The cause of his problem was Chronic Obstructive Pulmonary Disease - COPD for this patient had a long term history of smoking.
The amount and duration of smoking contribute to disease severity. Thus, a key step in the evaluation of patients with suspected COPD is to ascertain the number of pack-years smoked (packs of cigarettes per day multiplied by the number of years), as the majority (about 80 percent) of patients with COPD in Singapore have a history of cigarette smoking. A smoking history should include the age of starting and the age of quitting, as patients may underestimate the number of years they smoked. With enough smoking, almost all smokers will develop measurably reduced lung function. While studies have shown an overall "dose-response curve" for smoking and lung function, some individuals develop severe disease with fewer pack years and others have minimal to no symptoms despite many pack years.
The exact threshold for the duration/intensity of cigarette smoking that will result in COPD varies from one individual to another. In the absence of a genetic/environmental/occupational predisposition, smoking less than 10 to 15 pack-years of cigarettes is unlikely to result in COPD. On the other hand, the single best variable for predicting which adults will have airflow obstruction on spirometry is a history of more than 40 pack-years of smoking.
Symptoms and pattern of onset — 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 (table 2A). However, any of these symptoms may develop independently and with variable intensity.
There are three typical ways in which patients with COPD present
●Patients who have an extremely sedentary lifestyle but few complaints require careful questioning to elicit a history that is suggestive of COPD. Some patients unknowingly avoid exertional dyspnea by shifting their expectations and limiting their activity. They may be unaware of the extent of their limitations or that their limitations are due to respiratory symptoms, although they may complain of fatigue.
●Patients who present with respiratory symptoms generally complain of dyspnea and chronic cough. The dyspnea may initially be noticed only during exertion. However, it eventually becomes noticeable with progressively less exertion or even at rest. The chronic cough is characterized by the insidious onset of sputum production, which occurs in the morning initially, but may progress to occur throughout the day. The daily volume rarely exceeds 60 mL. The sputum is usually mucoid but becomes purulent during exacerbations.
●Patients who present with episodes of increased cough, purulent sputum, wheezing, fatigue, and dyspnea that occur intermittently, with or without fever. Diagnosis can be problematic in such patients. The combination of wheezing plus dyspnea may lead to an incorrect diagnosis of asthma. Conversely, other illnesses with similar manifestations are often incorrectly diagnosed as a COPD exacerbation (eg, heart failure, bronchiectasis, bronchiolitis) The interval between exacerbations decreases as the severity of the COPD increases.
Physical examination — The findings on physical examination of the chest vary with the severity of the COPD
●Early in the disease, the physical examination may be normal or may show only prolonged expiration or wheezes on forced exhalation.
●As the severity of the airway obstruction increases, physical examination may reveal hyperinflation (eg, increased resonance to percussion), decreased breath sounds, wheezes, crackles at the lung bases, and/or distant heart sounds . Features of severe disease include an increased anteroposterior diameter of the chest ("barrel-shaped" chest) and a depressed diaphragm with limited movement based on chest percussion.
●Patients with end-stage COPD may adopt positions that relieve dyspnea, such as leaning forward with arms outstretched and weight supported on the palms or elbows. This posture may be evident during the examination or may be suggested by the presence of callouses or swollen bursae on the extensor surfaces of forearms. Other physical examination findings include use of the accessory respiratory muscles of the neck and shoulder girdle, expiration through pursed lips, paradoxical retraction of the lower interspaces during inspiration (ie, Hoover's sign) cyanosis, asterixis due to severe hypercapnia, and an enlarged, tender liver due to right heart failure. Neck vein distention may also be observed because of increased intrathoracic pressure, especially during expiration.
●Yellow stains on the fingers due to nicotine and tar from burning tobacco are a clue to ongoing and heavy cigarette smoking.
Clubbing of the digits is not typical in COPD (even with associated hypoxemia) and suggests comorbidities such as lung cancer, interstitial lung disease, or bronchiectasis.
Laboratory — No laboratory test is diagnostic for COPD, but certain tests are sometimes obtained to exclude other causes of dyspnea and comorbid diseases.
Assessment for anemia is an important step in the evaluation of dyspnea. Measurement of plasma brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) concentrations is useful as a component of the evaluation of suspected heart failure (HF).
Testing for alpha-1 anti-trypsin (AAT) deficiency should be obtained in all symptomatic adults with persistent airflow obstruction on spirometry. Especially suggestive subsets include the presence of emphysema in a young individual (eg, age 45 years), emphysema in a nonsmoker or minimal smoker, emphysema characterized by predominantly basilar changes on the chest radiograph, or a family history of emphysema.
Pulmonary function tests — Pulmonary function tests (PFTs), particularly spirometry, are the cornerstone of the diagnostic evaluation of patients with suspected COPD In addition, PFTs are used to determine the severity of the airflow limitation, assess the response to medications, and follow disease progression.
Spirometry — When evaluating a patient for possible COPD, spirometry is performed pre and post-bronchodilator administration (eg, inhalation of albuterol 400 mcg) to determine whether airflow limitation is present and whether it is partially or fully reversible. Airflow limitation that is irreversible or only partially reversible with bronchodilator is the characteristic physiologic feature of COPD. Screening spirometry is not currently recommended.
