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1) Brief Description of the Chronic Obstructive Pulmonary Disease (COPD), detail the necessary review of systems and what would be seen on physical for this complaint/problem

2) List the differential diagnoses related to COPD and include your rationale supporting your diagnosis

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3) Compare and contrast two different clinical guidelines for COPD. Analyze the differences in order to determine the best treatment plan

4) Develop you evidence based diagnostic plan, including appropriate first line diagnostic tests and expected results

5) Evidence Based Management plan, including pharmacology, patient/caregiver education, follow up, referrals, focus on culture, literacy, and costs related to patient’s ability to pay

 

  • cription of the common complaint selected, detail the necessary review of systems and what would be seen on physical for this complaint/problem

Chronic obstructive pulmonary disease (COPD) is airflow limitation cau

Brief Des sed by an inflammatory response to inhaled toxins, often cigarette smoke. Alpha-1 antitrypsin deficiency and various occupational exposures are fewer common causes in nonsmokers.

The cardinal pathophysiologic feature of COPD is airflow limitation caused by airway narrowing and/or obstruction, loss of elastic recoil, or both.

Airway narrowing and obstruction are caused by inflammation-mediated mucus hypersecretion, mucus plugging, mucosal edema, bronchospasm, peribronchial fibrosis, and remodelling of small airways or a combination of these mechanisms. Alveolar septa are destroyed, reducing parenchymal attachments to the airways and thereby facilitating airway closure during expiration.

Enlarged alveolar spaces sometimes consolidate into bullae, defined as airspaces ≥ 1 cm in diameter. Bullae may be entirely empty or have strands of lung tissue traversing them in areas of locally severe emphysema; they occasionally occupy the entire hemithorax. These changes lead to loss of elastic recoil and lung hyperinflation.

Increased airway resistance increases the work of breathing. Lung hyperinflation, although it decreases airway resistance, also increases the work of breathing. Increased work of breathing may lead to alveolar hypoventilation with hypoxia and hypercapnia, although hypoxia and hypercarbia can also be caused by ventilation/perfusion (V/Q) mismatch.

Symptoms are productive cough and dyspnea that develop over years; common signs include decreased breath sounds, prolonged expiratory phase of respiration, and wheezing. Severe cases may be complicated by weight loss, pneumothorax, frequent acute decompensation episodes, right heart failure, and/or acute or chronic respiratory failure. Chronic obstructive pulmonary disease (COPD), caused by chronic bronchitis and emphysema, is a condition that limits the lungs’ ability to function properly.

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Symptoms and Signs

The three cardinal symptoms of COPD are dyspnea, chronic cough, and sputum production and the most common early symptom is exertional dyspnea. Less common symptoms include wheezing and chest tightness. However, any of these symptoms may develop independently and with variable intensity.

 

COPD takes years to develop and progress. Most patients have smoked ≥ 20 cigarettes/day for > 20 yr.

  • Productive cough usually is the initial symptom, developing among smokers in their 40s and 50s.
  • Dyspnea that is progressive, persistent, exertional, or worse during respiratory infection appears when patients are in their late 50s or 60s.

Symptoms usually progress quickly in patients who continue to smoke and in those who have a higher lifetime tobacco exposure. Morning headache develops in more advanced disease and signals nocturnal hypercapnia or hypoxemia.

Signs of COPD include wheezing, a prolonged expiratory phase of breathing, lung hyperinflation manifested as decreased heart and lung sounds, and increased anteroposterior diameter of the thorax (barrel chest). Patients with advanced emphysema lose weight and experience muscle wasting that has been attributed to immobility, hypoxia, or release of systemic inflammatory mediators, such as TNF-alpha.

Signs of advanced disease include pursed-lip breathing, accessory respiratory muscle use, paradoxical inward movement of the lower rib cage during inspiration (Hoover sign), and cyanosis. Signs of cor pulmonale include neck vein distention, splitting of the 2nd heart sound with an accentuated pulmonic component, tricuspid insufficiency murmur, and peripheral edema. Right ventricular heaves are uncommon in COPD because the lungs are hyperinflated.

