CHAPTER 11. PULMONARY DISEASE
Kim K. Kuebler and Rhalene Gabuat Patajo
The increased prevalence of nonmalignant pulmonary disease is often underestimated because chronic obstructive pulmonary disease (COPD) is often underdiagnosed and poorly defined (Global Initiative for Chronic Obstructive Lung Disease [GOLD], 2005; Voelkel & Agusti, 2004). COPD is a major cause of morbidity and mortality throughout the world and is the fourth leading cause of death in the United States. In 2000, COPD was listed as the underlying cause of death for almost 119,000 American adults, which is a 67% increase compared with 52,000 deaths in 1980 (Centers for Disease Control and Prevention [CDC], 2002). By 2020, COPD is predicted to become the third leading cause of death in the United States and worldwide (GOLD, 2005; National Heart, Lung, and Blood Institute [NHLBI], 2001).
The increase in age-adjusted mortality rates for COPD between 1965 and 1998 distinguishes it from other diseases such as coronary heart disease or stroke, which have demonstrated a decrease in mortality rates over the same period of time (Anderson, 2002; Minino, Arias, Kochanek et al., 2002). COPD is the only leading cause of death in the United States for which the death rate is increasing (Doherty, 2005). The World Health Organization (WHO) estimates that 2.5 million deaths worldwide were the result of COPD in 2001 (WHO, 2003). In 2002 in the United States, the annual direct costs for COPD were more than $32 billion (Hilleman, Dewan, Malesker et al., 2000; NHLBI, 2002). Because of the morbidity and mortality associated with COPD, the economic implications of COPD in the United States are significant.
Of the estimated 24 million cases in the United States, less than 50% of these patients are given an accurate diagnosis of COPD (Mannino, Homa, Akinbami et al., 2002). The lack of proper diagnosis is fueled in part by clinical misconceptions of the demographics of this disease (Dransfield & Bailey, 2005). For the first time in history, the number of deaths in the United States from COPD was higher among women than among men in 2000, and the COPD death rate for women tripled from between 1980 and 2000 (CDC, 2002). In addition, the majority of COPD cases occur in patients younger than 65 years; in 2000, only 30% of reported cases occurred in older age groups. This evidence challenges the traditional assumption that COPD is a disease of the elderly male patient (CDC, 2003).
Pulmonary function and exercise abilities differ between geriatric and younger populations (Chan & Welsh, 1998). The elderly are susceptible to an increased risk of pulmonary disease over time, and the presentation of these diseases will differ in the middle-aged adult and the elderly (Chan & Welsh, 1998). The elderly patient will have less respiratory reserve to blunt a hypoxic or hypercarbic drive or to perceive the experience of dyspnea (Chan & Welsh, 1998). The burden of COPD in an increasingly aging society is likely only to increase, and so the importance of integrating palliative management for the myriad accompanying symptoms is critical.
DEFINITION
The current and widely accepted definition of COPD was proposed by WHO and NHLBI through an initiative identified as GOLD (2005). This collaborative project identified new guidelines for the diagnosis and treatment of COPD (Bramen & Peters, 2005). Prior to the GOLD guidelines, COPD was defined as a disease process caused by chronic bronchitis and emphysema. This definition has been replaced by new information suggesting that COPD is a result of airflow limitation—a reaction to the abnormal inflammatory response in the lungs from prolonged exposure to noxious gases. The American Thoracic Society (ATS) and the European Respiratory Society (ERS) offer a joint definition of COPD identical to the GOLD guidelines, describing COPD as “a preventable and treatable disease state characterized by airflow limitation that is not fully reversible” (ATS, 2004). “Airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles of gases primarily caused by cigarette smoking” (ATS, 2004). Although the new GOLD definition for COPD no longer identifies this disease as an irreversible process, both guidelines recommend the use of staging criteria to prognosticate COPD, ranging from “at risk” to “very severe” disease (ATS, 2004; GOLD, 2005). However, COPD is considered a progressive disease, and the goal of care is often to reduce the progression of disability and symptoms.