Lower limit of normal FEV1/FVC — GOLD guidelines support using the traditional postbronchodilator FEV1/FVC ratio less than 0.7 as the threshold that indicates airflow limitation . However, the FEV1/FVC ratio decreases with age, so use of the fifth percentile lower limit of normal (LLN) of the FEV1/FVC ratio, rather than the absolute value of <0.7, has been advocated by some as a dividing point for the diagnosis of COPD.
Global Lung Initiative equations — As an alternative to using the LLN of FEV1/FVC to define normal airflow on spirometry, a new approach may utilize equations developed by the Global Lung Initiative (GLI) [8,76,77]. Using GLI equations, z scores (number of standard deviations above or below mean) were calculated for FEV1, FVC, and FEV1/FVC and compared with fixed ratio data.
Forced expiratory volume in six seconds — The forced expiratory volume in six seconds (FEV6), obtained by stopping the expiratory effort after 6 seconds rather than at cessation of airflow, is an acceptable surrogate for the FVC.
Peak expiratory flow — Peak expiratory flow (PEF) is often used as a measure of airflow limitation in asthma but may underestimate the degree of airflow limitation in COPD . In addition, a low PEF is not specific for airflow limitation and requires corroboration with spirometry.
Lung volumes — Lung volume measurement is not needed for all patients with suspected COPD. However, when a reduced FVC is noted on postbronchodilator spirometry, lung volume measurement by body plethysmography is used to determine whether the reduction in FVC is due to air trapping, hyperinflation, or a concomitant restrictive ventilatory defect. Decreased inspiratory capacity (IC) and vital capacity, accompanied by an increased total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV) are indicative of hyperinflation. An increased FRC with a normal TLC is indicative of air trapping without hyperinflation.
Diffusing capacity — The diffusing capacity for carbon monoxide (DLCO) is an excellent index of the degree of anatomic emphysema in smokers with airflow limitation, but is not needed for routine assessment of COPD . The indications for performing a DLCO measurement include hypoxemia by pulse oximetry (eg, arterial oxygen tension [PaO2] <92 mmHg), breathlessness out of proportion to the degree of airflow limitation, and evaluation for lung resection or lung volume reduction surgery.
Pulse oximetry and arterial blood gases — Pulse oximetry is a noninvasive, easily performed test that assesses blood oxygen saturation. It has reduced the number of patients who require arterial blood gases (ABGs), as supplemental oxygen is not needed when the pulse oxygen saturation (SpO2) is >88 percent. However, pulse oximetry does not provide information about alveolar ventilation or hypercapnia (PaCO2 >45mmHg), and assessment of oxygenation by pulse oximetry may be inaccurate in the setting of an acute exacerbation of COPD.
The indications for measuring ABGs (eg, PaO2, PaCO2, and acidity [pH]), which must be considered in the clinical context, include the following:
●Low FEV1 (eg, <50 percent predicted)
●Low oxygen saturation by pulse oximetry (eg, <92 percent)
●Depressed level of consciousness
●Acute exacerbation of COPD
●Assessment for hypercapnia in at risk patients 30 to 60 minutes after initiation of supplemental oxygen.
Imaging — Chest radiography and computed tomography (CT) are typically performed in patients with COPD when the cause of dyspnea or sputum production is unclear and during acute exacerbations to exclude complicating processes (eg, pneumonia, pneumothorax, heart failure). Imaging is not required to diagnose COPD.
Chest radiography — The main reasons to obtain a chest radiograph when evaluating a patient for COPD are to exclude alternative diagnoses, evaluate for comorbidities (eg, lung cancer with airway obstruction, bronchiectasis, pleural disease, interstitial lung disease, heart failure), or to look for complications of COPD (eg, pneumonia, pneumothorax) that might be suggested by a change in symptoms.
Plain chest radiographs have poor sensitivity for detecting COPD. As an example, only about half of patients with COPD of moderate severity are identified as having COPD by a plain chest radiograph (ie, the sensitivity of 50 percent).
Computed tomography — CT has greater sensitivity and specificity than standard chest radiography for the detection of emphysema. This is particularly true with high resolution CT (ie, collimation of 1 to 2 mm) [86-89]. The use of expiratory scans, particularly when used in conjunction with the inspiratory scans, can also be used to assess non-emphysematous air trapping as a surrogate measure for small airway abnormality.
The diagnosis of COPD is confirmed by the following
●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] PLUS an FEV1 less than 80 percent of predicted) that is incompletely reversible after the administration of an inhaled bronchodilator (table 2A-B). (See 'Pulmonary function tests' above.)
●The absence of an alternative explanation for the symptoms and airflow limitation. 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 suggests repeating spirometry on a separate occasion to demonstrate the 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.
●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.
●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.
●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 5). 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 4 and figure 5) . A high-resolution CT scan with three-dimensional reconstruction can be helpful. The gold standard for diagnosis is direct visualization.
●Bronchiectasis – Bronchiectasis, a condition of an 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.
●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 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.
●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. Thus, tuberculosis is both a risk factor for COPD and potential comorbidity
●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 6). Symptoms include the 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.
●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.
●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.
●SG 0: Normal spirometry
●SG 1: Mild, postbronchodilator FEV1/FVC ratio <0.7, FEV1 ≥60 percent predicted
●SG 2: Moderate, postbronchodilator FEV1/FVC ratio <0.7, 30 percent ≤FEV1 <60 percent predicted
●SG 3: Severe, postbronchodilator FEV1/FVC ratio <0.7, FEV1 <30 percent predicted
●SG U: Undefined, postbronchodilator FEV1/FVC ratio >0.7, FEV1 <80 percent predicted