Spontaneous pneumothorax may occur (possibly related to rupture of bullae) and should be suspected in any patient with COPD whose pulmonary status abruptly worsens.

 

COPD is currently the fourth leading cause of death in the United States. Further, COPD is the cause of significant patient morbidity, affecting the daily lives of millions. COPD is also associated with periodic exacerbations that result in a significant number of emergency department and in-patient visits. Several new interventions, including discharge bundles, telemedicine, and tele-rehabilitation, have been pro- posed to reduce readmission.

In 2015, COPD accounted for 3 million deaths world- wide, or 5% of all deaths.14 Compared with 1990, COPD accounted for 10% more deaths and had a 44% greater prevalence in 2015.14 The morbidity and mortality attributable to COPD both globally and nationally is probably even greater than reported due to underdiagnosis and undertreatment of COPD. An estimated 29 million Americans age 20–79 y (15% of this age group) are living with obstructive lung disease, but only 13 million, or 6.5%, of these adults are aware of their diagnosis. COPD exacerbations accounted for 1.8 million emergency department visits in 2012 with an estimated 20% subsequently admitted to the hospital. As COPD progresses, patients become more debilitated and dependent on others for daily living and for management of their chronic condition. These informal caregivers, ranging from unpaid family members to friends, also incur indirect costs, with 7% of caregivers suffering an average of 1.7 lost days of work per year.

 

The prevalence of COPD increases with age. As life expectancy increases and treatment advances, COPD prevalence is expected to grow. Further burdening the aging COPD population is their increased risk for multimorbidity. Common comorbid conditions in the COPD population include hypertension, hyperlipidemia, depression, cataracts, osteoporosis, and cancer.  FEV1 worsened in subjects with COPD who also had cardiovascular disease, hypertension, and/or dia- betes, these subjects had higher significant hospitalization and nonsignificant mortality rates, compared with those without these comorbid conditions.

 

For the past few decades, prevalence of COPD in women has exceeded that in men, despite overall less lifetime cigarette consumption. Since 2000, mortality in women has surpassed that in men. National Center for Health Statistics report found that age- adjusted death rates from COPD have decreased for white and African-American men (2000 –2014) but increased for African-American women and remained stagnant for white women during that same time period.31 Women may also experience greater lung function decline than men after controlling for the amount of tobacco exposure.32-34 Proposed factors include female-specific genetic predisposition to del- eterious effects of inhaled tobacco, greater reported dyspnea burden, and a deleterious effect on health-related quality of life and increased airway hyperreactivity in women.34-36 More- over, decreases in estrogen during menopause are thought to promote alveolar loss, possibly increasing women’s suscep- tibility to COPD development.37

Within COPD, there is an inverse relationship between prevalence and income level.16,30 COPD prevalence is 1.5–3 times higher in those with low socioeconomic status com- pared with those in higher socioeconomic groups.38 Low- socioeconomic status patients account for an estimated two thirds of the COPD population despite comprising 20% of the general population.38 In general, those who are economically disadvantaged tend to have higher smok- ing rates, more occupational exposure to inhalant toxins, and greater exposure to air pollution, leading to increased risk for COPD development.38 Unfortunately, lower so- cioeconomic status has also been linked to poorer out- comes, including more severe disease, worse lung func-

.

 

  • List the differential diagnoses related to your common complaint and include your rationale supporting your diagnosis

 

Among patients who present in mid or later life with dyspnea, cough, and sputum production, the differential diagnosis is broad (eg, heart failure, COPD, interstitial lung disease, thromboembolic disease) (table 3). Typically, the finding of persistent airflow limitation on pulmonary function testing and the absence of radiographic features of heart failure or interstitial lung disease direct the clinician to a narrower differential of COPD, chronic obstructive asthma, bronchiectasis, tuberculosis, constrictive bronchiolitis, and diffuse panbronchiolitis [8]. Importantly, these conditions can commonly occur together, for example, patients with asthma may develop COPD and patients with COPD may have concurrent bronchiectasis.