COPD encompasses both chronic bronchitis and emphysema. Chronic bronchitis occurs in most patients with COPD in the earlier phases of the disease, whereas emphysema is less common and often presents much later in the course of disease, accompanied by significant symptom burden (cachexia, dyspnea, fatigue, etc.). Chronic bronchitis is defined by the ATS/ERS guidelines as “chronic productive cough, lasting for three months over two successive years in a patient in whom other causes of productive cough have been excluded” (ATS, 2004). Emphysema is further defined as “permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of the walls of the alveoli without obvious fibrosis” (ATS, 2004).
THE COPD PATIENT
Many clinicians hold stereotypical views on the “typical” COPD patient as being elderly and male. The validity of this traditional approach to COPD was analyzed through a retrospective study of more than 2100 COPD patients managed by the National Jewish Medical and Research Center (Tinkelman & Corsello, 2003). This study was designed to evaluate the socioeconomic, demographic, and resource utilization of current COPD patients. The investigators concluded that COPD patients are younger than previously identified and are typically described by the following characteristics:
▪ Continues to smoke cigarettes despite having moderate to severe disease
▪ Just as likely to be female (52.7%) as male (47.3%)
▪ Older than 40 years
▪ Just as likely to be employed as unemployed
▪ Is not diagnosed in the early stages of disease
▪ Has increased use of health care services compared to same-age individuals in the general population (Doherty, 2005; Tinkelman & Corsello, 2003)
The diagnosis of COPD has been historically assigned to patients who have emphysema, chronic bronchitis, or a mixture of the two. Many patients will complain of having increased dyspnea over several years and are positive for chronic cough, poor exercise tolerance, and evidence of airway obstruction such as overinflated lungs and poor gas exchange (West, 2003). Appropriate diagnosis, therefore, is absolutely essential when effectively managing a specific pulmonary disease.
ETIOLOGY AND PATHOPHYSIOLOGY
The classic epidemiologic studies of Fletcher and Peto (1977) revealed that death and disability from COPD were related to an accelerated decline in lung function over time, with a loss of more than 50 mL per year in the forced expiratory volume over 1 second (FEV 1) compared with a normal loss of approximately 20 mL per year. A reduction in FEV 1 in the face of progressive disease over time contributes to increased dyspnea on exertion and slowly advances to respiratory failure (Barnes, 2004).
There is considerable debate regarding the reasons for the accelerated loss of FEV 1 and its relation to the pathogenesis of COPD. However, there are four major mechanisms that have been implicated (Barnes, 2004):
1. Loss of elasticity and the destruction of the alveolar attachments of airways during expiration
2. Increased cholinergic bronchomotor tone in the airways via release of acetylcholine by way of the parasympathetic nervous system
3. Narrowing of small airways as a result of inflammation and scarring
4. Mucus blocking of small airways
All four of these mechanisms can interact with one another and are often induced from cigarette smoking and the inhalation of noxious particles. Narrowing of the small airways results in hyperinflation of the lungs and air trapping contributing to dyspnea and cough (Barnes, 2004). The structural changes that occur in the aging lung and chest wall produce predictable alterations in pulmonary function tests. The elderly patient will tend to have a decrease in his or her vital capacity, which is a direct result of the following (Chan & Welsh, 1998):
▪ Increased chest wall stiffness (muscle atrophy, weakness, arthritis, etc.)
▪ Loss of elastic recoil of the lung and supportive connective tissue
▪ Decreased respiratory force generated by respiratory muscles
Obstructive and Restrictive Airway Disease
The differentiations in obstructive and restrictive airway diseases are often blurred and may give rise to the difficulties in definition, diagnosis, and management of specific diseases (i.e., asthma, COPD, bronchitis, emphysema, and malignancies). Obstructive airway disease is an increased resistance to airflow and can be caused by conditions that occur inside the pulmonary lumen, within the wall of the airway, and/or in the peribronchial region (West, 2003). Airway lumen, for example, may be blocked by excessive secretions often found in patients with chronic bronchitis. Other examples of airway lumen blockage include a partially occluded lumen from pulmonary edema, aspiration of a foreign object, or any substance that creates a partial or complete blockage within the airway lumen (West, 2003).
