National COPD Month on November, 2018: Today I was diagnosed with COPD by a Dr. He gave me disability papers
November, 2018 is National COPD Month 2018. COPD - Update Quarter 1 2013 (Volume 7, Issue 1), NHLBI, NIH National COPD Awareness Month
In order to qualify for Social Security Disability Insurance (SSDI) benefits, through the Social Security Administration (SSA), you must prove your disability prevents you from doing any type of Substantial Gainful Activity (SGA).
SGA income for 2013 is $1040.00/mo. Anything over that amount of income will disqualify you for SSDI benefits (unless you are blind). This is not as easy as it may seem. You must be able to prove that you cannot do your previous work as well as ANY other work in the national economy. This includes such mundane work as surveillance monitor, envelope stuffer or any other sedentary work. Just because you cannot do your previous job does not necessarily mean that you cannot do ANY work at SGA level.
Of course, it does not depend just on SGA. It also depends on the severity of your medical condition, your age, and a number of other requirements. On average, it takes about two years to get approval for SSDI if you qualify.
Chronic Obstructive Pulmonary Disease?
Chronic obstructive pulmonary disease (COPD) is arguably the most important lung disease encountered in the United States, for the following reasons:
The large number of patients with this disorder.
The high frequency of physician encounters in both outpatient and inpatient settings.
The substantial debility, physical impairment, and reduced quality of life caused by the condition.
The need for continued outpatient management.
The associated medical morbidity and need for hospital care during acute exacerbations.
The high utilization of medical resources associated with hospital care for exacerbations as well as with chronic treatment, eg, longterm oxygen therapy.
The disease is the fourth-ranked cause of death in the United States and currently kills more than 100,000 Americans each year. Beginning in 2000, the number of females dying annually from COPD exceeded the number of males.
The definition and diagnostic evaluation of COPD are reviewed here. Other issues, including the etiology and management of COPD are presented elsewhere. (See appropriate topic reviews).
DEFINITION — It is important to realize the difference between the definition of a disease and its diagnostic criteria . The defining characteristics of a disease are the common properties specifying the group of abnormal persons on whom the description of the disease is based. The definition of a disease is important in communication.
Diagnostic criteria are features of the disease chosen from its description that are found by empirical research to best distinguish the disease from others which resemble it. The diagnostic criteria may or may not include features of the defining characteristics and frequently include features that do not appear in the definition . The diagnostic criteria are much more important than definitions in both clinical practice and research. As long as diagnostic criteria are clearly stated, the definition is of lesser importance [2,3] (show table 1). (See "ATS/ERS Summary: Standards for the diagnosis and treatment of patients with COPD" section on diagnosis).
A number of expert panels, including the American Thoracic Society, European Respiratory Society, and the British Thoracic Society have all defined COPD using slightly different over the past ten years . The Global Initiative for Chronic Obstructive Lung Disease (GOLD), a report produced by an expert panel convened jointly by the National Heart, Lung, and Blood Institute and the World Health Organization, defined COPD as :
"A disease state characterized by airflow limitation that is not fully reversible. Airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases."
Airflow obstruction is the result of both small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema). The relative contributions of each vary from person to person, and can be accompanied by partially reversible airways hyperreactivity [2-4].
Earlier definitions have also focused on the terms emphysema, chronic bronchitis, and asthma, which are not included in the definition provided above [3,5,6].
Chronic bronchitis is a clinical diagnosis defined by the presence of chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough have been excluded . (See "Evaluation of subacute and chronic cough in adults")
Emphysema is a pathological term describing the abnormal permanent enlargement of airspaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis; there is no fibrosis visible to the naked eye . Emphysema is frequently present in patients with moderate and severe COPD .
Asthma is defined as an inflammatory disease of the airways characterized by an increased responsiveness of the trachea and bronchi to various stimuli, and manifested by a widespread narrowing of the airways that changes in severity either spontaneously or as a result of therapy . (See "Epidemiology of asthma").
