Chronic obstructive pulmonary disease
Easily preventable, chronic obstructive pulmonary disease (COPD) remains the nation's fourth largest killer and could—if smoking cessation rates don't rapidly improve—become No. 3 within the next 15 years.
Because of its connection to smoking, COPD has long had the stigma of a self-inflicted disease, creating guilt in patients and evoking little sympathy from the public. But life for COPD patients is getting better, according to Michael R. Littner, MD, chief of pulmonary medicine at the Sepulveda Campus of the Veterans Affairs Greater Los Angeles Healthcare System in Sepulveda, Calif., and professor of medicine at the David Geffen School of Medicine at University of California, Los Angeles.
Emphysema (shown here in a chest X-ray as yellow areas to the left and right) can support a chronic obstructive pulmonary disease (COPD) diagnosis. COPD can be present, however, without emphysema.
At one time, Dr. Littner pointed out, physicians could do little more than urge patients to quit smoking. "But new treatments can improve a patient's quality of life," he said—a fact that is now encouraging more funding for COPD research.
Still, the disease presents a host of clinical challenges. For one, COPD can be easily confused with asthma.
"That is probably the most important clinical distinction to make in terms of a differential diagnosis," said Dr. Littner, a pulmonary specialist who authored PIER's COPD module. To make that distinction, internists shouldn't jump to a diagnosis too quickly and they need to ask the right questions: Did patients' symptoms begin after age 40? Are symptoms progressive instead of episodic? Is there a lack of history of atopy and/or childhood asthma, and a current or previous history of cigarette smoking?
And "COPD may not be the primary cause of symptoms," Dr. Littner added. "If patients come in with coronary artery disease and are short of breath because they have congestive heart failure and have COPD—which disease caused the patient's shortness of breath?"
Exacerbations, which intensify and become more frequent as the disease progresses, pose another treatment challenge. They also add to the disease's toll of frequent patient visits, medication changes and hospitalizations.
And COPD still presents its historical dilemma: how to convince patients to stop smoking. With only 15% to 25% of smokers going on to develop COPD, it becomes a risk many smokers appear willing to take. (See "Smoking cessation: the golden rule of COPD.")
"They think, 'I'll throw the dice and gamble that it won't have any real impact—and I'll quit if it causes a problem,' " Dr. Littner said. "Patients do not seem to realize that once symptoms start, it is too often late to prevent permanent damage." He stressed, however, that quitting smoking may reduce or prevent further damage.
This edition of ACP Observer Special Focus is designed to help improve your ability to diagnose, treat and manage patients with COPD.
Cigarette smoking causes as many as 90% of all COPD cases. To prevent COPD, advise all patients not to smoke. Refer smokers to a cessation program, including group meetings, counseling, and drug therapy with nicotine replacement or bupropion.
Because a COPD diagnosis requires demonstrable airway obstruction based on spirometry, unselected screening for COPD is not recommended. However, consider testing individuals who have the following:
a history of cough or sputum production or findings compatible with emphysema on chest X-ray.
limiting symptoms such as dyspnea inappropriate to their activity level; frequent episodes of acute bronchitis related to upper respiratory tract infections; difficulty sleeping due to cough and dyspnea; or general diminished activity levels and energy from breathing difficulties.
no other clinical COPD characteristics, but are now or used to be a heavy smoker.
Use history, physical exam, degree of dyspnea, exercise tolerance and pulmonary function measurements to diagnose and stage COPD severity.
Rely on those same elements, particularly patient history, to exclude other airway-obstruction disorders, such as asthma, bronchiectasis and cystic fibrosis.
Clubbing and/or rales found on examination suggest another disease, such as bronchiectasis, interstitial lung disease or left heart failure.
Base your documentation of airflow obstruction and its severity on pulmonary function testing, including spirometry with a forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) ratio of <0.70 and on lung volumes and diffusing capacity, if necessary. (See "Staging COPD severity by spirometry.")
Besides spirometry, obtain pulse oximetry readings in patients with suspected COPD. Obtain an arterial blood gas reading if oximetry does not provide enough information on oxygenation or if you suspect hypercapnia.
A COPD diagnosis is supported by evidence of chronic bronchitis, emphysema or both. (Keep in mind, however, that COPD can be present without such symptoms or evidence of emphysema.)
Suspect emphysema on consistent physical exam findings of hyperinflation, including increased anteroposterior and lateral diameter; a flattened, poorly moving diaphragm; a hyperresonant percussion note; or distant breath sounds. A chest X-ray can help support an emphysema diagnosis if bullae are present. If necessary for clinical purposes, confirm emphysema with a high resolution CT chest scan.
You can base a chronic bronchitis diagnosis on at least two consecutive years of at least 90 days of cough and sputum production. And you should consider ordering an alpha1-antitrypsin level test if patients are age 45 or younger, or if they have emphysema without a recognized risk factor, such as smoking.
COPD exacerbations, which play a major role in treatment considerations, are characterized by acute deterioration in respiratory status. One common diagnostic approach uses three different major criteria: an increase in sputum volume; presence of sputum purulence (generally yellow or green); and worsening dyspnea.
