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Chronic Obstructive Pulmonary Disease in Long-Term Care
Chronic obstructive pulmonary disease (COPD) is a disease with a progressive and complex nature, and therefore is commonly found in nursing home residents. COPD has been found to be as likely as kidney disease to lead to admission to a skilled nursing facility in elderly patients who underwent coronary artery bypass surgery. Whereas death from heart disease and stroke are declining, the death rate from COPD is on the increase. According to one study, one in every six admissions to nursing homes was for patients with a history of emphysema or COPD. Tobacco smoking is the primary cause of COPD in 80-90% of persons who have the disease. This article discusses relevant issues for persons with COPD residing in LTC facilities.
Chronic obstructive pulmonary disease (COPD) occurs in about 5% to 6% of the U.S. adult population. The typical patient with COPD is an elderly person who smoked cigarettes for years, has multiple comorbidities, and is significantly limited by his or her disease(s). Tobacco smoking is the primary cause of COPD in 80-90% of persons who have the disease1 and is characterized by a progressive decline in lung function and functional impairment. COPD has a significant impact on society; the death rate from COPD is increasing, whereas death due to heart disease and stroke are declining. Because of the progressive and complex nature of COPD, it is a common disease encountered in the nursing home resident. This review article will discuss relevant issues for persons with COPD residing in long-term care (LTC) facilities.
COPD in the Nursing Home
A significant number of individuals with COPD are admitted to LTC facilities at some point in their disease. According to one study, about one of every six admissions to nursing homes was for patients with a history of emphysema or COPD.2 In the last 12 months of COPD patients’ lives, one recent study reported there was a 40% likelihood of being admitted to a LTC facility.3 The presence of COPD was as likely as kidney disease to lead to admission to a skilled nursing facility (SNF) in elderly patients who underwent coronary artery bypass surgery.4 In 2004, 10% of patients with COPD enrolled in California Medicare were admitted to a SNF.5 In a Medicaid COPD population, approximately 22% of the respiratory-related healthcare costs are nursing home costs; a greater amount was spent on hospitalizations (approximately 50%).6
COPD Guidelines
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, an international effort, became available in 2001 and has been updated annually (www.goldcopd.org).7 The American Thoracic Society (ATS) and European Respiratory Society (ERS) also developed joint guidelines in 2004, similar to GOLD in many regards, but they provide additional information on some topics (www.thoracic.org). There likely will be increased quality assurance healthcare initiatives involving patients with COPD based on these guidelines.
Definition/Prognosis
Chronic obstructive pulmonary disease is defined as a disease characterized by airflow limitation (obstruction) that is not fully reversible. The airflow limitation is progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases (eg, tobacco smoke). The ATS defines chronic bronchitis as a chronic productive cough for 3 months in each of 2 consecutive years in a patient in whom other causes of chronic cough have been excluded. Emphysema is pathologically defined as the presence of permanent enlargement of airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Many persons with COPD have a mixture of these two diseases, and a notable portion also have concurrent asthma.
Anywhere between 15% and 50% of smokers develop COPD.8 As airflow limitation progresses, lung hyperinflation and gas trapping develop. This leads to breathlessness on exertion and a diminished ability to participate in activities that require exertion, obviously impacting on quality of life. Premature death is expected in persons with COPD.
Prevalence
In contrast to other common diseases associated with death, such as stroke and coronary heart disease, the mortality rate associated with COPD continues to increase, and in 1998 was the fourth leading cause of death due to chronic diseases. There appears to be a shift in the male:female ratio for this disease; in 2000 there were more deaths from COPD in women than in men.9 COPD has been diagnosed in 16 million people—14 million with chronic obstructive bronchitis and 1.8 million with significant clinical emphysema. In a U.S. survey of more than 16,000 persons, which included pulmonary function testing, 24% of smokers had airflow obstruction, 13% of ex-smokers, and 7% of never-smokers.10
Comorbidities in COPD
COPD is a systemic disease—many organs are affected.11 Due to advanced age and smoking history, the typical COPD patient has multiple comorbidities. A recent study showed that the most common causes of death in COPD are respiratory, cardiac, and cancer.12 The typical individual with COPD admitted to a LTC facility will have multiple health issues, and depending on the patient, COPD may or may not be the primary health problem. The majority of persons with COPD have cardiovascular disease including coronary artery disease, heart failure, and hypertension.13 Stroke occurs in a significant portion of persons with COPD. About 25% of persons with COPD have concurrent asthma. Disability is common as the disease progresses. Age-related and steroid-induced osteoporosis occur frequently in persons with the disease, and COPD is a risk factor for nursing home–associated pneumonia. A significant number of persons with COPD have obstructive sleep apnea. Depression and anxiety are also common in COPD; one study found that 40% of persons with COPD have depressive symptoms.14 Diabetes mellitus occurs in about 25% of persons with COPD.5
Malnutrition is a significant issue in some individuals with COPD. Substantial chronic airway obstruction leads to greater energy requirements due to the increased work of breathing, as well as inactivity from deconditioning. Chronic systemic steroids (eg, prednisone) also contribute to skeletal muscle breakdown and weakness.