  • Chronic obstructive asthma– In some patients with chronic asthma, a clear distinction from COPD is not possible. As an example, a patient, who has had atopic asthma since childhood and smoked cigarettes for 15 years in their twenties and thirties could present in their fifties with a combination of asthma and COPD. The importance of recognizing the coexistence of these diseases is in devising a treatment plan that is adapted to reflect both underlying disease processes. (See‘Interrelationships among asthma, chronic bronchitis, and emphysema’ above and “Asthma in adolescents and adults: Evaluation and diagnosis”.)
  • Chronic bronchitis with normal spirometry– A small portion of cigarette smokers have a chronic productive cough for three months in two successive years, but do not have airflow limitation on pulmonary function tests. They are not considered to have COPD, although they may develop COPD if they continue to smoke. Some treatments for COPD may improve their cough. (See‘Interrelationships among asthma, chronic bronchitis, and emphysema’ above.)
  • Central airway obstruction– Central airway obstruction can be caused by numerous benign and malignant processes and can mimic COPD with a slowly progressive dyspnea on exertion followed by dyspnea with minimal activity (table 6). Monophonic wheezing or stridor may be present. Symptoms are minimally improved by inhaled bronchodilator, if at all. A high index of suspicion is needed as conventional chest radiographs are rarely diagnostic. Though insensitive, flow volume loops can show the characteristic changes of central airway obstruction, frequently before abnormalities in the spirometric volumes are noted (figure 4and figure 5) [104]. A high resolution CT scan with three-dimensional reconstruction can be helpful. The gold standard for diagnosis is direct visualization. (See “Clinical presentation, diagnostic evaluation, and management of central airway obstruction in adults”, section on ‘Diagnostic evaluation and initial management’.)
  • Bronchiectasis– Bronchiectasis, a condition of abnormal widening of the bronchi that is associated with chronic or recurrent infection, shares many clinical features with COPD, including inflamed and easily collapsible airways, obstruction to airflow, and exacerbations characterized by increased dyspnea and sputum production. Bronchiectasis is suspected on the basis of prominent symptoms of cough and daily mucopurulent sputum production. The diagnosis is usually established clinically based on the characteristic cough and sputum production and the presence of bronchial wall thickening and luminal dilatation on chest computed tomographic (CT) scans. (See“Clinical manifestations and diagnosis of bronchiectasis in adults”.)
  • Heart failure– Heart failure is a common cause of dyspnea among middle-aged and older patients and some patients experience chest tightness and wheezing with fluid overload due to heart failure. Occasionally, airflow limitation is noted, although a restrictive pattern is more common. Heart failure is usually differentiated by the presence of fine basilar crackles, radiographic evidence of an increased heart size and pulmonary edema. The brain natriuretic peptide is typically increased in heart failure, but can also be increased during right heart strain from cor pulmonale. (See“Evaluation of the patient with suspected heart failure”.)
  • Tuberculosis– In an area endemic for tuberculosis, the overall prevalence of airflow obstruction was 31 percent among those with a past history of tuberculosis compared with 14 percent among those without. This association was unchanged after adjustment for respiratory disease in childhood, smoking, and exposure to dust and smoke [105,106]. Thus, tuberculosis is both a risk factor for COPD and a potential comorbidity [8]. (See“Clinical manifestations and complications of pulmonary tuberculosis”.)
  • Constrictive bronchiolitis– Constrictive bronchiolitis, also known as bronchiolitis obliterans, is characterized by submucosal and peribronchiolar fibrosis that causes concentric narrowing of the bronchiolar lumen. Constrictive bronchiolitis is most commonly seen following inhalation injury, transplantation (eg, bone marrow, lung), or in the context of rheumatoid lung or inflammatory bowel disease (table 7). Symptoms include progressive onset of cough and dyspnea associated with hypoxemia at rest or with exercise. Crackles may be present. Pulmonary function tests show a progressive and irreversible airflow limitation. Findings on inspiratory CT scan include centrilobular bronchial wall thickening, bronchiolar dilation, tree-in-bud pattern, and a mosaic ground-glass attenuation pattern. (See“Overview of bronchiolar disorders in adults”, section on ‘Bronchiolitis obliterans’.)
  • Diffuse panbronchiolitis– Diffuse panbronchiolitis is predominantly seen in male nonsmokers of Asian descent. Almost all have chronic sinusitis. On pulmonary function testing, an obstructive defect is common, although a mixed obstructive-restrictive pattern may also be seen. Chest radiographs and high resolution CT scans show diffuse centrilobular nodular and linear opacities corresponding to thickened and dilated bronchiolar walls with intraluminal mucous plugs. (See“Diffuse panbronchiolitis”, section on ‘Diagnosis’.)
  • Lymphangioleiomyomatosis– Lymphangioleiomyomatosis (LAM) is seen primarily in young women of childbearing age. Pulmonary function testing frequently reveals mild airflow obstruction, although a mixed obstructive-restrictive pattern may be seen. CT scans typically demonstrate small, thin-walled cysts that can at times be confused with emphysema. However, the airspaces in emphysema are not actually cysts but are caused by the destruction of alveolar walls and permanent enlargement of distal airspaces, so the “walls” are typically inapparent. (See‘Diagnosis’ above and “Sporadic lymphangioleiomyomatosis: Epidemiology and pathogenesis”.)