Disease interrelationships — Although neither chronic bronchitis nor emphysema is a required element in the definition of COPD, there is substantial overlap among all of the entities described above. Figure 1 is a nonproportional Venn diagram showing the relationship of chronic bronchitis, emphysema, asthma, and airflow obstruction; the shaded area delineates COPD (show figure 1). Specific issues related to some of the subsets on this diagram include:
Patients with asthma (subset 9) whose airflow obstruction is completely reversible are not considered to have COPD.
It is virtually impossible in many cases to differentiate patients with asthma whose airflow obstruction does not remit completely from persons with COPD who have partially reversible airflow obstruction and airway hyperreactivity . Because of this difficulty, patients with nonremitting asthma are classified as having COPD (subsets 6 to 8).
Chronic bronchitis and emphysema with airflow obstruction usually occur together (subset 5) . Some patients may have asthma associated with these two disorders (subset 8).
Persons with asthma who are exposed to chronic irritation, as from cigarette smoke, may develop chronic productive cough, a feature of chronic bronchitis (subset 6). In the United States, such patients are often referred to as having asthmatic bronchitis or the asthmatic form of COPD.
Persons with chronic bronchitis  or emphysema  without airflow obstruction are not classified as COPD; they are classified as Stage 0: At Risk, in the GOLD Staging system (show table 4) (subsets 1, 2, and 11).
Patients with airways obstruction due to diseases with known etiology or specific pathology, such as cystic fibrosis or obliterative bronchiolitis (subset 10), are not included in the definition of COPD. (See "Bronchiolitis in adults", and see "Clinical manifestations of pulmonary disease in cystic fibrosis").
Evidence suggests that the bronchial inflammation of COPD is pathophysiologically different from that of asthma, thus adding justification for separating asthma from COPD when possible [12-14]. COPD is associated with CD-8+ lymphocytes, neutrophils and CD-68+ monocytes/macrophages predominate (show histology 1) [15-18]. In contrast, asthma is associated with CD4+ (helper) T-lymphocytes, eosinophils, and inccreased interleukin (IL)-4 and IL-5, (a Th2-type response) (show figure 2). There are many patients with pathologic overlap suggesting that the terms COPD and asthma fail to identify the phenotypes that exist .
From the clinical and epidemiologic viewpoints, asthma affects all ages and has a low mortality-to-prevalence ratio. COPD is predominantly a disease of the sixth decade of life and later and has a high ratio of mortality to prevalence. (See "Natural history and prognosis of COPD").
A number of animal models of induction of emphysema by cigarette smoking have been reported [19,20]. Why then should we not define COPD in terms of cigarette smoking as its main etiology? The reason is that there are other harmful inhalants that contribute to the pathogenesis of COPD. Furthermore, only about 15 to 20 percent of smokers develop COPD suggesting that host factors (most likely genetic) also contribute to pathogenesis of the disease. (See "Risk factors for COPD").
Alpha-1 antitrypsin deficiency — The only established genetic abnormality that predisposes to lung disease clinically and pathologically similar to COPD is alpha-1 antitrypsin [AAT] deficiency . For convenience, this lung disease will be referred to as AAT-COPD. (See "Clinical manifestations, diagnosis, and natural history of alpha-1-antitrypsin deficiency").
Severe AAT deficiency has a frequency of about 1 in 3,000 live births. About 95 percent of severely deficient persons have Pi*ZZ alleles rather than the normal Pi*MM. These individuals may have liver disease in infancy or in old age, or they may develop AAT-COPD in their thirties or forties, especially if they smoke. (See "Extrapulmonary manifestations of alpha-1-antitrypsin deficiency").