Diagnosis
Diagnosis of COPD is based on clinical history—a history of exposure to risk factors (smoking) and the presence of airflow obstruction that is partially reversible, with or without the presence of symptoms.7 Spirometry pulmonary function testing assesses the expiratory volumes and flow rates of the respiratory system. Basic spirometry estimates the individual’s forced expiratory volume in 1 second (FEV1) and the forced vital capacity (FVC). In an obstructed patient, the FEV1 is reduced in proportion to the FVC; a ratio of FEV1/FVC less than 70% is consistent with obstructive lung disease. The FEV1 is further used to stage the severity of COPD (eg, mild COPD FEV1/FVC < 70%, and FEV1 > 80% predicted). The diagnosis of COPD should be considered in people older than age 40 years with exposure to risk factors (typically being a smoker) and/or persistent symptoms associated with COPD (Table).7
Guidelines for Management
Currently, various staging systems are used to classify the severity of COPD. The Table denotes the staging of COPD severity and general information about treatment.
Management of Stable COPD
The overall approach to the management of stable COPD is a stepwise increase in drug treatment depending on the disease severity.7 The goals for management include the following: (1) early and accurate diagnosis; (2) prevention of disease progression (deterioration of pulmonary function); (3) relief of symptoms; (4) improvement in exercise tolerance and health status; (5) prevention and treatment of exacerbations and complications; (6) improvement in quality of life; and (7) reduction in mortality.
Management of stable COPD includes drug therapy, smoking cessation, oxygen, pulmonary rehabilitation, and nutritional intervention. Attention to all of these issues are necessary for optimal management of the person with COPD.
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Drug Therapies
Drug therapies for COPD include inhaled beta2-agonists, inhaled anticholinergics, theophylline, corticosteroids, mucolytics, expectorants, and antibiotics. The COPD guidelines provide general recommendations on their use in COPD. For the pharmacotherapy of stable mild to very severe COPD, patients should be receiving short-acting bronchodilators such as ipratropium. As the patient reaches moderate-severity disease, long-acting bronchodilators can be added, and in some patients inhaled corticosteroids (ICS). Based on the currently available evidence, ICS are recommended only in patients with severe and very severe COPD (FEV1 < 50% by GOLD classification) and who have frequent exacerbations.7 According to COPD guidelines, bronchodilator medications are central to the symptomatic management. These agents help with dyspnea, quality of life, and lessening of the frequency of exacerbations.
Some basic concepts about the agents in COPD include:
• Starting with short-acting agents.
• Combining beta2-agonists with anticholinergics provides additive bronchodilation above either agent alone.
• Adding long-acting agents to short-acting agents may provide additional bronchodilation when given in combination with short-acting agents.
Beta2-Agonists. Short-acting agents, albuterol and levalbuterol (isomer of albuterol), are generally very effective bronchodilators in COPD. These agents provide bronchodilation for 4-8 hours. Long-acting beta2-agonists are salmeterol, arformoterol nebulized solution, and formoterol nebulized solution and dry powder inhaler (DPI). Salmeterol begins working within 30-45 minutes, peaks at 1 hour, and lasts 12 hours. Formoterol and arformoterol induce bronchodilation within 5 minutes, achieve near-maximal bronchodilation by 30 minutes, and last 12 hours. A new once-a-day inhaled beta2-agonist, indacaterol, will likely be marketed in the near future. Side effects of beta2-agonists seen in the elderly person with COPD include tremors, tachycardia, and headache. The concerns about increased mortality with long-acting beta2-agonists, as described in asthma, have not been proven in the COPD population.12
Anticholinergics. Inhaled anticholinergics are ipratropium bromide and tiotropium bromide. Ipratropium provides bronchodilation within 30 minutes and typically lasts 6 hours. Tiotropium is a long-acting agent (dosed once daily) with an onset of about 20-30 minutes and a duration of 24 hours. Tiotropium is a more potent bronchodilator than ipratropium at usual doses because of differences in affinity for muscarinic receptors in the airways. It is recommended to discontinue ipratropium when initiating tiotropium. Ipratropium adds little additional bronchodilation to tiotropium, likely only adding anticholinergic side effects. A recent meta-analysis suggested that inhaled anticholinergics increase the risk of cardiovascular deaths; this is unproven at present but needs further investigation.15 The combination of albuterol and ipratropium will be administered in a different inhaler by 2010, due to removal of chlorofluorocarbons (CFCs) in metered dose inhalers (MDIs).
