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CHRONIC OBSTRUCTIVE
PULMONARY DISEASE(COPD)
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·
INTRODUCTION
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Chronic Obstructive
Pulmonary Disease (COPD) is a major cause of chronic morbidity and mortality
throughout the world. Many people suffer from this disease for years and die
prematurely from it or its complications. COPD is the fourth leading cause of
death in the world, and further increases in its prevalence and mortality can
be predicted in the coming decades.
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In United States
approximately 14.2 million people have COPD.Since 1982, the patients diagnosed
with COPD increased by 41.5%. Researchers estimate the prevalence of chronic
airflow obstruction in the United States as 8-17% for men and 10-19% for women.
The prevalence rates increased in women by 30% in the last decade.
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Mortality/Morbidity
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Absolute mortality rates
for US patients aged 55-84 years (1985) were 200 per 100,000 males and 80 per
100,000 females. Internationally, a marked variation in overall mortality rates
from COPD exists. The extremes are the more than 400 deaths per 100,000 males
aged 65-74 years in Romania and the fewer than 100 deaths per 100,000 in Japan.
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Sex
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Researchers estimate that
4-6% of white male adults and 1-3% of white female adults have emphysema or
COPD. Men have a higher mortality rate than women, but mortality due to COPD in
women is expected to increase.
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PATHOLOGY
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Pathological changes
characteristic of COPD are found in the proximal airways, peripheral airways,
lung parenchyma,and pulmonary vasculature. The pathological changes include
chronic inflammation, with increased numbers of specific inflammatory cell
types in different parts of the lung, and structural changes resulting from
repeated injury and repair. In general, the inflammatory and structural changes
in the airways increase with disease severity and persist on smoking cessation.
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Pathological Changes in COPD
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Proximal airways
(trachea, bronchi more 2 mm internal diameter)
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Inflammatory cells: increasing of macrophages, CD8+ (cytotoxic)
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T- lymphocytes, few
neutrophils or eosinophils
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Structural changes: Goblet cells, enlarged submucosal glands (both
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leading to mucus
hypersecretion), squamous metaplasia of epithelium
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Peripheral airways
(bronchioles less 2mm )
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Inflammatory cells: Macrophages, T lymphocytes (CD8+ more than CD4+),
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B lymphocytes, lymphoid
follicles, fibroblasts, few neutrophils
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or eosinophils
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Structural changes: Airway wall thickening, peribronchial fibrosis, luminal
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inflammatory exudate,
airway narrowing (obstructive bronchiolitis)
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Increased inflammatory
response and exudate correlated with disease
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severity
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Lung parenchyma
(respiratory bronchioles and alveoli)
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Inflammatory cells: Macrophages, CD8+ T lymphocytes
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Structural changes: Alveolar wall destruction, apoptosis of epithelial
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and endothelial cells
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• Centrilobular
emphysema: dilatation and destruction of respiratory
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bronchioles; most
commonly seen in smokers
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• Panacinar emphysema:
destruction of alveolar sacs as well as respiratory
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bronchioles; most
commonly seen in alpha-1 antitrypsin deficiency
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Pulmonary vasculature
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Inflammatory cells: Macrophages, T lymphocytes
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Structural changes: Thickening of intima, endothelial cell dysfunction,
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smooth muscle pulmonary
hypertension.
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PATHOGENESIS
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Inflammatory Cells
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COPD is characterized by
a specific pattern of inflammation involving neutrophils, macrophages, and
lymphocytes. These cells release inflammatory mediators and interact with
structural cells in the airways and lung parenchyma.
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Inflammatory Mediators
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The wide variety of
inflammatory mediators that have been shown to be increased in COPD patients
attract inflammatory cells from the circulation (chemotactic factors), amplify
the inflammatory process (proinflammatory cytokines), and induce structural
changes (growth factors).
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Oxidative Stress
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Oxidative stress may be
an important amplifying mechanism in COPD. Biomarkers of oxidative stress (e.g.,
hydrogen peroxide, 8-isoprostane) are increased in the exhaled breath
condensate, sputum, and systemic circulation of COPD patients. Oxidative stress
is further increased in exacerbations. Oxidants are generated by cigarette
smoke and other inhaled particulates, and released from activated inflammatory
cells such as macrophages and neutrophils. There may also be a reduction in
endogenous antioxidants in COPD patients. Oxidative stress has several adverse
consequences in the lungs, including activation of inflammatory genes,
inactivation of antiproteases, stimulation of mucus secretion, and stimulation
of increased plasma exudation. Many of these adverse effects are mediated by
peroxynitrite, which is formed via an interaction between superoxide anions and
nitric oxide. In turn, the nitric oxide is generated by inducible nitric oxide
synthase, which is expressed in the peripheral airways and lung parenchyma of
COPD patients. Oxidative stress may also account for a reduction in histone
deacetylase activity in lung tissue fromCOPD patients, which may lead to
enhanced expression of inflammatory genes and also a reduction in the
antiinflammatoryaction of glucocorticosteroids.
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Protease-Antiprotease
Imbalance
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There is compelling
evidence for an imbalance in the lungs of COPD patients between proteases that
break down connective tissue components and antiproteases that protect against
this. Several proteases, derived from inflammatory cells and epithelial cells,
are increased in COPD patients. There is increasing evidence that they may
interact with each other. Protease-mediated destruction of elastin, a major
connective tissue component in lung parenchyma, is an important feature of
emphysema and is likely to be irreversible.