 

  • Compare and contrast two different clinical guidelines for your diagnosis. Analyze the differences in order to determine the best treatment plan

 

  1. United Preventive Task Force guidelines for Diagnosis and treatment of COPD

 

The USPSTF recommends against screening for COPD using spirometry, regardless of a patient’s age, smoking status, or family history of COPD. This recommendation does not apply to persons with a family history of alpha1-antitrypsin deficiency.

The potential benefit of spirometry-based screening for COPD is the prevention of one or more exacerbations by treating patients with previously undetected airflow obstruction. Even in groups with the greatest prevalence of airflow obstruction, hundreds of patients would need to be screened with spirometry to defer one exacerbation. Under the best-case assumptions about response to therapy, an estimated 455 adults between 60 and 69 years of age would need to be screened to defer one exacerbation. This small benefit would likely be outweighed by the inconvenience of spirometry, the possibility of false-positive screening results, and the adverse effects of subsequent unnecessary therapy.

  • Good evidence indicates that history and physical examination are not accurate predictors of airflow limitation in asymptomatic patients.

 

  1. American College of Physicians guidelines for Diagnosis and Treatment of COPD
Spirometry should be obtained to diagnose airflow obstruction in patients with respiratory symptoms. (Grade: strong.) Spirometry should not be used to screen for airflow obstruction in patients without respiratory symptoms. (Grade: strong.)
Inhaled bronchodilators may be used for patients with stable COPD who have respiratory symptoms and FEV1 of 60% to 80% of predicted. (Grade: weak.)
Inhaled bronchodilators are recommended for patients with stable COPD who have respiratory symptoms and FEV1 < 60% of predicted. (Grade: strong.)
Monotherapy with a LABA or long-acting anticholinergic is recommended for symptomatic patients with COPD who have FEV1 < 60% of predicted. (Grade: strong.) The choice of specific therapy should be based on patient preference, cost, and adverse effect profile.
Combination inhaled therapies (LABA, long-acting anticholinergic, or inhaled corticosteroid) may be used for symptomatic patients with stable COPD who have FEV1 < 60% of predicted. (Grade: weak.)
Pulmonary rehabilitation is recommended for symptomatic patients with FEV1 < 50% of predicted. (Grade: strong.) Pulmonary rehabilitation may be considered for symptomatic or exercise-limited patients with FEV1> 50% of predicted. (Grade: weak.)
Continuous oxygen therapy is recommended for patients with COPD who have severe resting hypoxia (arterial partial pressure of oxygen ≤ 55 mm Hg, oroxygen saturation ≤ 88%). (Grade: strong.)

According to Global Initiative for Chronic Obstructive Lung Disease (GOLD)guidelines

 

Patients’ airflow limitation with a post-bronchodilator forced expiratory volume/forced vital capacity (FEV1/FVC) <0.7 is further classified as either GOLD 1 (mild), GOLD 2 (moderate), GOLD 3 (severe), or GOLD 4 (very severe). Patients’ symptom burden and risk of exacerbation are classified into GOLD groups A through D; this is used to guide patients’ therapy. Classification of airflow limitation (grades 1-4) and symptom burden with exacerbation risk (groups A-D) is patient-specific and can occur in a variety of combinations.