Disease that affects the internal wall of the airway includes the contraction of the bronchial smooth muscle that occurs in asthma as a result of the inflammatory process of the airway epithelium. Hypertrophy of the mucus glands that accompanies chronic bronchitis can also interfere with airway obstruction within the lumen (West, 2003). Prolonged exposure to noxious gas contributes to the destruction of the lung parenchyma, which causes a loss of the radial traction of the connective tissues within the lung and consequent airway narrowing (West, 2003).
Cigarette smoke accounts for more than 90% of cases of COPD in developed countries; however, COPD occurs in only a minority of smokers (10% to 20%), indicating individual variations in susceptibility to this disease (Barnes, 2004). Research in this area is ongoing and includes evaluation of patient-specific phenotype, pathologic mediators of disease, involved cellular mechanisms, and newly identified environmental factors.
Emphysema
Emphysema is characterized by an enlargement of the air spaces (alveoli) distal to the terminal bronchiole with associated airway lumen destruction (West, 2003). The associated loss of elasticity and the destruction of the alveolar attachments in the lung promote narrow airways and air trapping (hyperinflation) (Barnes, 2004). Cigarette smoke may stimulate the neutrophil to release excessive amounts of the enzyme lysosomal elastase. This results in the destruction of elastin, an important structural protein in the lung (West, 2003). Neutrophil elastase also binds to type IV collagen, an important molecule that influences the strength of the pulmonary capillary and the integrity of the alveolar wall (West, 2003).
Chronic Bronchitis
This disease is associated with an excessive production of mucus secretions within the bronchial tree. Hypertrophy of the mucus glands in the large airway and chronic inflammation of the airway contribute to airway narrowing—a result of lumen thickening, inflammation, and scarring in the small airways (West, 2003). In chronic bronchitis, excessive amounts of mucus are found in the airways, and thickened mucus may occlude some small bronchi (West, 2003). Small airways are narrowed and show inflammatory changes that include cellular infiltration and airway edema. Granulation tissue and peribronchial fibrosis occur over time (West, 2003).
Asthma
Asthma is an inflammatory response of the airways to various stimuli (antigens) that potentiate airway narrowing. The airways of an asthmatic patient respond to stimuli by hypertrophied smooth muscle that contracts and produces bronchoconstriction. The bronchial airway contains hypertrophy of the mucus glands and edema of the bronchial wall with an increased integration of eosinophils and lymphocytes (West, 2003).
Restrictive Disease
Restrictive diseases are those in which the expansion of the lung is restricted because of alterations in the lung parenchyma or because of disease of the pleura, chest wall, or neuromuscular apparatus. They are characterized by a reduced vital capacity and a small resting lung volume, but the airway resistance is not increased. It is important to note that restrictive and obstructive conditions can be present concurrently.
▪ Diffuse interstitial pulmonary fibrosis Thickening of the interstitium of the alveolar wall may be caused by an immunologic reaction. The patient presents with dyspnea, rapid and shallow breathing, and an irritating, unproductive cough.
▪ Sarcoidosis Granulomatous tissue is present in several organs (lymph nodes, lungs, skin, eyes, liver, spleen, etc.). Fibrotic changes in the alveolar walls are seen, and pulmonary fibrosis and cor pulmonale may develop.
▪ Hypersensitivity pneumonitis This occurs with exposure to inhaled organic dusts. Fibrotic changes occur in advanced cases, and the patient is frequently dyspneic.