Methylxanthines. Theophylline is generally reserved for persons with COPD who do not respond or cannot take inhaled long-acting bronchodilators. It provides additive effects on symptoms and breathing tests with inhaled beta2-agonists and anticholinergics. Theophylline also decreases breathing muscle fatigue, stimulates central breathing drive, and exerts mild anti-inflammatory effects. A theophylline level in the range of 8-12 mcg/mL (not the traditional 10-20 mcg/mL) is preferred. This decreases the risk of adverse effects and the impact of drug interactions. Theophylline levels should be monitored with initiation of therapy, changes in dosing, suspicion of adverse effects (eg, nausea, vomiting, tachycardia), sometimes to assess the impact of drug interactions, and perhaps annually. Generic sustained-release theophylline is a relatively inexpensive long-acting bronchodilator. Agents that work like theophylline, phosphodiesterase inhibitors, are currently under investigation.
Inhaled Corticosteroids. ICS are used in a significant portion of persons with COPD. The primary benefit shown among studies is the decreased frequency of respiratory exacerbations in COPD. A large, prospective, randomized, placebo-controlled study compared inhaled high-dose fluticasone, salmeterol, high-dose fluticasone/salmeterol, and placebo in persons with moderate and severe COPD.12 The primary outcome measure, all-cause mortality, showed a favorable trend but was not statistically different among the treatments. Exacerbations were less frequent in the fluticasone and fluticasone/salmeterol groups. Of note, bacterial pneumonias were more common in the ICS groups.
The two marketed combination agents are fluticasone/salmeterol and budesonide/formoterol, the latter of which is not currently approved for COPD in the United States. The recommended dose of fluticasone/salmeterol for COPD is 250 mcg/50 mcg, although some studies have used higher doses. There are no compelling data that the higher strength of fluticasone/salmeterol 500 mcg/50 mcg provides additional benefit in COPD. Side effects may be greater with the higher dose.
Oral Corticosteroids. Systemic steroids, usually oral prednisone, are more commonly used for COPD exacerbations and less commonly chronically in persons with the most severe COPD. A meta-analysis found that some persons with COPD responded favorably to steroids.16 Reported rates of improvement in FEV1 in those responding to oral steroids ranged from 0% to 56% as compared to those responding to placebo. Chronic or frequent use of systemic steroids warrants the use of agents to prevent steroid-induced osteoporosis, including calcium/vitamin D and bisphosphonates. Of note, many persons with COPD receive acid-suppressive agents such as proton pump inbibitors. Calcium citrate is the preferred calcium salt to optimize gastrointestinal absorption in this situation.
Expectorants/Mucolytics. Mucolytics and/or expectorants, such as guaifenesin, are sometimes used in persons with COPD. A Cochrane review indicated that mucolytics can decrease exacerbations in COPD and improve quality of life.17 Oral (and rarely inhaled) acetylcysteine may be useful as a mucolytic in COPD. Inhaled N-acetylcysteine may cause bronchospasm. Inhaled dornase alfa is not recommended for COPD.
Vaccinations. The severity of respiratory infections, the primary cause of acute exacerbations in COPD, can be reduced by the use of influenza and pneumococcal vaccines. An annual influenza vaccination has been shown to result in fewer outpatient visits and hospitalizations.18 The ATS/ERS guidelines recommend influenza and pneumococcal vaccinations for persons with COPD. The intranasal influenza vaccination should not be used in persons with COPD, due to the potential for respiratory reactions.
