History
Most patients with chronic obstructive pulmonary disease (COPD) seek medical attention late in the course of their disease. Patients often ignore the symptoms because they start gradually and progress over the course of years. Patients often modify their lifestyle to minimize dyspnea and ignore cough and sputum production. With retroactive questioning, a multiyear history can be elicited.
Patients typically present with a combination of signs and symptoms of chronic bronchitis, emphysema, and reactive airway disease. These include cough, worsening dyspnea, progressive exercise intolerance, sputum production, and alteration in mental status. Symptoms include the following:
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Productive cough or acute chest illness
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Breathlessness
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Wheezing
Systemic manifestations (decreased fat-free mass, impaired systemic muscle function, osteoporosis, anemia, depression, pulmonary hypertension, cor pulmonale, left-sided heart failure
A productive cough or an acute chest illness is common. The cough usually is worse in the mornings and produces a small amount of colorless sputum.
Breathlessness is the most significant symptom, but it usually does not occur until the sixth decade of life (although it may occur much earlier). By the time the FEV1 has fallen to 50% of predicted, the patient is usually breathless upon minimal exertion. Despite the fact that FEV1 is the most common variable used to grade the severity of COPD, although it is not the best predictor of mortality.
Wheezing may occur in some patients, particularly during exertion and exacerbations.
The value of patient history and physical examination was addressed in the 2011 update to the American College of Physicians/American College of Chest Physicians/American Thoracic Society/European Respiratory Society (ACP/ACCP/ATS/ERS) guideline for diagnosis and management of stable COPD. According to the 2011 guideline, a history of more than 40 pack-years of smoking was the best single predictor of airflow obstruction; however, the most helpful information was provided by a combination of the following 3 signs [34] :
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Self-reported smoking history of more than 55 pack-years
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Wheezing on auscultation
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Self-reported wheezing
If all 3 signs are absent, airflow obstruction can be nearly ruled out. [34]
With disease progression, intervals between acute exacerbations become shorter, and each exacerbation may be more severe. The rate of COPD exacerbations appears to reflect an independent susceptibility phenotype. [35]
COPD is now known to be a disease with systemic manifestations, and the quantification of these manifestations has proved to be a better predictor of mortality than lung function alone. Many patients with COPD may have decreased fat-free mass, impaired systemic muscle function, osteoporosis, anemia, depression, pulmonary hypertension, cor pulmonale, and even left-sided heart failure. Depression is not uncommon in subjects with COPD. [36]
In a study by Spitzer et al in Germany, airflow limitation as measured by spirometry was significantly more common in adults with posttraumatic stress disorder than in controls. Results were adjusted for lifestyle, clinical, and sociodemographic factors. [37]
In addition, COPD appears to increase the risk for mild cognitive impairment (MCI). Investigators from the Mayo Clinic Study of Aging—a population-based, cross-sectional study of 1,927 participants—reported an association between COPD and an increased risk of having MCI, MCI subtypes, and memory loss in elderly patients. [38, 39] They also observed a dose-response relationship between COPD duration and an increased risk for cognitive problems.
The prevalence of MCI was significantly higher in patients with COPD (n = 288) (27%) than in those without COPD (15%), and there was a nearly twofold higher odds ratio (1.87) for MCI in patients with COPD. Moreover, the odds ratio increased from 1.6 in patients with COPD for 5 years or less to 2.1 in those who had COPD for longer than 5 years. [38, 39]
Some important clinical and historical differences may help distinguish between the types of COPD. Classic findings for patients with chronic bronchitis include productive cough with gradual progression to intermittent dyspnea; frequent and recurrent pulmonary infections; and progressive cardiac/respiratory failure with edema and weight gain. Classic findings for patients with emphysema include a long history of progressive dyspnea with late onset of nonproductive cough; occasional mucopurulent relapses; and eventual cachexia and respiratory failure.
Physical Examination
The sensitivity of a physical examination in detecting mild to moderate COPD is relatively poor; however, physical signs are quite specific and sensitive for severe disease. Patients with severe disease experience tachypnea and respiratory distress with simple activities.
The respiratory rate increases in proportion to disease severity. Use of accessory respiratory muscles and paradoxical indrawing of lower intercostal spaces is evident (known as the Hoover sign). In advanced disease, cyanosis, elevated jugular venous pulse (JVP), and peripheral edema can be observed.