▪ Interstitial disease caused by drugs, poisons, radiation Busulfan, nitrofurantoin, amiodarone, bleomycin, antineoplastic drugs, and oxygen may cause an acute pulmonary reaction, which can proceed to interstitial fibrosis. Therapeutic radiation causes acute pneumonitis followed by fibrosis.
▪ Collagen disease Interstitial fibrosis may be found in patients with generalized scleroderma, systemic lupus erythematosus, or rheumatoid arthritis.
▪ Lymphangitis carcinomatosa Spread of carcinoma tissue through pulmonary lymphatics leads to prominent dyspnea.
▪ Pneumothorax This occurs in a variety of conditions, including rupture of a bulla in COPD, rupture of a cyst in advanced fibrotic disease, or during mechanical ventilation with high airway pressures, and often precipitates breathlessness/dyspnea.
▪ Pleural effusion Fluid in the pleural space frequently accompanies serious disease, and the patient often reports dyspnea if the effusion is large.
▪ Scoliosis Bone deformities can cause an increased work of breathing.
▪ Ankylosing spondylitis Gradual immobility of the vertebral joints and fixation of the ribs result in reduced movement of the chest wall.
▪ Neuromuscular disorders Poliomyelitis, Guillain-Barré syndrome, amyotrophic lateral sclerosis, myasthenia gravis, and muscular dystrophies affect the muscles or nerves of respiration (West, 2003).
HISTORY AND PHYSICAL EXAMINATION
History
Diagnosing and managing advanced pulmonary disease require a history of exposure to risk factors that contribute to airflow limitation with or without symptoms (GOLD, 2005). COPD, however, should be considered in any patient who has had cough, sputum production, or dyspnea and who smokes or is exposed to noxious gases (Table 11-1).
| Signs and Symptoms | |
|---|---|
| Chronic cough | Intermittent or every other day |
| Occurs throughout the day | |
| Rarely occurs only during nocturnal hours | |
| Chronic sputum production | Any pattern of chronic sputum production |
| Dyspnea | Progressive (worsens over time) |
| Persistent, daily | |
| Patient complains of an increased effort to breathe | |
| Unable to exercise | |
| Worse during respiratory infections | |
| Risk factors | Tobacco smoke |
| Occupational dusts and chemicals | |
| Smoke from home cooking, heating fuels |
▪ Past medical history of asthma, allergies, sinusitis, frequent respiratory infections in childhood, nasal polyps, and/or other respiratory difficulties in the adult patient
▪ Family history of COPD, α-1 deficiency, or other chronic respiratory diseases
▪ Pattern of symptom development that would include age of onset, dyspnea in colder temperatures, with physical exertion, aggravating/relieving factors, and so on
▪ History of respiratory exacerbations and/or frequent hospitalizations
▪ Concomitant comorbidities such as respiratory infections, ischemic heart disease, hypertension, congestive heart failure, or asthma (Kesten, 2001)
▪ Review of current medications (β-blockers are contraindicated in COPD patients)
▪ Patient-perceived quality of life
▪ Whether social and family support are available
▪ Reduction of risk factors (GOLD, 2005)
As patients develop moderate to severe COPD (FEV 1 less than 50%), they often present with
▪ Sleep apnea or nocturnal O 2 desaturation
▪ Pulmonary hypertension with exertion (exercise)
▪ Hypercarbia
▪ Weight loss, muscle wasting (cachexia)
▪ Increased incidence of depression
▪ Pulmonary hyperinflation (on chest radiograph) (Voelkel & Agusti, 2004)
Physical Examination
Objective evaluation of the COPD patient may vary from patient to patient, but common findings often include the following (GOLD, 2005):
▪ Central cyanosis or a bluish, pale discoloration of the mucous membranes
▪ Chest wall structural abnormalities that resemble a “barrel-shaped” chest, horizontal ribs, and/or protruding abdomen
▪ Reduction in cardiac dullness, difficulty in auscultation heart apex beat, due to pulmonary hyperinflation (best auscultated over the xiphoid area)
▪ Resting shallow respiratory rate of 20 breaths per minute, reduced breath sounds
▪ Prolonged expiratory effort, pursed lip breathing, and use of accessory muscles to breathe
DIAGNOSTICS
It is important to efficiently decide and administer diagnostics that will not add further symptom burden to the pulmonary patient, bearing in mind that a major differential diagnosis for COPD is asthma. In patients with chronic asthma, a clear distinction from COPD is not possible by using current imaging and physiological diagnostics (GOLD, 2005). It is assumed that both COPD and asthma coexist in this patient population. Other differential diagnoses are easier to differentiate from COPD (GOLD, 2005).
