Dyspnea (Chronic Obstructive Pulmonary Disease) case file

Dyspnea (Chronic Obstructive Pulmonary Disease) case file

Eugene C. Toy MD, Donald Briscoe, MD, FA  AFP, Bruce Britton, MD, Joel J. Heidelbaugh, MD, FA  AFP, FACG

Case 1

A 52-year-old man presents to your office for an acute visit because of coughing and shortness of breath. He is well known to you because of multiple office visits in the past few years for similar reasons. He has a chronic "smoker's cough;' but reports that in the past 2 days his cough has increased, his sputum has changed from white to green in color, and he has had to increase the frequency with which he uses his albuterol inhaler. He denies having a fever, chest pain, peripheral edema, or other symptoms. His medical history is significant for hypertension, peripheral vascular disease, and two hospitalizations for pneumonia in the past 5 years. He has a 60-pack-year history of smoking and continues to smoke two packs of cigarettes a day.

On examination, he is in moderate respiratory distress. His temperature is 98.4°F, his blood pressure is 152/95 mm Hg, his pulse is 98 beats/min, his respiratory rate is 24 breaths/min, and he has an oxygen saturation of 94% on room air. His lung examination is significant for diffuse expiratory wheezing and a prolonged expiratory phase of respiration. There are no signs of cyanosis. The remainder of his examination is normal. A chest x-ray done in your office shows an increased anteroposterior (AP) diameter and a flattened diaphragm, but otherwise he has clear lung fields.

⯈ What is the most likely cause of this patient's dyspnea?

⯈ What acute treatment(s) are most appropriate at this time?

⯈ What interventions would be most helpful to reduce the risk of future exacerbations of this condition?

ANSWER TO CASE 2:

Dyspnea (Chronic Obstructive Pulmonary Disease) 

Summary: A 52-year-old man with a long history of smoking presents with dyspnea,

increased sputum production, change in sputum character, coughing, and wheezing.

• Most likely cause of current symptoms: Acute exacerbation of chronic obstructive pulmonary disease (COPD)
• Appropriate treatment of exacerbation: Antibiotic, bronchodilators, systemic corticosteroids
• Interventions to reduce exacerbations: Smoking cessation, long-acting bronchodilator, inhaled corticosteroid, influenza and pneumococcal polysaccharide vaccination

ANALYSIS

Objectives

1. Be able to diagnose and determine the stage of COPD in adults.
2. Know the management of stable COPD and COPD exacerbations.

Considerations

Two of the most common causes of dyspnea and wheezing in adults are asthma and COPD. There can be substantial overlap between the two diseases, as patients with chronic asthma can develop chronic obstructive disease over time. As in most medical situations, the patient's history will usually provide the key information to the appropriate diagnosis. Asthma often presents earlier in life, may or may not be associated with cigarette smoking, and is characterized by episodic exacerbations with return to relatively normal baseline lung functioning. COPD, on the other hand, tends to present in midlife or later, is usually the result of a long history of smoking, and is a slowly progressive disorder in which measured pulmonary functioning never returns to normal.

In the setting of an acute exacerbation, the differentiation between an exacerbation of asthma and an exacerbation of COPD is not necessary for determination of the immediate management. The assessment of the patient presenting with dyspnea should always start with the ABCs-Airway, Breathing, and Circulation. Intubation with mechanical ventilation should be performed when the patient is unable to protect his own airway ( eg, when he has a reduced level of consciousness), when he is tiring because of the amount of work required to overcome his airway obstruction, or when adequate oxygenation cannot be maintained.