Patients have a mild exacerbation if they have one of those three major criteria, and one or more of the following:
- an upper respiratory infection in the past five days
- fever without another apparent cause
- increased wheezing or cough
- increase in respiratory rate or heart rate 20% above baseline
Patients are suffering a moderate exacerbation if they meet two of the three major criteria, plus have an infection, fever, increased wheezing or cough, or increased respiratory rate. They are having a severe exacerbation if they meet all three major criteria.
All smokers with COPD should enroll in a smoking cessation program. Patients should also avoid risk factors; get an influenza vaccination if they have no sensitivity to egg protein, as well as a pneumococcal vaccination; and receive exercise training and patient education.
Base COPD drug therapy primarily on symptoms and secondarily on FEV1 staging, and use step therapy to treat chronic COPD. Use the lowest level of therapy that relieves symptoms and maximizes activity level.
And make sure patients are adhering to their regimen and properly using medications before escalating therapy. As an adjunct to drug therapy, consider prescribing exercise and other techniques to improve lung function and quality of life.
In most cases, you should begin therapy with inhaled rather than systemic agents. Metered-dose inhalers (MDIs) and nebulizers work equally well, and dry-powder inhalers are as effective as MDIs. Nebulizers may benefit patients who have coordination problems or physical conditions such as arthritis.
Patients should use a short-acting bronchodilator—an anticholinergic or beta2-agonist—when needed. Bronchodilators alleviate shortness of breath and improve exercise tolerance.
Patients should use a short-acting anticholinergic on a regular, not an as-needed, basis. Patients should start with two puffs four times a day and go to higher doses if needed, such as four puffs four times a day or more.
Because anticholinergics work more slowly than short-acting beta2-agonists, consider prescribing a short-acting beta2-agonist on at least an as-needed basis to alleviate transient increases in symptoms.
Consider combination therapy with the regular use of a beta2-agonist and an anticholinergic. For patients who regularly take both inhaled short-acting anticholinergics and beta2-agonists, consider prescribing an inhaler that contains both.
Patients with moderate COPD should begin treatment with either short-acting bronchodilators as for mild COPD, or with one or more long-acting bronchodilators, depending on symptom severity.
Consider a long-acting anticholinergic, such as inhaled tiotropium, once a day, or an inhaled long-acting beta2-agonist twice a day. Do not, however, prescribe an inhaled long-acting beta2-agonist as rescue therapy. (Keep inhaled short-acting beta2-agonists for that purpose.) Combining a long-acting beta2-agonist and a long-acting anticholinergic may be superior to using either alone.
Reserve oral bronchodilators for patients who cannot take inhaled medications, and consider adding sustained-release theophylline to a beta2-agonist or anticholinergic. Patients can usually get relief with a blood level of between 5 µg/mL and 12 µg/mL, with only mild side effects.
Theophylline can be useful in controlling nighttime symptoms, but it may also cause insomnia. Discontinue use if you don't reach your clinical objective within several weeks or if there are substantial side effects.
Also consider short-term pulmonary rehabilitation programs of less than six months for patients with moderate COPD, particularly those with the following:
- anxiety with activity
- breathlessness and limitations on activity
- loss of independence
Severe to very severe COPD
In addition to short- and long-acting bronchodilators, consider inhaled corticosteroids for patients with severe COPD, particularly if they have frequent moderate to severe exacerbations. Evidence shows that inhaled corticosteroids, when combined with a bronchodilator, can prevent exacerbations, relieve symptoms and improve quality of life for these patients.
Consider using high-dose inhaled corticosteroids, such as fluticasone, triamcinolone or budesonide, and increase doses as needed. You should not use oral corticosteroids for maintenance therapy because of side effects. If needed, however, patients should take them every other day at the lowest effective dose in combination with inhaled corticosteroids.
Patients typically derive greater benefit from combining an inhaled corticosteroid with a long-acting beta2-agonist. Such a combination may prevent exacerbations and improve symptoms and morning pre-dosing FEV1, more than either alone.
Patients with severe COPD should also enroll in long-term pulmonary rehabilitation programs of six months or longer. And patients with severe or very severe COPD may require long-term oxygen therapy if:
their resting, exercise or sleeping arterial partial pressure of oxygen (PaO2) is <55 mm Hg or their arterial oxygen saturation (SaO2) is <88% with or without hypercapnia; or
their PaO2 is between 56 mm Hg and 60 mm Hg or their SaO2 is 89%, if they have pulmonary hypertension or peripheral edema suggesting congestive heart failure or polycythemia.
Oxygen therapy should be used around-the-clock for patients with resting hypoxemia, and for exercise and/or sleep if these are when hypoxemia is present.
Also consider referring patients with severe to very severe COPD for lung volume reduction surgery (LVRS). While LVRS can improve patients' chances for better exercise capacity, lung function and quality of life, it does not improve overall survival over medical therapy alone.
Survival may be improved, however, in patients with predominantly upper lobe emphysema and poor exercise tolerance. Do not consider LVRS for patients whose predicted FEV1 is <20% and who have either homogenous emphysema or carbon monoxide diffusing capacity of <20% predicted. LVRS is also not recommended in patients with non-upper-lobe emphysema and high baseline exercise capacity.