Thoracic examination reveals the following:
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Hyperinflation (barrel chest)
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Wheezing – Frequently heard on forced and unforced expiration
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Diffusely decreased breath sounds
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Hyperresonance on percussion
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Prolonged expiration
In addition, coarse crackles beginning with inspiration may be heard.
Certain characteristics allow differentiation between disease that is predominantly chronic bronchitis and that which is predominantly emphysema.
Chronic bronchitis characteristics include the following:
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Patients may be obese
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Frequent cough and expectoration are typical
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Use of accessory muscles of respiration is common
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Coarse rhonchi and wheezing may be heard on auscultation
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Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and cyanosis
Emphysema characteristics include the following:
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Patients may be very thin with a barrel chest
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Patients typically have little or no cough or expectoration
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Breathing may be assisted by pursed lips and use of accessory respiratory muscles; patients may adopt the tripod sitting position
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The chest may be hyperresonant, and wheezing may be heard
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Heart sounds are very distant
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Overall appearance is more like classic COPD exacerbation
Staging
The severity of airflow obstruction was the primary means of staging COPD until the American Thoracic Society (ATS) provided criteria for staging COPD based on the presence of obstruction (ratio of FEV1 to forced vital capacity [FEV1/FVC] < 70%) and its severity as measured by percent of predicted FEV1.
ATS and Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria for assessing the severity of airflow obstruction (based on the percent predicted postbronchodilator FEV1 when the FEV1/FVC is < 70%) are as follows:
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Stage I (mild) - FEV1 80% or greater of predicted
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Stage II (moderate) - FEV1 50-79% of predicted
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Stage III (severe) - FEV1 30-49% of predicted
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Stage IV (very severe) - FEV1 less than 30% of predicted or FEV1
However, these staging systems have limited utility in predicting mortality. The recognition that COPD is a systemic disease has helped in developing criteria that are better at predicting mortality than is assessment of airway obstruction alone. A widely used system for COPD prognosis is the BODE index (body mass index, obstruction [FEV1], dyspnea [modified Medical Research Council dyspnea scale], and exercise capacity [6MWD]). [28]
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Venn diagram of chronic obstructive pulmonary disease (COPD). Chronic obstructive lung disease is a disorder in which subsets of patients may have dominant features of chronic bronchitis, emphysema, or asthma. The result is airflow obstruction that is not fully reversible.
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Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells.
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Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells (high-powered view).
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Gross pathology of advanced emphysema. Large bullae are present on the surface of the lung.
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Gross pathology of a patient with emphysema showing bullae on the surface.
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At high magnification, loss of alveolar walls and dilatation of airspaces in emphysema can be seen.
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Posteroanterior (PA) and lateral chest radiograph in a patient with severe chronic obstructive pulmonary disease (COPD). Hyperinflation, depressed diaphragm, increased retrosternal space, and hypovascularity of lung parenchyma are demonstrated.
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A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragm on lateral chest radiograph.
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A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragm on posteroanterior chest radiograph.
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Severe bullous disease as seen on a computed tomography (CT) scan in a patient with chronic obstructive pulmonary disease (COPD).
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Pressure volume curve comparing lungs with emphysema, lungs with restrictive disease, and normal lungs.
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Flow volume curve of a patient with emphysema shows marked decrease in expiratory flow, hyperinflation, and air trapping (patient B) compared with a patient with restrictive lung disease, who has reduced lung volumes and preserved flow (patient A).
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Forced expiratory volume in 1 second (FEV1) can be used to evaluate the prognosis in patients with emphysema. The benefit of smoking cessation is shown here because the deterioration in lung function parallels that of a nonsmoker, even in late stages of the disease. Redrawn from Fletcher C, Peato R. The natural history of chronic airflow obstruction. Br Med J 1977; 1: 1645-1648.
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Oxygen therapy via nasal cannula.
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Home supplemental oxygen.
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Bilevel positive airway pressure (BiPAP).
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Pulmonary rehabilitation.
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Chronic obstructive pulmonary disease (COPD). Pulmonary rehabilitation.
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Chest radiograph of an emphysematous patient shows hyperinflated lungs with reduced vascular markings. Pulmonary hila are prominent, suggesting some degree of pulmonary hypertension (Correa da Silva, 2001).
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Schematic representation of another sign of emphysema on the lateral chest radiograph. When the retrosternal space (defined as the space between the posterior border of the sternum and the anterior wall of the mediastinum) is larger than 2.5 cm, it is highly suggestive of overinflated lungs. This radiograph is from a patient with pectus carinatum, an important differential diagnosis to consider when this space is measured (Correa da Silva, 2001).