Because COPD is a progressive disease, the monitoring of pulmonary function through spirometry is ideal when evaluating worsening of disease. Evaluating arterial blood gas measurement is recommended for patients with a FEV 1 less than 40% predicted or if respiratory failure or right-side heart failure is present. This should be considered only in the patient who is seeking aggressive interventions and not in the patient seeking only symptom management. Chest radiographs and spirometry may be the only diagnostic measurements needed in the palliative care setting to discern changes in pulmonary function. A complete blood cell count with differential can also identify dyspnea that is related to anemia. It is important to note that polycythemia (hematocrit greater than 55%) can develop in the presence of atrial hypoxemia and in patients who currently smoke (GOLD, 2005).
PHARMACOLOGIC INTERVENTIONS
Several guidelines have been established to help clinicians treat patients with COPD. As previously mentioned, major treatment guidelines have been endorsed by organizations such as GOLD and ATS/ERS. According to these organizations, the goals of COPD treatment should include the following (ATS, 2004; GOLD, 2005):
▪ Prevent disease progression
▪ Relieve symptoms of dyspnea and improve airflow limitation and lung function
▪ Improve exercise tolerance
▪ Improve quality of life
▪ Prevent and/or treat complications
▪ Prevent and/or treat exacerbations
▪ Reduce mortality
Currently, there is no treatment modality available to stop the progression of this irreversible disease. Because smoking is the leading cause of approximately 90% of all cases of COPD, smoking cessation is recommended to slow down disease progression (Decramer, 2005). Long-term oxygen therapy, used properly, has been shown to decrease mortality. However, because no treatment actually stops disease progression, the major focus in COPD treatment is to treat the symptoms and complications associated with the disease, to improve health status, and to improve exercise tolerance (GOLD, 2005).
There are several classes of drugs that are used to treat COPD: anticholinergics, β-agonists, steroids, theophylline, and others. Treatments are also available that combine different drug classes into one convenient form. The major COPD guidelines have recommended specific uses for each of the classes based on the patient’s disease severity, as measured by airflow limitation (FEV 1).
Inhaled medications are preferred for COPD, to deliver the drug directly to the site of action and to minimize the systemic side effects. This is particularly important in elderly patients who may have comorbid conditions. However, it is ultimately patient factors such as tolerability, convenience, proper inhaler technique, and cost that drive the choice of medications (Dolovich, Ahrens, Hess et al., 2005).
Anticholinergics
Because cholinergic activity is an important and distinctive feature in COPD, anticholinergics are recommended as first-line treatment in national and international COPD guidelines (GOLD, 2005; ATS, 2004). Anticholinergics decrease bronchoconstriction, decrease mucus secretion, and decrease bronchial vasodilation, thereby decreasing the symptoms of dyspnea and cough.
For several decades, only short-acting anticholinergics have been available, with ipratropium being the agent most commonly used. Tiotropium became the first long-acting anticholinergic agent approved for once-daily administration. All anticholinergics affect the muscarinic receptors in the airways. Tiotropium, however, has specific selectivity for the M 1 and M 3 receptors, providing long duration of action. Tiotropium has shown to improve lung function, improve dyspnea, reduce COPD exacerbations and related hospitalizations, and improve health-related quality of life (Barr, Bourbeau, Camargo et al., 2005).