Studies in Europe and the United States indicate that only about 10 percent of those predicted on the basis of genetic screening studies are diagnosed with AAT deficiency. Undiagnosed individuals with severe deficiency either have no lung disease, or have lung disease masquerading as COPD or non-remitting asthma. The relative proportions of these two groups are unknown. However, as many as 2 percent of patients with COPD or sustained asthma may have severe AAT deficiency.
For these reasons, the World Health Organization , the American Thoracic Society, the European Respiratory Society and a number of medical organizations  recommend that persons with known COPD, or asthma with non-remittent airflow obstruction, be screened for AAT deficiency. (See "ATS/ERS statement: Standards for the diagnosis and management of individuals with AAT deficiency II. Lung disease" and see "ATS/ERS statement: Standards for the diagnosis and management of individuals with AAT deficiency IV. Genetic testing").
History — Patients with COPD have usually been smoking at least 20 cigarettes per day for 20 or more years before symptoms develop. Chronic productive cough, sometimes with wheezing, often begins when patients are in their forties, although the patients are frequently less aware of these symptoms than the persons they live with (show table 1).
An acute chest illness, generally when patients are in their fifties, may prompt a visit to the doctor. Dyspnea on effort does not usually begin until the mid sixties or early seventies. Sputum production is insidious, initially occurring only in the morning; the daily volume rarely exceeds 60 mL. Sputum is usually mucoid but becomes purulent with an exacerbation. Key elements in the diagnostic assessment are presented in Table 2A-2B (show table 2A-2B).
Acute chest illnesses may occur intermittently, and are characterized by increased cough, purulent sputum, wheezing, dyspnea, and occasionally fever. The history of wheezing and dyspnea may lead to the erroneous diagnosis of asthma. Conversely, other diseases with respiratory symptoms are commonly mistaken for COPD, especially in patients who also smoke cigarettes (show table 3).
With disease progression, the intervals between acute exacerbations shorten. Late in the course of the illness, an exacerbation may give rise to hypoxemia with cyanosis; the latter is accentuated by erythrocytosis. Associated findings also include:
Weight loss - Approximately 20 percent of patients with moderate and severe disease experience weight loss and loss of fat free body mass. There is increased muscle protein breakdown that is believed to be due to systemic factors such as systemic effects of lung inflammation, oxidative stress, and an excess of circulating cytokines. These abnormalities of muscle contribute to decreased exercise performance. (See "ATS/ERS Summary: Standards for the diagnosis and treatment of patients with COPD" section on management of stable COPD: nutrition, and see "Natural history and prognosis of COPD" section on Body Mass).
Hypercapnia with more severe hypoxemia in the setting of end-stage disease.
Morning headache, which suggests hypercapnia.
Cor pulmonale with right heart failure and edema - These abnormalities can develop in patients with hypoxemia and hypercapnia.
Hemoptysis - Since bronchogenic carcinoma occurs with increased frequency in smokers with COPD, an episode of hemoptysis raises the possibility that carcinoma has developed. However, most episodes of hemoptysis are due to bronchial mucosal erosion. (See "Etiology and evaluation of hemoptysis in adults").
Physical examination — Physical examination of the chest early in the disease may show only prolonged expiration and wheezes on forced exhalation. As obstruction progresses, hyperinflation becomes evident, and the anteroposterior diameter of the chest increases. The diaphragm is depressed and limited in its motion. Breath sounds are decreased and heart sounds often become distant . Coarse crackles may be heard at the lung bases. Wheezes are frequently heard, and permit the diagnosis of airflow obstruction (show table 2A-2B).
Although airflow obstruction can be caused by many conditions, if the history and chest radiograph are compatible, a clinical diagnosis of COPD may be made. However, a forced expiratory spirogram before and after bronchodilator is always necessary for confirmation and quantification of the airflow obstruction. (See "Overview of pulmonary function testing in adults").
Patients with end-stage COPD may adopt positions which relieve dyspnea, such as leaning forward with arms outstretched and weight supported on the palms. Other signs in a patient with end-stage disease may include:
The full use of the accessory respiratory muscles of the neck and shoulder girdle.
