DIAGNOSING COPD

Your doctor will diagnose COPD based on your signs and symptoms, your medical and family histories, and test results. Your doctor may ask whether you smoke or have had contact with lung irritants, such as secondhand smoke, air pollution, chemical fumes, or dust.

If you have an ongoing cough, let your doctor know how long you've had it, how much you cough, and how much mucus comes up when you cough. Also, let your doctor know whether you have a family history of COPD.

Your doctor will examine you and use a stethoscope to listen for wheezing or other abnormal chest sounds. He or she also may recommend one or more tests to diagnose COPD.

Lung Function Tests

Lung function tests measure how much air you can breathe in and out, how fast you can breathe air out, and how well your lungs deliver oxygen to your blood.

The main test for COPD is spirometry (spi-ROM-eh-tre). Other lung function tests, such as a lung diffusion capacity test, also might be used. During this painless test, a technician will ask you to take a deep breath in. Then, you'll blow as hard as you can into a tube connected to a small machine. The machine is called a spirometer.

The machine measures how much air you breathe out. It also measures how fast you can blow air out.

Your doctor may have you inhale medicine that helps open your airways and then blow into the tube again. He or she can then compare your test results before and after taking the medicine.

Spirometry can detect COPD before symptoms develop. Your doctor also might use the test results to find out how severe your COPD is and to help set your treatment goals.

Other Tests

Your doctor may recommend other tests, such as:

• A chest x-ray or chest CT scan. These tests create pictures of the structures inside your chest, such as your heart, lungs, and blood vessels. The pictures can show signs of COPD. They also may show whether another condition, such as heart failure, is causing your symptoms.
• An arterial blood gas test. This blood test measures the oxygen level in your blood using a sample of blood taken from an artery. The results from this test can show how severe your COPD is and whether you need oxygen therapy.

NEWS IN COPD DIAGNOSIS: CDSS

An important problem in healthcare is the significant gap between optimal evidence-based medical practice and the care actually applied. A systematic review of adherence to chronic obstructive pulmonary disease (COPD) guidelines by clinicians found that the assessment of the disease and the therapy applied to patients were suboptimal. This situation exists across all chronic-disease care in general: in a multinational survey of chronically ill adults, 14-23% of cases reported at least one medical error in the previous two years.

Clinical decision support systems (CDSSs) can be defined as "software that is designed to be a direct aid to clinical decision-making in which the characteristics of an individual patient are matched to a computerized clinical knowledge base (KB), and patient-specific assessments or recommendations are then presented to the clinician and/or the patient for a decision". CDSSs have the potential to enhance healthcare and health, and to help close the gap between optimal practice and actual clinical care.

The CDSS operates by receiving and sending standardized messages, and relies on an existing HIS to present its recommendations to the healthcare professional on screen or via the issuance of a report. Two such HISs have successfully implemented the CDSS web services. The CDSS response time for all decision support services was acceptable (within seconds) to the clinical task at hand, and thus allowed a seamless integration into the existing HIS.

The performance of the CDSS diagnosis service was compared with an anonymised database of patients from Primary Care centres participating in forced-spirometry training in a web-based remote support program to enhance quality of forced spirometry done by non-expert professional in the Basque Country region of Spain. Forced-spirometry testing was done using a Sibel 120 SIBELMED spirometer. The spirometry quality and diagnosis evaluation was done by one respiratory specialist. Inclusion criteria to form the validation data set were:

(i) age of the patient greater than or equal to 40;

(ii) forced spirometry taken and recorded as an electronic record before and after the application of bronchodilators;

(iii) respiratory specialist used option menu to select the appropriate diagnosis (rather than entered through the free text field).

After applying the inclusion criteria, the validation set was formed containing 323 cases. The use of the dataset for validation purposes was approved by the Ethical Committee of the Hospital Clinic í Provincial de Barcelona.

References: 

-Velickovski, F., Ceccaroni, L., Roca, J., Burgos, F., Galdiz, J. B., Marina, N., & Lluch-Ariet, M. (2014). Clinical Decision Support Systems (CDSS) for preventive management of COPD patients. Journal of Translational Medicine, 12(Suppl 2), S9. doi:10.1186/1479-5876-12-S2-S9

-http://www.nhlbi.nih.gov/

Additional Question: What contributes to mortality and morbidity from this disease? Once again, COPD is the third leading cause of death in the US. Chronic/acute respiratory failure and has been found to be the primary contributor to deaths in COPD patients (mortality), though in the past researchers have also blamed coexisting/associated lung cancer. However, people can live and have been living long(ish) with this condition. In 2011, 12.7 million U.S. adults (aged 18 and over) were estimated to have COPD. However, close to 24 million U.S. adults have evidence of impaired lung function, indicating an under diagnosis of COPD. An estimated 715,000 hospital discharges were reported in 2010; a discharge rate of 23.2 per 100,000 population. COPD is an important cause of hospitalization in our aged population. Approximately 65% of discharges were in the 65 years and older population in 2010. The cause of these morbidity rates is due to the gradual/ongoing manifestation of COPD.