  • Develop you evidence based diagnostic plan, including appropriate first line diagnostic tests and expected results

 

 

Diagnosis is based on history, physical examination, chest x-ray, and pulmonary function tests.

The presence of symptoms compatible with COPD (eg, dyspnea at rest or on exertion, cough with or without sputum production, progressive limitation of activity) are suggestive of the diagnosis, especially if there is a history of exposure to triggers of COPD (eg, tobacco smoke, occupational dust, indoor biomass smoke), a family history of chronic lung disease, or presence of associated comorbidities (table 5).

The diagnosis of COPD is confirmed by the following [8,9]:

  • Spirometry demonstrating airflow limitation (ie, a forced expiratory volume in one second/forced vital capacity [FEV1/FVC] ratio less than 0.7 or less than the lower limit of normal [LLN]) that is incompletely reversible after the administration of an inhaled bronchodilator (table 2A-B). (See ‘Pulmonary function tests’above.)
  • Absence of an alternative explanation for the symptoms and airflow limitation (table 3) [8]. The differential diagnosis of COPD is discussed below. (See ‘Differential diagnosis’below and “Approach to the patient with dyspnea”.)
  • The Global Initiative for COPD (GOLD) guidelines suggest repeating spirometry on a separate occasion to demonstrate persistence of airflow limitation (FEV1/FVC <0.7 or less than the LLN) for patients with an initial FEV1/FVC between 0.6 and 0.8 [8,101,102].

After confirming the presence of COPD, the next step is to consider the cause. For the majority of patients, the etiology is long-term cigarette smoking. However, it is important to review with the patient whether underlying asthma, workplace exposures, indoor use of biomass fuel, a prior history of tuberculosis, or familial predisposition is contributory, because mitigation of ongoing exposures may reduce disease progression.

It is appropriate to screen all patients with COPD for alpha-1 antitrypsin (AAT) deficiency by obtaining an AAT serum level and AAT genotyping, possibly excepting areas with a low prevalence of AAT deficiency [8,103]. (See ‘Laboratory’ above and “Chronic obstructive pulmonary disease: Risk factors and risk reduction” and “Clinical manifestations, diagnosis, and natural history of alpha-1 antitrypsin deficiency”, section on ‘Laboratory testing’.)

  • Evidence Based Management plan, including pharmacology, patient/caregiver education, follow up, referrals, focus on culture, literacy, and costs related to patient’s ability to pay

Smoking cessation

Inhaled bronchodilators, corticosteroids, or both

Supportive care (eg, oxygen therapy, pulmonary rehabilitation)

Treatment of chronic stable COPD aims to prevent exacerbations and improve lung and physical function. Relieve symptoms rapidly with primarily short-acting beta-adrenergic drugs and decrease exacerbations with inhaled corticosteroids, long-acting beta-adrenergic drugs, long-acting anticholinergic drugs, or a combination

 

Recommended drug therapy.

Inhaled bronchodilators are the mainstay of COPD management; drugs include

  • Beta-agonists
  • Anticholinergics (antimuscarinics)

These two classes of drugs are equally effective. Patients with mild (group A—see table Classification and Treatment of COPD) disease are treated only when symptomatic. Patients with moderate to severe (group B, C, or D—see table) COPD should be taking drugs from one or both of these classes regularly to improve pulmonary function and increase exercise capacity.

The frequency of exacerbations can be reduced with the use of anticholinergics, inhaled corticosteroids, or long-acting beta-agonists. However, there is no convincing evidence that regular bronchodilator use slows deterioration of lung function. The initial choice among short-acting beta-agonists, long-acting beta-agonists, anticholinergics, and combination beta-agonist and anticholinergic therapy is often a matter of tailoring cost and convenience to the patient’s preferences and symptoms.