Expiration through pursed lips.
Paradoxical retraction of the lower interspaces during inspiration (Hoover's sign) .
An enlarged, tender liver secondary to right heart failure. Neck vein distention, especially during expiration, may be observed in the absence of heart failure because of increased intrathoracic pressure.
Asterixis due to severe hypercapnia.
Plain chest radiography — Since emphysema is defined in anatomical terms, radiographic images of the lungs provide the clearest evidence of its presence. Nevertheless, the plain chest radiograph is insensitive for diagnosing emphysema; only about half of the instances are detected when the disease is of moderate severity.
Overdistention of the lungs is indicated on frontal chest radiographs by a low, flat diaphragm and a long, narrow heart shadow. Flattening of the diaphragmatic contour and an increased retrosternal airspace are observed on the lateral projection. Rapid tapering of the vascular shadows accompanied by hypertransradiancy of the lungs is a sign of emphysema.
Bullae, presenting as radiolucent areas larger than one centimeter in diameter and surrounded by arcuate hairline shadows, are proof of the presence of emphysema. However, bullae reflect only locally severe disease and are not necessarily indicative of widespread emphysema.
Pulmonary hypertension and right ventricular hypertrophy are indicated by prominent hilar vascular shadows and encroachment of the heart shadow on the retrosternal space as the right ventricle enlarges anteriorly . The cardiac enlargement may become evident only on comparison with previous chest radiographs.
Computed tomography — Computed tomography (CT), especially high resolution CT (collimation of 1 to 2 mm), has much greater sensitivity and specificity than standard chest radiography for the diagnosis of emphysema (show radiograph 1 and show radiograph 2) [27,28]. (See "High resolution computed tomography of the lungs").
As an example, one study of 41 patients with emphysema as determined by high resolution CT found that 16 had no evidence of emphysema by chest radiograph . Ten of these sixteen, however, had decreased gas exchange as detected by carbon monoxide diffusion studies. The degree of abnormal gas exchange was inversely related to the severity of disease as determined by high resolution CT.
CT may also identify the specific anatomic type of emphysema, (ie, panacinar or centriacinar); either can occur alone in COPD but most often they occur together.
Centriacinar emphysema occurs preferentially in the upper lobes and produces holes in the center of the secondary pulmonary lobules (show radiograph 1).
Panacinar emphysema more commonly involves the lung bases, resulting in a generalized paucity of vascular structures; it also affects the entire secondary pulmonary lobule (show radiograph 2).
However, since this information rarely alters therapy, CT has no place in the routine care of patients with COPD. It is the main imaging tool for estimating the benefit of pulmonary resection for giant bullous disease and for diagnosing complicating bronchiectasis. Along with ventilation-perfusion scintiscanning, CT also plays a major role in evaluating emphysematous patients for lung volume reduction surgery. (See "Lung volume reduction and bullectomy in COPD").
Pulmonary function tests — Pulmonary function measurements are necessary for diagnosing and assessing the severity of airflow obstruction, and are helpful in following its progress. Airflow obstruction is an important indicator of impairment and the likelihood of blood gas abnormalities. The FEV1 is easily measurable and has less variability than other measurements of airways dynamics, and its normal value is predictable from age, gender, and height. (See "Overview of pulmonary function testing in adults").
The FVC is also readily measured, although it is dependent on the expiratory time in severe COPD. In the mildest degree of airflow obstruction, the FEV1/FVC ratio falls below 0.70 and the FEV1 percent predicted is normal. The FEV1 and the FEV1/FVC ratio fall progressively as the severity of COPD increases. As noted earlier, up to 30 percent of patients have an increase of 15 percent or more in their FEV1 following inhalation of a beta-agonist aerosol. However, the absence of a bronchodilator response during a single test never justifies withholding bronchodilator therapy. No tests of airflow obstruction can distinguish between chronic bronchitis and emphysema.