Etiology: Causes

Long-term exposure to lung irritants that damage the lungs and the airways usually is the cause of COPD. In the US, the most common irritant that causes COPD is cigarette smoke. Pipe, cigar, and other types of tobacco smoke also can cause COPD, especially if the smoke is inhaled.

Breathing in secondhand smoke, air pollution, or chemical fumes or dust from the environment or workplace also can contribute to COPD. (Secondhand smoke is smoke in the air from other people smoking.)

Rarely, a genetic condition called alpha trypsin 1 deficiency may play a role in causing COPD. People who have this condition have low levels of alpha-1 antitrypsin (AAT)—a protein made in the liver.

Having a low level of the AAT protein can lead to lung damage and COPD if you're exposed to smoke or other lung irritants. If you have this condition and smoke, COPD can worsen very quickly.

Although uncommon, some people who have asthma can develop COPD. Asthma is a chronic (long-term) lung disease that inflames and narrows the airways. Treatment usually can reverse the inflammation and narrowing. However, if not, COPD can develop.

Pathophysiology: How COPD manifests

Inhaled irritants cause inflammatory cells such as neutrophils, CD8⁺ T-lymphocytes, B cells and macrophages to accumulate.² When activated, these cells initiate an inflammatory cascade that triggers the release of inflammatory mediators such as tumour necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), matrix-metalloproteinases (MMP-6, MMP-9), C-reactive protein (CRP), interleukins (IL-1, IL-6, IL-8) and fibrinogen. These inflammatory mediators sustain the inflammatory process and lead to tissue damage as well as a range of systemic effects. Chronic inflammation is present from the outset of the disease and leads to structural changes in the lung which further perpetuate airflow limitation. This chronic inflammatory cascade is illustrated at left. 

COPD is characterized by chronic inflammation of the airways, lung tissue and pulmonary blood vessels as a result of exposure to inhaled irritants such as tobacco smoke. 

Airway remodeling in COPD is a direct result of the inflammatory response associated with COPD and leads to narrowing of the airways. Three main factors contribute to this: peribronchial fibrosis, build-up of scar tissue from damage to the airways and over-multiplication of the epithelial cells lining the airways.

Parenchymal destruction is associated with loss of lung tissue elasticity, which occurs as a result of destruction of the structures supporting and feeding the alveoli (emphysema). This means that the small airways collapse during exhalation, impeding airflow, trapping air in the lungs and reducing lung capacity 

Smoking and inflammation enlarge the mucous glands that line airway walls in the lungs, causing goblet cell metaplasia and leading to healthy cells being replaced by more mucus-secreting cells. Additionally, inflammation associated with COPD causes damage to the mucociliary transport system which is responsible for clearing mucus from the airways. Both these factors contribute to excess mucus in the airways which eventually accumulates, blocking them and worsening airflow.

Key References:

-Saqib A. Gowani, Sana S. Memon, and Javaid A. Khan "A Major Cause of Death in COPD and Risk Factors for Lung Cancer—a Dilemma or a Mistake?" American Journal of Respiratory and Critical Care Medicine, Vol. 176, No. 6 (2007), pp. 624-625.
-Centers for Disease Control and Prevention. National Center for Health Statistics. National Hospital Discharge Survey raw data, 2010. Analysis performed by the American Lung Association Research and Health Education Division using SPSS software.
-Centers for Disease Control and Prevention. National Center for Health Statistics. National Health Interview Survey Raw Data, 2011. Analysis performed by the American Lung Association Research and Health Education Division using SPSS and SUDAAN software. 
-Chung KF. The role of airway smooth muscle in the pathogenesis of airway remodelling in COPD. Proc Am Thorac Soc 2005;2:347-54. 
-Laperre TS, Sont JK, van Schadewijk A, et al. Smoking cessation and bronchial epithelial remodelling in COPD: a cross-sectional study. Respir Res 2007;8:85-93.
-Danahay H & Jackson AD. Epithelial mucus-hypersecretion and respiratory disease. Curr Drug Targets Inflamm Allergy 2005;4:651-64
-National Institute of Health: National Heart, Lung, and Blood Institute: http://www.nhlbi.nih.gov/health/health-topics/topics/copd/causes