For both asthma and COPD exacerbations, the mainstays of medical therapy are oxygen, bronchodilators, and steroids. All dyspneic patients should have an assessment of their level of oxygenation. Clinical signs of hypoxemia, such as cyanosis of the perioral region or digits, should be noted on examination. Objective levels of oxygenation using pulse oximetry or arterial blood gas measurements should also be performed. Hypoxemia must be addressed by providing supplemental oxygen. Inhaled β2-agonists, most commonly albuterol, can rapidly result in bronchodilation and reduction in airway obstruction. The addition of an inhaled anticholinergic agent, such as ipratropium, may work synergistically with the β-agonist. Corticosteroids, given systemically (orally, intramuscularly, or intravenously), act to reduce the airway inflammation that underlies the acute exacerbation. Clinically significant effects of steroids take hours to occur; consequently, steroids should be used with bronchodilators because bronchodilators act rapidly. Steroids used in combination with bronchodilators significantly improve short-term outcomes in the management of acute exacerbations of asthma and COPD.

Approach To:

Chronic Obstructive Pulmonary Disease

DEFINITIONS

CHRONIC BRONCHITIS: Cough and sputum production on most days for at least 3 months during at least 2 consecutive years

EMPHYSEMA: Shortness of breath caused by the enlargement of respiratory bronchioles and alveoli caused by destruction of lung tissue

CLINICAL APPROACH

Evaluation

COPD is the third leading cause of death in the United States, affecting more than 5% of the adult population. COPD is defined as airway obstruction that is not fully reversible, is usually progressive, and is associated with chronic bronchitis, emphysema, or both. The most common etiology is cigarette smoking, which is associated with approximately 90% of cases of COPD. Other etiologies of COPD include passive exposure to cigarette smoke ("second-hand smoke") and occupational exposures to dusts (including mining, cotton, silica, plastics), chemicals, and fumes (welding, heavy metals). Patients with symptoms of COPD, who do not smoke and work in high-risk occupations, warrant further evaluation. A rare cause of COPD is a genetic deficiency in α1-antitrypsin, which is more common in Caucasians and should be considered when emphysema develops at younger ages ( <45 years), especially in nonsmokers. COPD is a disease of inflammation of the airways, lung tissue, and vasculature. Pathologic changes include mucous gland hypertrophy with hypersecretion, ciliary dysfunction, destruction of lung parenchyma, and airway remodeling. The results of these changes are narrowing of the airways, causing a fixed airway obstruction, poor mucous clearance, cough, wheezing, and dyspnea.

The most common initial symptom of COPD is cough, which is at first intermittent and then frequently becomes a daily occurrence. The cough is often productive of white, thick mucus. Patients will present with intermittent episodes of worsening cough, with change in mucus from clear to yellow I green, and often with wheezing. These exacerbations are usually caused by viral or bacterial infections.

As COPD progresses, lung function continues to deteriorate and dyspnea develops. Dyspnea is the primary presenting symptom of COPD. Dyspnea also tends to worsen over time-initially the dyspnea will occur only with significant effort, then with any exertion, and finally at rest. By the time dyspnea develops, lung function (as measured by forced expiratory volume in the first second of expiration [FEV1]) has been reduced by about half and the COPD has been present for years. When evaluating the patient with dyspnea, it is important to consider other diagnoses. Eightyfive percent of dyspnea causes are due to one of the following conditions: congestive heart failure, COPD, asthma, interstitial lung disease, pneumonia, and psychogenic disturbances (including anxiety).

Examination of a patient with mild or moderate COPD, who is not having an exacerbation, is usually normal. As the disease progresses, patients are often noted to have "barrel chests" (increased anteroposterior chest diameter) and distant heart sounds, as a result of hyperinflation of the lungs. Breath sounds may also be distant and expiratory wheezes with a prolonged expiratory phase of respiration may be noted. During an acute exacerbation, patients often appear anxious and tachypneic; they may be using accessory muscles of respiration, usually have wheezes or rales, and may have signs of cyanosis.

Chest x-rays in patients with COPD are typically normal until the disease is advanced. In more severe cases, hyperinflation of the lungs with an increased posteroanterior (PA) diameter and flattening of diaphragms may be seen. Bullaeareas of pulmonary parenchymal destruction-can also be seen in x-rays in more severe disease.