Lung volume measurements reveal an increase in total lung capacity, functional residual capacity, and residual volume, and often a decrease in the vital capacity. The single breath carbon monoxide diffusing capacity is decreased in proportion to the severity of emphysema because of the loss of alveolar-capillary bed. The test is not specific, nor can it detect mild emphysema. (See "Diffusing capacity for carbon monoxide").
Arterial blood gases reveal mild or moderate hypoxemia without hypercapnia in the early stages. As the disease progresses, hypoxemia becomes more severe and hypercapnia supervenes. Hypercapnia is observed with increasing frequency as the FEV1 falls below one liter. Blood gas abnormalities worsen during acute exacerbations and may worsen during exercise and sleep. (See "Interpretation of arterial oxygen tension").
Erythrocytosis is infrequently observed in patients living at sea level who have arterial PO2 levels above 55 mmHg; the frequency of erythrocytosis increases as arterial PO2 falls below 55 mmHg. The response of the bone marrow to hypoxemia is complex, resulting in a variable relation between blood oxygen level and red cell mass in COPD.
Sputum examination — In stable chronic bronchitis, sputum is mucoid and the predominant cell is the macrophage. During an exacerbation, sputum usually becomes purulent with an influx of neutrophils. The Gram stain usually shows a mixture of organisms. The most frequent pathogens cultured from the sputum are Streptococcus pneumoniae and Haemophilus influenzae. Other oropharyngeal flora such as Moraxella catarrhalis have been shown to cause exacerbations. However, cultures and even Gram stains are rarely necessary before instituting antimicrobial therapy in the outpatient setting. (See "Role of infection in chronic obstructive pulmonary disease").
STAGING COPD — A staging system for COPD, in which the need for diagnostic evaluation and therapy is stratified by stage, has also been proposed although not yet validated (show table 4) . In an observational cohort study, 14,223 subjects had spirometry performed at baseline and five and 15 years later . Six percent of subjects met criteria for Stage 0 (symptomatic smokers with normal spirometry). Compared to a control group of asymptomatic smokers, individuals in the Stage 0 group did not demonstrate an accelerated decline in lung function, suggesting that Stage 0 is of little help in identifying smokers at risk of developing COPD . In a cross sectional study of more than 18,000 subjects from Europe, 12 percent were classified as Stage 0; they had the same risk factors for COPD as those suffering from the disease and the same increased medical care needs .
Subsequently, a novel staging system was constructed . The BODE index is a multidimensional 10-point scale based on:
B - body-mass index
O - obstruction of airflow quantified by the FEV1
D - dyspnea and quantified by the modified Medical Research council dyspnea scale (MMRC)
E - exercise capacity (quantified by the six-minute walk test).
Higher scores indicate a higher risk of death. The hazard ratio for death from any cause per one-point increase in the BODE score was 1.34 (95% CI, 1.26 to 1.42; P<0.001), and the hazard ratio for death from respiratory causes was 1.62 (95% CI, 1.48 to 1.77; P<0.001). The BODE index was better than the FEV1 at predicting the risk of death from any cause and from respiratory causes among patients with COPD.
We believe that spirometry, the BMI, and the MMRC staging of dyspnea should be used routinely for staging; the 6 min walk test is not easily done in the clinic setting. (See "Natural history and prognosis of COPD", section on BODE index and see "ATS/ERS Summary: Standards for the diagnosis and treatment of patients with COPD").
RECOMMENDATIONS — COPD is characterized by airflow limitation that is not fully reversible, and that is usually both progressive and associated with an abnormal inflammatory response to noxious particles or gases. There is substantial overlap among COPD, chronic bronchitis, and emphysema; however, these terms are not synonymous.