COPD in the US

Epidemiology:
According to recent statistics, chronic bronchi- tis affects approximately 10 million people in the United States, the majority of which are between 44 and 65 years of age. Among them, 24.3% with chronic bronchitis are older than 65 years, and surprisingly 31.2% are between the ages of 18 and 44 years. The numbers affected by chronic bronchitis dramatically increase with smoking. Pelkonen et al. followed 1711 Finnish men in rural com- munities for 30 years and found the incidence of chronic bronchitis was 42% in continuous smokers, 26% in ex-smokers, and 22% in never-smokers. In a recent cross-sectional study of over 5000 adult current or ex-smokers with over a 10-pack-year history, the prevalence of chronic bronchitis, using the classic definition, was a striking 34.6%. The prevalence of chronic bronchitis is higher in COPD patients, affecting 14 – 74% of all COPD patients.

Are some populations more at risk?: Debatable.
Chronic bronchitis seems to affect whites more than blacks, but the majority of studies have been composed of mostly whites. A recent study of non-Hispanic whites and blacks found that COPD patients were more likely to be white than black, but the differences in racial distribution between those with and without chronic bronchitis were small. Sex has also been a matter of debate. Many studies have found that chronic bronchitis affects men more than women. How- ever, according to the 2013 American Lung Association study, the prevalence rates of chronic bronchitis in women were nearly twice that in men (59.7 vs. 29.6 per 1000 persons). A 10-year study of 21 130 Danish patients showed that the cumulat- ive prevalence of chronic mucus secretion was 10.7% in women vs. 8.7% in men. The reasons for the higher prevalence of chronic bronchitis in women compared to that in men are unclear, but may be due to hormonal influences, sex differences in symptom reporting, and sex diagnostic bias; for example, in the European Respiratory Society Study on Chronic Obstructive Pulmonary Disease (EUROSCOP) study, women reported more dyspnea and cough, but less phlegm symptoms than men

Until next time: here's a great animation just on Emphysema!

Key Articles:
Kim, V. (2015). The chronic bronchitis phenotype in chronic obstructive pulmonary disease: Features and implications. Current Opinion, 21(00), 1-9. Retrieved January 17, 2015.

Searched databases: NIH, WHO, PubMed, Medline.
Search Terms: "COPD", "COPD US", "COPD epidemiology", "US epidemiology COPD" "COPD US prevalence"

Uh, what is COPD?

Chronic obstructive pulmonary disease (COPD) refers to a group of lung diseases that block airflow and make breathing difficult. Emphysema and chronic bronchitis are the two most common conditions that make up COPD. Chronic bronchitis is an inflammation of the lining of your bronchial tubes, which carry air to and from your lungs. Emphysema occurs when the air sacs (alveoli) at the end of the smallest air passages (bronchioles) in the lungs are gradually destroyed.

Here's a great animation from Nucleus Medical Media to help introduce the lungs, COPD, and how its different presentations it develop.

COPD Epidemiology & Pathophysiology:

Epidemiology: Chronic obstructive pulmonary disease (COPD) is estimated to affect 32 million persons in the United States and is the fourth leading cause of death in this country. Patients typically have symptoms of chronic bronchitis and emphysema, but the classic triad also includes asthma.

Pathophysiology: COPD is characterized by airflow limitation that is poorly reversible. Cumulative, chronic exposure to cigarette smoking is the number one cause of the disease, but repeated exposure to secondhand smoke, air pollution and occupational exposure (to coal, cotton, grain) are also important risk factors.

Chronic inflammation plays a major role in COPD pathophysiology. Smoking and other airway irritants cause neutrophils, T-lymphocytes, and other inflammatory cells to accumulate in the airways. Once activated, they trigger an inflammatory response in which an influx of molecules, known as inflammatory mediators, navigate to the site in an attempt to destroy and remove inhaled foreign debris.

Under normal circumstances, the inflammatory response is useful and leads to healing. In fact, without it, the body would never recover from injury. In COPD, repeated exposure to airway irritants perpetuates an ongoing inflammatory response that never seems to shut itself off. Over time, this process causes structural and physiological lung changes that get progressively worse.

As inflammation continues, the airways constrict, becoming excessively narrow and swollen. This leads to excess mucus production and poorly functioning cilia, a combination that makes airway clearance especially difficult. When people with COPD can't clear their secretions, they develop the hallmark symptoms of COPD, including a chronic, productive cough, wheezing and dyspnea. Finally, the build-up of mucus attracts a host of bacteria that thrive and multiply in the warm, moist environment of the airway and lungs. The end result is further inflammation, the formation of diverticula (pouch-like sacs) in the bronchial tree, and bacterial lung infection, a common cause of COPD exacerbation.