Anticholinergics are available in metered-dose inhalers, dry powder inhalers, and nebulized forms. Short-acting anticholinergics can be given as needed for symptom relief or on a regular basis to prevent exacerbations, whereas long-acting anticholinergics are used as maintenance therapy to prevent exacerbations.
With anticholinergics, the most common side effect is dry mouth. This may be particularly pronounced in the elderly COPD patient, although this side effect decreases over time, allowing the patient to maintain therapy without the need for withdrawal (Tashkin & Cooper, 2004).
β-Agonists
As bronchodilators, β-agonists are also recommended as first-line treatment for COPD. β-Agonists cause bronchodilation indirectly by blocking the adrenergic receptors found on airway smooth muscle. β-Agonists improve lung function, decrease symptoms, improve exercise-induced dyspnea, decrease exacerbations, and increase health-related quality of life (Sin, McAlister, Man et al., 2003).
Short-acting and long-acting β-agonists are available in metered-dose inhalers, dry-powder inhalers, solutions for nebulization, and other combinations. For patients with intermittent episodes of dyspnea or COPD exacerbations, short-acting β-agonists may be used. Long-acting β-agonists may be used as an option for convenient maintenance therapy.
Tremor and tachycardia are a class effect of β-agonist use and are unlikely to be problematic unless the patient has preexisting heart conditions (Tashkin, 2005). Tremors can be most troublesome in older patients and may limit the dose that is tolerated (GOLD, 2005).
Corticosteroids
The exact mechanism is unknown, but corticosteroids work by affecting the inflammation cascade in COPD, although the inflammation in COPD is not completely suppressed by corticosteroids. This may be due to the fact that corticosteroids prolong the survival of neutrophils rather than suppress the neutrophilic inflammation in COPD (Barnes, 2000).
There are several forms of treatment with corticosteroids: oral, nebulized, and inhaled. Due to the side effect profile of oral corticosteroids, clinicians are encouraged to use the least amount for the shortest period of time (approximately 2 weeks) and then to transition to an inhaled corticosteroid for maintenance treatment if the patient is classified as severe or for very severely affected patients who experience frequent exacerbations (GOLD, 2005).
Oral corticosteroids have demonstrated a beneficial effect in treating acute exacerbations of COPD, improving clinical outcome and reducing the length of hospitalization. The reasons for this discrepancy between the responses to corticosteroids in acute and chronic COPD may be related to differences in the inflammatory response (e.g., increased numbers of eosinophils) or airway edema in exacerbations (Barnes, 2000).
According to COPD guidelines, inhaled corticosteroids should be reserved for the more severe patients in late-stage COPD (GOLD, 2005). The benefit of inhaled corticosteroids has not been established with regard to FEV 1 or hyperinflation. There is, however, a benefit seen in reducing exacerbations, thus acknowledging its place in treating more severe patients who experience an increased number of exacerbations.
When using corticosteroids, caution is warranted with regard to adverse effects. The most common adverse effects include oral thrush (with inhaled formulations), dysphonia (with inhaled formulations), and skin bruising (Man & Sin, 2005). In general, use of inhaled corticosteroids appears to be relatively safe compared with prolonged courses of oral corticosteroids, especially patients with more severe COPD who may find that the benefits outweigh the side effect risks (Calverley, 2005).
Theophylline
Even with the availability of new and more tolerable medications for COPD, theophylline is still widely used. Although the exact mechanism is unknown, theophylline improves lung function and ventilatory capacity by causing dilatation of the small airways and improves arterial blood gas tensions with effects on respiratory muscles (Ram, 2005).
The role for theophylline is established in asthma but is not fully defined in COPD, as only very small studies have been done. It is generally reserved as a last resort, according to guideline recommendations for theophylline and other xanthine derivatives (GOLD, 2005). It may benefit patients who remain symptomatic after the failure of first-line therapy.