For home treatment of chronic stable disease, drug administration by metered-dose inhaler or dry-powder inhaler is preferred over administration by nebulizer; home nebulizers are prone to contamination due to incomplete cleaning and drying. Therefore, nebulizers should be reserved for people who cannot coordinate activation of the metered-dose inhaler with inhalation or cannot develop enough inspiratory flow for dry powder inhalers.

For metered-dose inhalers, patients should be taught to exhale to functional residual capacity, inhale the aerosol slowly to total lung capacity, and hold the inhalation for 3 to 4 sec before exhaling. Spacers help ensure optimal delivery of drug to the distal airways and reduce the importance of coordinating activation of the inhaler with inhalation. Some spacers alert patients if they are inhaling too rapidly. New or not recently used metered-dose inhalers require 2 to 3 priming doses (different manufacturers have slightly different recommendations for what is considered “not recently used,” ranging from 3 to 14 days).

Beta-agonists

Beta-agonists relax bronchial smooth muscle and increase mucociliary clearance. Albuterol aerosol, 2 puffs (90 to 100 mcg/puff) inhaled from a metered-dose inhaler 4 to 6 times/day prn, is usually the drug of choice.

Long-acting beta-agonists are preferable for patients with nocturnal symptoms or for those who find frequent dosing inconvenient. Options include salmeterol powder, 1 puff (50 mcg) inhaled bid, indacaterol 1 puff (75 mcg) inhaled once/day (150 mcg once/day in Europe), and olodaterol 2 puffs once/day at the same time each day. Also available are nebulized forms of arformoterol and formoterol. The dry-powder formulations may be more effective for patients who have trouble coordinating use of a metered-dose inhaler.

Patients should be taught the difference between short-acting and long-acting drugs, because long-acting drugs that are used as needed or more than twice/day increase the risk of cardiac arrhythmias.

Adverse effects commonly result from use of any beta-agonist and include tremor, anxiety, tachycardia, and mild, temporary hypokalemia.

Anticholinergics

Anticholinergics (antimuscarinics) relax bronchial smooth muscle through competitive inhibition of muscarinic receptors (M1, M2, and M3).

Ipratropium is a short-acting anticholinergic; dose is 2 to 4 puffs (18 mcg/puff) from a metered-dose inhaler q 4 to 6 h. Ipratropiumhas a slower onset of action (within 30 min; peak effect in 1 to 2 h), so a beta-agonist is often prescribed with it in a single combination inhaler or as a separate as-needed rescue drug.

Tiotropium is a long-acting quaternary anticholinergic inhaled as a powder formulation. Dose is 1 puff (18 mcg) once/day. Aclidinium bromide is available as a multidose dry-powder inhaler. Dose is 1 puff (400 mcg/puff) bid. Umeclidinium can be used as a once/day combination with vilanterol (a long-acting beta-agonist) in a dry-powder inhaler. Glycopyrrolate (an anticholinergic) can be used bid in combination with indacaterol or formoterol (long-acting beta-agonists) in a dry-powder or metered-dose inhaler.

Adverse effects of all anticholinergics are pupillary dilation (and risk of triggering or worsening acute angle closure glaucoma), urinary retention, and dry mouth.

Inhaled corticosteroids

Corticosteroids are often part of treatment. Inhaled corticosteroids seem to reduce airway inflammation, reverse beta-receptor down-regulation, and inhibit leukotriene and cytokine production. They do not alter the course of pulmonary function decline in patients with COPD who continue to smoke, but they do relieve symptoms and improve short-term pulmonary function in some patients, are additive to the effect of bronchodilators, and diminish the frequency of COPD exacerbations. They are indicated for patients who have repeated exacerbations or symptoms despite optimal bronchodilator therapy. Dose depends on the drug; examples include fluticasone 500 to 1000 mcg/day and beclomethasone 400 to 2000 mcg/day.

The long-term risks of inhaled corticosteroids in elderly people are not proved but probably include osteoporosiscataract formation, and an increased risk of nonfatal pneumonia. Long-term users therefore should undergo periodic ophthalmologic and bone densitometry screening and should possibly receive supplemental calcium, vitamin D, and a bisphosphonate as indicated.