The primary diagnostic test of lung function is spirometry. In normal aging, both the forced vital capacity (FVC) (a measure of the total amount of air that can be expired after a maximal inspiration) and FEV1 reduce gradually over time. In normal-functioning lungs, the ratio of the FEV1 to FVC is greater than 0.7. In COPD, both the FVC and FEV1 are reduced and the ratio of FEV1 to FVC is less than 0.7, indicating an airway obstruction. Reversibility is defined as an increase in FEV1 of greater than 12% or 200 mL. Using a bronchodilator may result in some improvement of both FVC and FEV1, but neither will return to normal, making the diagnosis of a fixed obstruction. The severity of COPD, which can help to determine treatment, can be assessed using these measurements (Table 2-1).

Management of Stable COPD

The goals of COPD management are to relieve symptoms, prevent/slow disease progression, reduce/prevent/treat exacerbations, and reduce/prevent/treat complications. Several components of treatment are common to all stages of COPD, whereas pharmacologic treatment is guided by the stage of disease.

All patients with COPD should be encouraged to quit smoking. The pulmonary function of smokers declines more rapidly than that of nonsmokers. Although smoking cessation does not result in significant improvement in pulmonary function, smoking cessation does reduce the rate of further deterioration to that of a nonsmoker. Cessation also reduces the risks of other comorbidities, including cardiovascular diseases and cancers. Case 7 more thoroughly discusses smoking cessation. All patients with COPD should be appropriately vaccinated. Those with chronic pulmonary diseases and all smokers should receive a pneumococcal vaccination and

Adapted from National Heart, Lung and Blood Institute/World Health Organization. Global initiative for chronic obstructive

lung disease. Executive summary. Updated 2009. Available at: http://www.goldcopd.com/Guide/ineitem.asp?/7 =

2&12 = 1&intld=2205. Accessed October 20, 2010.

annual influenza vaccination. Regular exercise and efforts to maintain normal body weight should be encouraged. Avoidance of second-hand smoke, aggravating occupational exposures, and indoor and outdoor pollution is recommended.

Although pharmacologic treatment cannot reverse lung changes or modify longterm decline in lung function, it does reduce the severity of symptoms, decrease the frequency of exacerbations, and improve exercise tolerance and overall health. Short-acting bronchodilators used as needed are the recommended treatment in stage I COPD. These include β2-agonists (albuterol) and anticholinergics (ipratropium). Inhaled medications are preferred over oral, as they tend to have fewer side effects. The choice of specific agent is based on availability, individual response to therapy, and side effects.

In stage II COPD, a long-acting bronchodilator should be added. Commonly used agents in the United States are salmeterol (an inhaled β2-agonist) and tiotropium (an inhaled anticholinergic ). Oral methylxanthines ( aminophylline, theophylline) are also options, but have narrow therapeutic windows (high toxicity) and multiple drug-drug interactions, making their use less common. The use of long-acting bronchodilators is more convenient and more effective than using short-acting agents, but is much more expensive and does not replace the need for short-acting agents for rescue therapy in exacerbations.

Inhaled steroids (fluticasone, triamcinolone, mometasone, etc) do not affect the rate of decline of lung function in COPD but do reduce the frequency of exacerbations. For that reason, inhaled steroids are recommended for stages III and IV COPD with frequent exacerbations. Long-term treatment with oral steroids is not recommended, as there is no evidence of benefit, and there can be multiple complications (myopathy, osteoporosis, glucose intolerance, etc). Although continuous prophylactic antibiotic use decreases the number ofCOPD exacerbations for a few years, there is no decrease in mortality and the risk of antibiotic resistance makes this a controversial issue.

Oxygen therapy is recommended in stage IV COPD if there is evidence of hypoxemia (PaO2 <55 mm Hg or SaO2 <88% at rest) or where the PaO2 is less than or equal to 60 mm Hg and there is polycythemia, pulmonary hypertension, or peripheral edema suggesting heart failure. Oxygen therapy is the only intervention that has been shown to decrease mortality and must be worn for at least 15 h/d.