Clinical indications of early COPD, including dyspnea and chronic productive cough, are outlined in Table 1 (show table 1). Tables 2A and 2B summarize key points of the history, physical examination, and laboratory evaluation of COPD (show table 2A-2B). Once the diagnosis has been established, assessment of disease severity may help guide therapy (show table 4). (See "Overview of management of stable chronic obstructive pulmonary disease").
Cigarette smoking is by far the largest preventable risk factor in the development of COPD, and smoking cessation counseling is a critical aspects of disease management. (See "Overview of smoking cessation").
What disease did cured ham have?
A US study has linked eating cured meat like bacon and hot dogs with increased risk of lung disease.
The study is published in the American Journal of Respiratory and Critical Care Medicine and examines the link between frequent consumption of cured meats and impaired lung function in terms of the increased odds of chronic obstructive pulmonary disease (COPD).
Chronic obstructive pulmonary disease (COPD), of which emphysema and chronic bronchitis are the most common form (and often co-exist), is characterized by swelling of the airways.
According to the American Lung Association, COPD is the fourth leading cause of death in the US and more women now die from it than men. In 2003 it claimed 122,283 American lives.
Other studies, mostly on animals, have shown a link between nitrite consumption and reduced lung function.
Nitrites are added to cured meat such as bacon, hot dogs and cured ham as preservative, colour or as anti-bacterial agents. They are thought to generate reactive nitrogen species in the body -- molecules that cause structural damage to lung tissue, in a similar way to emphysema.
This is the first study to establish a direct connection between cured meat consumption and COPD.
The research team of four scientists was led by Dr Rui Jiang of the Division of General Medicine, Department of Medicine, at Columbia University in New York.
They examined data on 7,352 Americans aged 45 and over (average age 64.5 years) who took part in the Third National Health and Nutrition Examination Survey between 1988 and 1994.
The results showed that, even after adjusting for smoking, diet, age and other factors:
-- The more cured meat they ate, the poorer the participants' lung function.
-- Those who consumed cured meat 14 times a month were 78 per cent more likely to have COPD than those who ate none or very little.
Lung function was a measure of the amount of air a participant could blow out in one second (Forced Expiratory Volume for 1 sec, or FEV1). The total amount of air they could blow out after a deep breath was also measured (Forced Vital Capacity, FVC), but there was little effect on this measure.
Dr Jiang and colleagues concluded that:
"Frequent cured meat consumption was associated independently with an obstructive pattern of lung function and increased odds of COPD."
Critics of the study say that cured meat no longer contains the levels of nitrites that were present ten or twenty years ago, and therefore these results do not reflect today's situation. There are other sources of nitrites in the average diet, where only about 5 per cent comes from cured meat, they say.
Dr Jiang and colleagues did find that participants who ate the most cured meat were also more likely to smoke, be male, and of lower socio-economic status. They were also more likely to consume more calories, and eat less fresh fruit and vegetables.
However, the researchers pointed out that they adjusted for these factors. They said more studies should be done to find out if eating cured meat directly causes COPD or whether something else links the two.
According to the US National Library of Medicine, the leading cause of COPD is smoking, and 15 to 20 per cent of long term smokers develop the condition.
Long term tobacco smoking causes inflammation in the lungs and destroys the air sacs.
Apart from smoking, risk factors also include passive smoke inhalation, being male, and spending long periods of time in polluted atmospheres.
There is also a rare emphysema that afflicts a very small number of smokers and non-smokers alike, caused by a deficiency in the enzyme alpha-1 anti-trypsin.
Symptoms of COPD include: persistent shortness of breath (dyspnea) lasting from months to years, wheezing, finding it hard to exercise for very long, and coughing (with or without phlegm).
"Cured Meat Consumption, Lung Function, and Chronic Obstructive Pulmonary Disease among United States Adults."
Rui Jiang, David C. Paik, John L. Hankinson, and R. Graham Barr.
Am. J. Respir. Crit. Care Med. 2007; 175: 798-804.
First published online January 25 2007 as doi:10.1164/rccm.200607-969OC