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Close-up image shows emphysematous bullae in the left upper lobe. Note the subpleural, thin-walled, cystlike appearance (Correa da Silva, 2001).
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A, Frontal posteroanterior (PA) chest radiograph shows no abnormality of the pulmonary vasculature, with normal intercostal spaces and a diaphragmatic dome between the 6th and 7th anterior ribs on both sides. B, Image in a patient with emphysema demonstrating reduced pulmonary vasculature resulting in hyperlucent lungs. The intercostal spaces are mildly enlarged, and the diaphragmatic domes are straightened and below the extremity of the seventh rib (Correa da Silva, 2001).
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A, Lateral radiograph of the chest shows normal pulmonary vasculature, a retrosternal space within normal limits (< 2.5 cm), and a normal angle between the diaphragm and the anterior thoracic wall. B, Lateral view of the chest shows increased pulmonary transparency, increased retrosternal space (>2.5 cm), and an angle between the thoracic wall and the diaphragm >90 degrees. Straightening of the diaphragm can be more evident in this projection than on others (Correa da Silva, 2001).
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High-resolution CT (HRCT) in a patient after viral bronchiolitis obliterans demonstrates areas of airtrapping, which is predominant in the inferior lobes and associated with bronchiectasis in the left lower lobe. Note that the decreased attenuation caused by the airtrapping can simulate emphysema (Correa da Silva, 2001).
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Pediatric high-resolution CT (HRCT) shows a hyperinflated right lung with large pulmonary bullae due to congenital lobar emphysema (Correa da Silva, 2001).
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High-resolution CT (HRCT) demonstrates areas of centriacinar emphysema. Note the low attenuation areas without walls due to destruction of the alveoli septae centrally in the acini. Red element shows the size of a normal acinus (Correa da Silva, 2001).
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High-resolution CT (HRCT) shows large bullae in both inferior lobes due to uniform enlargement and destruction of the alveoli walls causing distortion of the pulmonary architecture (Correa da Silva, 2001).
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Panacinar emphysema of the left lung in a patient with a right lung transplant. Note the red element showing the size of a normal acinus and its discrepancy with the destroyed and enlarged airspaces of the left lower lobe (Correa da Silva, 2001).
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High-resolution CT (HRCT) shows subpleural bullae consistent with paraseptal emphysema. Red mark shows the size of a normal acinus (Correa da Silva, 2001).
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High-resolution CT (HRCT) shows enlarged air-spaces or bullae adjoining pulmonary scars, consistent with paracicatricial emphysema. Red mark shows the size of a normal acinus (Correa da Silva, 2001).
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CT densitovolumetry of a nonsmoker, healthy young patient shows normal lungs. Less than 0.35% of lungs have attenuations below -950 HU (Correa da Silva, 2001).
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Expiratory CT densitovolumetry shows no areas of airtrapping (Correa da Silva, 2001).
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CT densitovolumetry in a patient with lung cancer. Three-dimensional (3D) image shows that the cancer is in the portion of the right lung that was less affected by emphysema in a patient with poor pulmonary function (Correa da Silva, 2001).
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CT densitovolumetry shows the attenuation mask. Green areas are those with attenuation below the selected threshold (here, -950 HU to evaluate emphysema), and pink areas are those with attenuations above the threshold. Area outside the patient is highlighted in green because of air (Correa da Silva, 2001).
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CT densitovolumetry demonstrates irregular distribution of the emphysema, with substantial predominance in the left lung (Correa da Silva, 2001).
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- Overview
- Presentation
- DDx
- Workup
- Treatment
- Approach Considerations
- Smoking Cessation
- Management of Inflammation
- Management of Infection
- Management of Sputum Viscosity and Secretion Clearance
- PPIs for Exacerbations and the Common Cold
- Oxygen Therapy and Hypoxemia
- Vaccination to Reduce Infections
- Alpha1-Antitrypsin Deficiency Treatment
- Inpatient Care
- Bullectomy
- Lung Volume Reduction Surgery
- Lung Transplantation
- Long-term Monitoring
- End-of-Life Care
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- Medication
- Medication Summary
- Beta2-Adrenergic Agonists, Short-Acting
- Beta2-Adrenergic Agonists, Long-Acting
- Anticholinergics, Respiratory
- Xanthine Derivative
- Phosphodiesterase-4 Inhibitors
- Corticosteroids, Inhalant
- Corticosteroids, Oral
- Beta-Adrenergic Agonist and Anticholinergic Agent Combinations
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