Smoking Cessation. Pharmacologic therapies increase smoking cessation rates. Bupropion, varenicline, and nicotine replacement therapies are all effective interventions. Bupropion may cause sleeplessness and, rarely, increases the risk of seizures and cardiac abnormalities. Recently, mental status changes have been reported with varenicline. Nicotine replacement therapies are generally safe in the elderly person and have a quicker onset than the other therapies, a consideration when an individual is admitted to the nursing home who has recently quit smoking.
Nonpharmacologic Management
COPD is preventable in its earliest phase and treatable in all stages. Certain nonpharmacologic interventions may be useful, such as smoking cessation, patient education, vaccinations, supplemental oxygen, pulmonary rehabilitation, and surgeries. Lung volume reduction surgery or lung transplantation may be undertaken in a minority of persons with COPD. Smoking cessation is probably the single most important intervention in COPD. Long-term oxygen therapy can prolong survival and improve exercise tolerance in persons with COPD who have low oxygen levels (PaO2 < 55 mm Hg). However, literature suggests that continuous long-term oxygen use for 15-18 hours per day is needed to affect outcomes.7 Nutrition is key in the person with COPD. The work of breathing markedly increases nutritional requirements in some individuals. Physical rehabilitation can also lead to significant improvements in persons with COPD.
Management of Acute Exacerbations of COPD
Most persons with COPD experience at least one or two acute exacerbations each year, more frequently with advanced disease. Exacerbations are defined as an acute worsening of a person’s normal day-to-day condition that necessitates a change in regular drug therapy (acute change in baseline dyspnea, cough, and sputum production). Episodic acute exacerbations affect the severity and outcome of COPD—they are a very important determinant of disease progression. Patients hospitalized for acute exacerbations have a 3% to 4% mortality rate; those requiring intensive care have a higher mortality rate. As COPD worsens, lung function progressively deteriorates, and the rate of acute exacerbations increases markedly.
Treatment for COPD exacerbations include drug therapies (increased use of short-acting bronchodilators, antibiotics, and systemic steroids such as prednisone), oxygen therapy, and assisted ventilation, such as bilevel positive airway pressure (BiPAP). Other conditions can mimic or complicate COPD exacerbations such as other lung diseases, pulmonary hypertension, heart failure, coronary artery disease, pneumonia, and pulmonary emboli.
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Selected Drug Therapy Issues in the Person with COPD
Impact of COPD Drug Therapies on Comorbid Diseases
Drug therapies used to treat comorbidities may have special considerations in the person with COPD. The use of systemic steroids for COPD flares may alter glucose control, lead to mental status changes, contribute to osteoporosis, and cause skeletal muscle breakdown. Even in a person with COPD without diabetes mellitus, prednisone may unmask glucose intolerance within 1-2 days after starting the systemic steroid. Chronic or frequent use of systemic steroids clearly increase the risk of osteoporosis in persons with COPD; this is a frequently overlooked issue. Osteoporosis preventive therapy is strongly recommended. Calcium plus vitamin D, as well as many bisphosphonates, have been shown to decrease the likelihood of steroid-induced osteoporosis. In addition, ICS use in persons with COPD may lead to dose-related decreases in bone density.19
Infrequently, inhaled anticholinergics may worsen urinary retention, especially in the presence of prostatic hypertrophy, or they can cause constipation. Inhaled beta2-agonists may increase heart rate, lower blood potassium, and worsen tremors. Inhaled steroids may lead to an increased risk of bacterial pneumonia and bone loss in susceptible individuals.
Antibiotics for COPD Exacerbations
The most common bacteria in COPD flares include Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Pseudomonas aeruginosa, and Staphylococcus aureus. Atypicals, such as Mycoplasma, appear to be uncommon in COPD flares. Commonly used antibiotics include macrolides, fluoroquinolones, tetracyclines, and beta-lactams. Special antiobiotic considerations in the elderly person with COPD include central nervous system side effects with quinolones (eg, mental status changes with ciprofloxacin), drug interactions with quinolones (eg, binding with cations, increased warfarin international normalized ratio with levofloxacin and ciprofloxacin). Separation of the oral quinolone from the oral cation may be inadequate to avoid decreased bioavailability. The author recommends temporary discontinuation of oral cations when patients receive oral quinolones. When antibiotics are used in combination with steroids, fungal infections are more likely.