Combinations of a long-acting beta-agonist (eg, salmeterol) and an inhaled corticosteroid (eg, fluticasone) are more effective than either drug alone in the treatment of chronic stable disease.

Oral or systemic corticosteroids should usually not be used to treat chronic stable COPD.

Theophylline

Theophylline plays only a small role in the treatment of chronic stable COPD now that safer, more effective drugs are available. Theophylline decreases smooth muscle spasm, enhances mucociliary clearance, improves right ventricular function, and decreases pulmonary vascular resistance and arterial pressure. Its mode of action is poorly understood but appears to differ from that of beta-2-agonists and anticholinergics. Its role in improving diaphragmatic function and dyspnea during exercise is controversial.

Theophylline can be used for patients who have not adequately responded to inhaled drugs and who have shown symptomatic benefit from a trial of the drug. Serum levels need not be monitored unless the patient does not respond to the drug, develops symptoms of toxicity, or is questionably adherent; slowly absorbed oral theophylline preparations, which require less frequent dosing, enhance adherence.

Toxicity is common and includes sleeplessness and GI upset, even at low blood levels. More serious adverse effects, such as supraventricular and ventricular arrhythmias and seizures, tend to occur at blood levels > 20 mg/L.

Hepatic metabolism of theophylline varies greatly and is influenced by genetic factors, age, cigarette smoking, hepatic dysfunction, diet, and some drugs, such as macrolide and fluoroquinolone antibiotics and nonsedating histamine2 blockers.

Phosphodiesterase-4 inhibitors

Phosphodiesterase-4 inhibitors are more specific than theophylline for pulmonary phosphodiesterase and have fewer adverse effects. They have anti-inflammatory properties and are mild bronchodilators. Phosphodiesterase-4 inhibitors such as roflumilastcan be used in addition to other bronchodilators for reduction of exacerbations in patients with COPD. Roflumilast should be started at a oral dose of 250 mcg once/day and increased to 500 mcg once/day as tolerated.

Common adverse effects include nausea, headache, and weight loss, but these effects may subside with continued use.

Macrolide antibiotics

Long-term azithromycin therapy is an effective adjunct to prevent COPD exacerbations in patients who are prone to repeated or severe exacerbations, particularly those who are not currently smoking. A dose of 250 mg po once/day has demonstrated efficacy. Erythromycin 250 mg po bid or tid has also been found effective.

Oxygen Therapy

Long-term oxygen therapy prolongs life in patients with COPD whose Pao2 is chronically < 55 mm Hg. Continual 24-h use is more effective than a 12-h nocturnal regimen. Oxygen therapy

  • Brings hematocrit toward normal levels
  • Improves neuropsychologic factors, possibly by facilitating sleep
  • Ameliorates pulmonary hemodynamic abnormalities
  • Increases exercise tolerance in many patients

Oxygen saturation should be measured during exercise and while at rest. Similarly, a sleep study should be considered for patients with advanced COPD who do not meet the criteria for long-term oxygen therapy while they are awake (see table Indications for Long-Term Oxygen Therapy in COPD) but whose clinical assessment suggests pulmonary hypertension in the absence of daytime hypoxemia. Nocturnal oxygen may be prescribed if a sleep study shows episodic desaturation to ≤ 88%. Such treatment prevents progression of pulmonary hypertension, but its effects on survival are unknown. Patients with moderate hypoxemia above 88% or exercise desaturation may benefit symptomatically from oxygen, but there is no improvement in survival or reduction in hospitalizations (1).

Some patients need supplemental oxygen during air travel because flight cabin pressure in commercial airliners is below sea level air pressure (often equivalent to 1830 to 2400 m [6000 to 8000 ft]). Eucapnic COPD patients who have a Pao> 68 mm Hg at sea level generally have an in-flight Pao> 50 mm Hg and do not require supplemental oxygen. All patients with COPD with a Pao≤ 68 mm Hg at sea level, hypercapnia, significant anemia (Hct < 30), or a coexisting heart or cerebrovascular disorder should use supplemental oxygen during long flights and should notify the airline when making their reservation. Airlines can provide supplemental oxygen, and most require a minimum notice of 24 h, a physician’s statement of necessity, and an oxygen prescription before the flight. Patients should bring their own nasal cannulas, because some airlines provide only face masks. Patients are not permitted to transport or use their own liquid oxygen, but many airlines now permit use of portable battery-operated oxygen concentrators, which also provide a suitable oxygen source on arrival.