As COPD is a chronic condition that is expected to worsen over time, routine follow-up is imperative. Spirometry is the best method to monitor lung function. The COPD Assessment Test (CAT) is a questionnaire given to patients every 3 months. The CAT is an objective tool to assess changes overtime and the impact that COPD is having on a patient's life. Depending on the stage of the patients, COPD, pulmonary rehabilitation, and possibly lung resection surgery should be considered with the appropriate specialists.

Management of Exacerbations of COPD

An acute COPD exacerbation is defined as a change in respiratory function causing worsening of symptoms which leads to a change in medication. Acute exacerbations of COPD are common and typically present with change in sputum color or amount, cough, wheezing, and increased dyspnea. Although respiratory tract infections (viral and bacterial) are the most common precipitant, air pollutants are another common cause of acute COPD exacerbations. Diagnoses that can cause similar symptoms ( eg, pulmonary embolism, congestive heart failure, myocardial infarction, pneumonia, pneumothorax, pleural effusion) must be excluded so that appropriate therapy can occur.

The severity of the exacerbation should be evaluated by history, examination, assessment of oxygenation using a pulse oximetry, and focused testing. The following questions from the medical history may help to assist in assessing the exacerbation: number of previous episodes and hospitalizations, other chronic conditions, current treatment regimen, history of intubation/ mechanical ventilation, and duration and new symptoms. Physical examination signs of severity include the use of respiratory muscles, worsening or new cyanosis, unstable blood pressure and heart rate, altered mental status, and peripheral edema. Oxygen should be given with a target saturation of 88% to 92% or PaO2 levels at about 60 mm Hg.

Patients with more severe symptoms, comorbidities, altered mental status, an inability to care for themselves at home, or whose symptoms fail to respond promptly to office or emergency room treatments should be hospitalized. If hospitalized, a baseline arterial blood gas should be ordered to evaluate for hypercapnia, hypoxemia, and respiratory acidosis. Ventilatory support with either noninvasive (nasal or face mask) or invasive ventilation (intubation) should be considered in deteriorating or critical patients.

All acute exacerbations should be treated with short-acting bronchodilators. Combinations of short-acting agents with different mechanisms of action (ie, β-agonist and anticholinergic) can be used until symptoms improve. Systemic steroids shorten the course of the exacerbation and may reduce the risk of relapse. A steroid dose of 40 mg prednisolone (or equivalent) for 10 to 14 days is recommended.

Exacerbations associated with increased amounts of sputum or with purulent sputum should be treated with antibiotics. A sputum culture should be performed. Pneumococcus, Haemophilus injluenzae, and Moraxella catarrhalis are the most common bacteria implicated. In milder exacerbations, treatment with oral agents directed against these pathogens is appropriate. In severe exacerbations, gram-negative bacteria (Klebsiella, Pseudomonas) can also play a role, so antibiotic coverage needs to be broader.

Measures taken to prevent COPD exacerbation should be discussed and reviewed at each patient encounter. The number of annual exacerbations can be reduced by receiving appropriate vaccinations (influenza and pneumococcal), smoking cessation counseling, education about current medications and their proper use. Patients should be encouraged to discuss social concerns, psychiatric problems (such as anxiety), and proper nutrition and exercise with their physician.

COMPREHENSION QUESTIONS

2.1 A 38-year-old woman presents with progressively worsening dyspnea and cough. She has never smoked cigarettes, has no known passive smoke exposure, and does not have any occupational exposure to chemicals. Pulmonary function testing shows obstructive lung disease that does not respond to bronchodilators. Which of the following is the most likely etiology?

A. Radon exposure at home

B. COPD

C. α1-Antitrypsin deficiency

D. Asthma

2.2 A 60-year-old man is diagnosed with moderately severe (stage II) COPD. He admits to a long history of cigarette smoking and is still currently smoking. In counseling him about the benefits of smoking cessation, which of the following statements is most accurate?