Inhalational Devices in the Elderly
Selection of the proper inhalational device is an issue in the older person with COPD. One question is whether to administer inhaled drugs via an inhaler versus a nebulizer. There is normally a higher cost associated with administering a drug via nebulization as compared to an MDI, with or without a spacer. The most effective inhalation strategy depends on the situation. For example, if a patient is in a facility for a few days, it might be cheaper to administer the agent(s) via nebulization rather than paying for a 15-day or 30-day supply of a MDI.
Medicare currently covers nebulizer equipment and some nebulized drugs for outpatient use. Elderly persons tend to have difficulty with inhaler technique.20 Elderly patients may be able to inhale drugs more effectively via a nebulizer. However, its use requires more time and also requires regular cleaning of the nebulizer; there are reports of patients developing lung infections due to contaminated nebulizers. The patient with advanced COPD may have difficulty with both deep and rapid inspiration. The author typically encourages patients to stand up when possible when using their inhalers to increase lung deposition of drug. The use of a spacer with an MDI can help with poor inhaler technique, as well as decrease local side effects.
An increasing number of drugs are available as DPIs. DPIs are more effort-dependent to ensure good drug delivery.21,22 The budesonide DPI and likely the formoterol fumerate DPI require rapid inspiratory rates for optimal lung deposition, which may be difficult for some persons with COPD to achieve. The author normally does not recommend these devices in persons with more advanced COPD. In one study, approximately 50% of persons with COPD were unable to generate an adequate inspiratory rate for one type of budesonide DPI.23 In one study, one tiotropium bromide DPI was reported to provide good lung delivery at low inspiratory rates in persons with COPD.24 There do not appear to be differences in efficacy between a MDI and nebulizer for exacerbations of COPD.25
Agents to Use with Caution in COPD
Certain agents should be used cautiously or should be avoided in the treatment of COPD. Some drugs may be more likely to have side effects in the elderly person with COPD. Cough suppressants may block the protective role of cough; however, most cough suppressants do not completely stop a cough, and thus patients are generally able to continue to expectorate sputum. Narcotics may cause respiratory depression if used in excessive doses or if used in combination with other respiratory depressants such as benzodiazepines. Benzodiazepines alone may also cause respiratory depression. Persons with COPD who are carbon dioxide retainers (maintain above-normal arterial CO2 levels) are more apt to develop respiratory depression from narcotics or benzodiazepines.
If necessary to use narcotics and/or benzodiazepines in the elderly person with COPD, use the lowest effective dose and monitor respiratory status (eg, respiratory rate, shallow vs deep breathing). Some persons with COPD do have difficulty with persistent anxiety for a variety of reasons including chronic dyspnea, so it’s best to use the lowest effective dose of benzodiazepine or use an alternative anti-anxiety agent such as buspirone. Zolpidem appears to be a relatively safe hypnotic in the elderly individual.26 Narcotics may be used to relieve severe dyspnea in persons with terminal disease (eg, a patient enrolled in hospice). The bedridden individual with COPD may be more susceptible to narcotic-induced constipation.
Beta blockers to treat coronary heart disease or heart failure are sometimes avoided in COPD because of concerns of worsening respiratory status. In a group of persons with heart failure, beta blockers were used infrequently (< 10%) in patients with concurrent COPD, likely due to concerns of worsened lung function.27 In this study, long-term survival was better if the persons with COPD were taking beta blockers. In contrast to persons with asthma, bronchospasm from beta1-selective agents appears to be uncommon in individuals with COPD. A large Cochrane meta-analysis indicated that cardioselective (eg, metoprolol) beta blockers did not lead to decrease in FEV1 or worsened respiratory symptoms in persons with COPD.28 However, care should be taken when first starting a beta blocker in a person with COPD—especially in the patient with concurrent asthma a cardioselective agent should be used. Less frequently, nonselective beta-blocker eye drops may also induce bronchospasm.
Summary
The prevalence of COPD and its associated healthcare costs are significant and growing, including in the LTC population. As the population ages, COPD will take an ever-increasing toll on already-strained healthcare resources. With early diagnosis and comprehensive drug treatment, coupled with smoking cessation, vaccines, and pulmonary rehabilitation, this course can be altered. Pharmacologic interventions, especially the use of bronchodilators, can lessen symptoms and improve patients’ quality of life. Steroids have a significant role in COPD as well. Long-term treatment and monitoring are essential if the management of COPD is to be successful; COPD is not an irreversibly disabling disorder.