Due to a very narrow therapeutic index, close laboratory monitoring is needed with theophylline therapy. Theophylline is associated with dose-related adverse effects, including nausea, vomiting, seizures, and arrhythmias. If a patient must be treated with theophylline, benefits must outweigh the risks of side effects and possible drug interactions (Rennard, 2004).
Opioids
Opioids are commonly used to treat dyspnea and pain in patients with advanced lung disease. As COPD progresses to more severe COPD, dyspnea may often be debilitating and opioids have been used to suppress the sensation of dyspnea in the patient with chronic, stable COPD. The possible mechanisms of action of opioids include reduction in the central perception of dyspnea (similar to the reduction in the central perception of pain), reduction in anxiety associated with dyspnea, reduction in sensitivity to hypercapnia, reduction in oxygen consumption, and improved cardiovascular function (Jennings, Davies, Higgins, et al., 2002).
Oral, parenteral, and nebulized opioids have been used to treat dyspnea and pain. However, available data support only the use of oral and parenteral formulations due to potential respiratory depression and worsening hypercapnia. Nebulized opioids should be discouraged, as current data do not support their use (Foral, Malesker, Huerta et al., 2004; GOLD, 2005).
Anxiolytics
The role of anxiety in dyspnea remains unclear. Many patients report anxiety concurrent with the feeling of breathlessness. Dyspnea can lead to anxiety, and anxiety can exacerbate dyspnea. Although anxiolytics (e.g., benzodiazepines) are commonly prescribed for anxiety related to dyspnea, the evidence for their effectiveness is not very persuasive (Thomas & von Gunten, 2002). Treatment of anxiety does have a role in a subset of patients for whom it is a significant source of distress, and benzodiazepines can be safely prescribed for those patients at appropriate doses (Thomas & von Gunten, 2002).
NONPHARMACOLOGIC INTERVENTIONS
Smoking Cessation
Patients with COPD and patients who are at risk for COPD should be encouraged to stop smoking. Although the damage may continue to progress, smoking cessation has proved to slow the rate of decline in lung function (Decramer, 2005). As illustrated in Fletcher and Peto (1977), even patients who are in the more severe stages of COPD should be encouraged to stop smoking as they may benefit from decreased symptoms and possible prolongation of life.
Influenza Vaccine
Viral infections are a major cause of COPD exacerbations and are associated with increased mortality. Influenza vaccination has been reported to reduce serious illness and death in COPD patients by 50%. It is imperative for patients with COPD and for patients at risk to receive the influenza vaccine every year, and this is recommended in the GOLD guidelines (GOLD, 2005). Doing so will decrease the frequency of exacerbations and decrease mortality in this already vulnerable population.
Pneumococcal Vaccination
The usefulness of the pneumococcal vaccine has not been clearly shown, although it has been suggested (Rennard, 2004). Because elderly patients are at increased risk of hospitalizations and pneumonia, the pneumococcal vaccine should be also be considered (Rennard, 2004; Sin et al., 2003).
Oxygen
Long-term administration of oxygen (>15 hours per day) has been shown to improve quality of life and increase survival in patients with severe COPD and chronic hypoxemia (Sin et al., 2003). The primary goal is to increase the baseline Pa o2 to at least 8.0 kPa (60 mm Hg) at sea level and rest and/or produce an Sao2 of at least 90%, which will provide adequate delivery of oxygen to preserve vital organ function (GOLD, 2005).
Other
Pulmonary rehabilitation and exercise are useful interventions to improve dyspnea and physical deconditioning. Other useful interventions can include positioning, relaxation techniques, and patient and family education.
CONCLUSION
The management of pulmonary disease can be complicated. Proper diagnosis is imperative when treating pulmonary disease, as there are many forms of obstructive and restrictive diseases. Although many medications are available, the treatment approach must be personalized since interpatient variability is common. Proper treatment may require the combination of drugs from several classes and the inclusion of nonpharmacologic interventions to treat symptoms, prevent exacerbations, improve quality of life, and reduce mortality.
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