 

Oxygen administration

Oxygen is administered by nasal cannula at a flow rate sufficient to achieve a Pao>60 mm Hg (oxygen saturation > 90%), usually ≤ 3 L/min at rest. Oxygen is supplied by electrically driven oxygen concentrators, liquid oxygen systems, or cylinders of compressed gas. Stationary concentrators, which limit mobility but are the least expensive, are preferable for patients who spend most of their time at home. Such patients require small oxygen tanks for backup in case of an electrical failure and for portable use. Portable concentrators that allow mobility can be used for patients who do not require high flow rates.

A liquid system is preferable for patients who spend much time out of their home. Portable canisters of liquid oxygen are easier to carry and have more capacity than portable cylinders of compressed gas. Large compressed-air cylinders are the most expensive way of providing oxygen and should be used only if no other source is available. All patients must be taught the dangers of smoking during oxygen use.

Various oxygen-conserving devices can reduce the amount of oxygen used by the patient, either by using a reservoir system or by permitting oxygen flow only during inspiration. Systems with these devices may correct resting hypoxemia as effectively as continuous flow devices. However, intermittent flow devices may not be as effective as continuous flow for exercise-associated hypoxemia.

Patient Education

Patient  is strongly encouraged to stop smoking and is offered tobacco cessation support classes and a nicotine-replacement agent. He is told to return for reevaluation in two weeks to ensure that his symptoms are controlled, to discuss any concerns, to confirm that he is using his medication appropriately, and to report on his progress with smoking cessation.

 

 

COPD Self-Management Goals

  • Smoking cessation
  • Avoid exposure to triggers

o Pollutants, smoke, dust, strong fumes

  • Increased physical activity

o Increased endurance
o Improved muscle tone and strength o Improved circulation

  • Medication management
  • Reduce risk of exacerbation o Annual flu vaccine
  • Pneumococcal vaccine o Annual spirometry

Patient is strongly encouraged to stop smoking and is offered tobacco cessation support classes and a nicotine-replacement agent. Patient should return for reevaluation in two weeks to ensure that his symptoms are controlled, to discuss any concerns, to confirm that he is using his medication appropriately, and to report on his progress with smoking cessation.

PMG Patient Education Materials:

  • “Breathing Better with COPD Diagnosis” (Brochure), American Heart Lung and Blood Institute
  • EMR Patient Instructions:

o Smoking Cessation, by ExtCare

 

 

 

 

 

 

 

 

 

 

References

American Lung Association. COPD.

https://www.lung.org/lung-health-diseases/lung-disease-lookup/copd

American Family Physicians (2017).  Chronic Obstructive Pulmonary Disease: Diagnosis and Management. Retrieved from https://www.aafp.org/afp/2017/0401/p433.html

Wise, R. Chronic Obstructive Pulmonary Disease (COPD).

https://www.merckmanuals.com/professional/pulmonary-disorders/chronic-obstructive-pulmonary-disease-and-related-disorders/chronic-obstructive-pulmonary-disease-copd?query=COPD

Criner, R., & Han, M. (2018). COPD care in the 21st century: A public health priority. Respiratory Care 63, (5), 591-600. Retrieved from http://rc.rcjournal.com/content/63/5/591

Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management and Prevention of chronic obstructive pulmonary disease: 2020 Report.  Retrieved from https://goldcopd.org/wp-content/uploads/2019/12/GOLD-2020-FINAL-ver1.2-03Dec19_WMV.pdf

 

  1. S. Preventive Task Force. Chronic Obstructive Pulmonary Disease: Screening.

https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/chronic-obstructive-pulmonary-disease-screening

 

 

 

 

 

 

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