yellow, green or dark grey in color. "Among otherwise healthy individuals, antibiotics have not demonstrated any consistent benefit in the symptomatology or natural history of acute bronchitis. Antibiotics are recommended to patients with bronchiectasis or COPD exacerbation or if purulent sputum production has lasted beyond 7 days without evidence of improvement to other conventional therapy." -- "Bronchitis" Article by Samer Qarah, MD, Pulmonary Critical Care Consultant, Department of Internal Medicine, Division of Pulmonary and Critical Care, The Brooklyn Hospital Center and Cornell University. http://www.emedicine.com/med/topic247.htm It is estimated that about 80% of COPD exacerbations are caused primarily by bacteria and / or viruses. Viral infections and other non-bacterial causes of COPD are believed to frequently set the stage for bacterial infections that will respond favorably to treatment with antibiotics (if the right antibiotic is chosen). In one study of Emergency room patients who were experiencing a severe COPD exacerbation, 19% of those who received antibiotic treatment returned to the ER due to persistent or worsening symptoms within 14 days, compared to 32% of those received a placebo (a fake antibiotic). Relapse rates for those who received amoxicillin were higher than for those who received a placebo. CONTROVERSY ABOUT USE OF CORTICOSTEROIDS "Corticosteroids reduce, reverse, and in some cases prevent irritation, swelling and mucus build-up in breathing tubes…Non-corticosteroids [Anti-Inflammatories and Anti-Leukotrienes] prevent swelling and mucus build up when you come in contact with an irritating substance." - COPD Self-management guide, Health Partners Carespan program In clinical practice I have generally seen doctors prescribe non-steroidal anti-inflammatory drugs (such as ibuprofen) or corticosteroids on a short term basis for COPD exacerbations. NICE guidelines state "None of the inhaled corticosteroids currently available are licensed for use alone in the treatment of COPD." Oral or inhaled corticosteroids are widely used for treatment of COPD exacerbations, usually in combination with a bronchodilator and antibiotics, and are generally approved for up to 14 days. Longer term corticosteroid treatment should generally be reserved for patients who are in the "severe" to "very severe" stages of COPD or asthmatics who cannot adequately control their symptoms with bronchodilators alone. Corticosteroids Inhaled Corticosteroids None of the inhaled corticosteroids currently available are licensed for use alone in the treatment of COPD*. The following recommendations therefore include usage outside licensed indications, and prescribers need to remember that responsibility for such prescribing lies with them. Grade A - Oral corticosteroid reversibility tests do not predict response to inhaled corticosteroid therapy and should not be used to identify which patients should be prescribed inhaled corticosteroids. Grade B - Inhaled corticosteroids should be prescribed for patients with an FEV1 less than or equal to 50% predicted, who are having two or more exacerbations requiring treatment with antibiotics or oral corticosteroids in a 12-month period. The aim of treatment is to reduce exacerbation rates and slow the decline in health status and not to improve lung function per se. Grade D - Clinicians should be aware of the potential risk of developing osteoporosis and other side effects in patients treated with high-dose inhaled corticosteroids (especially in the presence of other risk factors), and should discuss the risk with patients. http://www.guideline.gov/summary/summary.aspx?doc_id=5061



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