Treating and preventing exacerbations
Bronchodilators reduce the frequency of exacerbations in patients with chronic COPD. Add inhaled corticosteroids to patients' bronchodilator regimen if their COPD is severe and they continue to have repeated exacerbations.
Typically, moderate to severe outpatient exacerbations are treated with a course of up to two weeks of oral corticosteroids, generally beginning at 40 mg/day of prednisone or equivalent. Corticosteroids may not be necessary for mild exacerbations. Increase doses of short-acting bronchodilators to relieve dyspnea symptoms.
Consider antibiotics for outpatient COPD exacerbations if patients have signs or symptoms of pulmonary infection. Always consider antibiotics for patients with one major exacerbation criterion and an abnormal chest X-ray result or a predicted FEV1 <30%.
For mild exacerbations, consider a course of doxycycline or trimethoprim/sulfamethoxazole. For unresponsive mild exacerbations or for moderate or severe exacerbations, consider a beta-lactam/beta-lactamase inhibitor, extended-spectrum macrolides, second- or third-generation cephalosporins, or a fluoroquinolone.
And consider the following in patients with exacerbations to alleviate shortness of breath and sputum production:
chest physiotherapy, percussion and vibration, and postural drainage to enhance sputum clearance and alleviate shortness of breath;
relaxation techniques to reduce anxiety from shortness of breath;
breath control, pursed lip breathing and diaphragmatic breathing to alleviate shortness of breath; and
nutritional intervention if needed to achieve ideal body weight.
Hospitalize patients with severe COPD exacerbations who do not respond to outpatient management.
Refer patients to the emergency department if they experience loss of alertness or two or more of the following parameters, indicating a severe exacerbation:
- dyspnea at rest
- a respiratory rate of >25 or more breaths per minute
- a heart rate of >110 beats a minute or more
- the use of accessory muscles
Patients can be discharged from the emergency department only when they don't need to use inhaled bronchodilators more than every four hours and if they can be managed with oral or inhaled medication or both, not intravenous medication.
Admit COPD patients who are experiencing impending respiratory failure, acute respiratory failure with progressive deterioration or chronic respiratory failure. Place them in intensive care if they are confused, lethargic, have respiratory muscle fatigue or need assisted mechanical respiration.
Teach all COPD patients the following:
- proper inhaler technique
- the signs of condition deterioration and exacerbations
- the proper use of medications and exercise
- precautions to take when traveling by air, particularly if patients have borderline oxygenation
- the value of frequent visits and telephone contact to relieve symptoms
- possible medication side effects and medication interactions
Regularly evaluate COPD patients to monitor their disease progression, medical adherence and response to therapy.
Observe how they use inhalers and reinforce inhaler training. Also ask about exacerbations, dyspnea level and patients' activity level, and alter therapy accordingly.
Monitor pulmonary function periodically to determine if therapy needs to be changed, particularly if patients' respiratory status has changed. For patients who began oxygen therapy during an acute exacerbation, consider evaluating them within three months to see if oxygen is still needed to maintain an arterial oxygen saturation >90% or a PaO2 >60 mm HG.
|The PIER module for COPD is online.|
The information included herein should never be used as a substitute of clinical judgment and does not represent an official position of ACP.
A pulmonary specialist for close to 30 years, James F. Donohue, FACP, is a professor of medicine and chief of pulmonary and critical care medicine at the University of North Carolina at Chapel Hill School of Medicine. He spoke to ACP Observer Special Focus about COPD:
On the importance of quitting smoking:
There is no disease-modifying intervention in COPD except smoking cessation. We now know that inflammation, particularly in the small airways, continues after cessation, as does oxidative stress. So these interact, damaging the lungs, muscle, bone marrow, brain and other organs. There is no doubt that COPD is systemic.
On the controversy and benefits of early screening:
Identifying COPD by spirometry lets us redouble our efforts to work with the smoking problem. And if we see severity—apparent only through symptoms and spirometry—that can help tailor therapy and smoking cessation.
Because the key to therapeutic intervention is smoking cessation, some would say it doesn't matter if you screen, but I feel it's worthwhile.
On "steroid phobia":
Fear of prescribing these drugs is a major problem because internists are concerned with side effects. Oral steroids like prednisone and methylprednisolone can induce cataracts, myopathies, diabetes and osteoporosis. I favor inhaled steroids to prevent exacerbations and the bursts of oral systemic steroids.
On new drugs:
The new once-a-day drugs, like tiotropium, will enhance adherence, as will twice-a-day drugs like the long-acting beta2-agonist formoterol. But the costs are prohibitive: A one-month supply, on average, is $120 for one inhaler.
On COPD and coronary disease:
Studies are showing that COPD patients taking inhaled corticosteroids are suffering fewer coronary insults. While 120,000 die officially of COPD every year, the number of those who die of coronary artery disease with COPD listed as a contributing factor is twice as high.
In internal medicine, everybody we see has issues like diabetes, coronary disease and COPD—they all go together. The internist's role is ever more important because with COPD, you need to look at the total patient.
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