A. By quitting, his pulmonary function will significantly improve.

B. By quitting, his current pulmonary function will be unchanged, but the rate of pulmonary function decline will slow.

C. By quitting, his current pulmonary function and the rate of decline are unchanged, but there are cardiovascular benefits.

D. By quitting, his pulmonary function will approach that of a nonsmoker of the same age.

2.3 A 68-year-old patient of your practice with known COPD has pulmonary function testing showing an FEV1 of 40% predicted has been having frequent exacerbations of his COPD. His SaO2 by pulse oximetry is 91%. Which of the following medication regimens is the most appropriate?

A. Inhaled salmeterol BID and albuterol as needed

B. Oral albuterol daily and inhaled fluticasone BID

C. Inhaled fluticasone BID, inhaled tiotropium BID, and inhaled albuterol as needed

D. Inhaled fluticasone BID, inhaled tiotropium BID, inhaled albuterol as needed, and home oxygen therapy

2.4 A 59-year-old man with a known history of COPD presents with worsening dyspnea. On examination, he is afebrile. His breath sounds are decreased bilaterally. He is noted to have jugular venous distension (JVD) and 2+ pitting edema of the lower extremities. Which of the following is the most likely cause of his increasing dyspnea?

A. COPD exacerbation

B. Pneumonia

C. Cor pulmonale

D. Pneumothorax

ANSWERS

2.1 C. This patient has a fixed airway obstruction consistent with COPD. The airway obstruction of asthma would be at least partially reversible on testing with a bronchodilator. α1-Antitrypsin deficiency should be considered in a patient who develops COPD at a young age, especially if there is no other identifiable risk factor.

2.2 B. Smoking cessation will not result in reversal of the lung damage that has already occurred, but can result in a slowing in the rate of decline of pulmonary function. In fact, smoking cessation can result in the rate of decline returning to that of a nonsmoker.

2.3 C. This patient has stage III COPD with frequent exacerbations. He is best treated by a long-acting bronchodilator ( eg, tiotropium) and an inhaled steroid ( eg, fluticasone) used regularly, along with an inhaled, short-acting bronchodilator on an as-needed basis.

2.4 C. JVD and lower extremity edema are suggestive of cor pulmonale, which is right heart failure due to chronically elevated pressures in the pulmonary circulation. Right heart failure causes increased right atrial pressures and right ventricular end-diastolic pressures, which then lead to liver congestion, jugular venous distension, and lower extremity edema.

CLINICAL PEARLS

⯈ All smokers should be counseled on the benefits of smoking cessation before they develop symptomatic COPD; by the time symptoms develop, the patient's FEV1 will have reduced by approximately 50%.

⯈ Always remember to evaluate the ABCs-Airway, Breathing, Circulation when evaluating a dyspneic patient.

REFERENCES

Armstrong C. ACP updated guidelines on diagnosis and management of stable COPD. Am Fam Physician. 2012 Jan 15;85(2):204-205. 

Herath SC, Pooler P. Prophylactic antibiotic therapy for chronic obstructive pulmonary disease (COPD). Cochrane Database Syst Rev. 2013 Nov 28;11:CD009764. 

National Heart, Lung and Blood Institute/World Health Organization. Global initiative for chronic obstructive lung disease. Executive summary. Updated 2011. Available at: http://www.goldcopd. com/Guidelineitem.asprl1=2&12=l&intld=2205. Accessed January 28, 2015. 

Reilly JJ Jr., Silverman EK, Shapiro SD. Chronic obstructive pulmonary disease. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 19th ed. New York, NY : McGraw-Hill Education; 2015. Available at: http://accessmedicine.mhmedical. com. Accessed May 25, 2015.

HomeFamily Medicine Case FileDyspnea (Chronic Obstructive Pulmonary Disease) case file