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PATHOPHYSIOLOGY
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Airflow Limitation and
Air Trapping
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The extent of
inflammation, fibrosis, and luminal exudates in small airways is correlated
with the reduction in FEV1 and FEV1/FVC ratio, and probably with the
accelerated decline in FEV1 characteristic of COPD4. This peripheral airway
obstruction progressively traps air during expiration, resulting in
hyperinflation. Although emphysema is more associated with gas exchange
abnormalities than with reduced FEV1, it does contribute to air trapping during
expiration. This is especially so as alveolar attachments to small airways are
destroyed when the disease becomes more severe. Hyperinflation reduces
inspiratory capacity such that functional residual capacity increases,
particularly during exercise (when this abnormality is known as dynamic hyperinflation),
and this results in dyspnea and limitation of exercise capacity. It is now
thought that hyperinflation develops early in the disease and is the main
mechanism for exertional dyspnea. Bronchodilators acting on peripheral airways
reduce air trapping, thereby reducing lung volumes and improving symptoms and
exercise capacity.
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Gas Exchange
Abnormalities
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Gas exchange
abnormalities result in hypoxemia and hypercapnia, and have several mechanisms
in COPD. In general, gas transfer worsens as the disease progresses. The
severity of emphysema correlates with arterial PO2 and other markers of
ventilation-perfusion (VA/Q) imbalance. Peripheral airway obstruction also
results inVA/Q imbalance, and combines with ventilatory muscle impaired
function in severe disease to reduce ventilation, leading to carbon dioxide
retention. The abnormalities in alveolar ventilation and a reduced pulmonary
vascular bed further worsen the VA/Q abnormalities.
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Mucus Hypersecretion
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Mucus hypersecretion,
resulting in a chronic productive cough, is a feature of chronic bronchitis and
is not necessarily associated with airflow limitation. Conversely, not all
patients with COPD have symptomatic mucus hypersecretion. When present, it is
due to mucous metaplasia with increased numbers of goblet cells and enlarged
submucosal glands in response to chronic airway irritation by cigarette smoke
and other noxious agents. Several mediators and proteases stimulate mucus
hypersecretion and many of them exert their effects through the activation of epidermal
growth factor receptor (EGFR).
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Pulmonary Hypertension
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Mild to moderate
pulmonary hypertension may develop late in the course of COPD and is due to
hypoxic vasoconstriction of small pulmonary arteries, eventually resulting in
structural changes that include intimal hyperplasia and later smooth muscle
hypertrophy/hyperplasia17. There is an inflammatory response in vessels similar
to that seen in the airways and evidence for endothelial cell dysfunction. The
loss of the pulmonary capillary bed in emphysema may also contribute to
increased pressure in the pulmonary circulation. Progressive pulmonary
hypertension may lead to right ventricular hypertrophy and eventually to
right-side cardiac failure (cor pulmonale).
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Systemic features
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It is increasingly recognized
that COPD involves several systemic features, particularly in patients with
severe disease, and that these have a major impact on survival and comorbid
diseases. Cachexia is commonly seen in patients with severe COPD. There may be
a loss of skeletal muscle mass and weakness as a result of increased apoptosis
and/or muscle disuse. Patients with COPD also have increased likeliness of
having osteoporosis, depression and chronic anemia. Increased concentrations of
inflammatory mediators, including TNF- IL-6, and oxygen-derived free
radicals,may mediate some of these systemic effects. There is an increase in
the risk of cardiovascular diseases, which is correlated with an increase in
C-reactive protein (CRP)
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CLINICAL PRESENTATION
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1.
RISK FACTORS
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• Genes
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COPD is a polygenic
disease and a classic example of gene-environment interaction. The genetic risk
factor that is best documented is a severe hereditary deficiency of alpha-1
antitrypsin. A significant familial risk of airflow obstruction has been
observed in smoking siblings of patien with severeCOPD, suggesting that genetic
factors could influence this susceptibility. Through genetic linkage
analysis,several regions of the genome have been identified that likely contain
COPD susceptibility genes, including chromosome.Genetic association studies
have implicated a variety of genes in COPD pathogenesis, including transforming
growth factor beta 1 (TGF-_1) microsomal epoxide hydrolase 1 (mEPHX1), and
tumor necrosis factor alpha (TNF_). However, the results of these genetic
association studies have been largely inconsistent, and functional genetic
variants influencing the development of COPD (other than alpha-1 antitrypsin
deficiency) have not been definitively identified.
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• Inhalational Exposures
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Because individuals may
be exposed to a variety of different types of inhaled particles over their
lifetime, it is helpful to think in terms of the total burden of inhaled
particles. Each type of particle, depending on its size and composition, may
contribute a different weight to the risk, and the total risk will depend on
the integral of the inhaled exposures Of the many inhalational exposures that
may be encountered over a lifetime, only tobacco smoke and occupational dusts
and chemicals(vapors, irritants, and fumes) are known to cause COPD on their
own. Tobacco smoke and occupational exposures also appear to act additively to
increase the risk of developing COPD. However this may reflect an inadequate
data base from populations who are exposed to other risk factors, such as heavy
exposures to indoor air pollution from poorly vented biomass cooking and
heating.
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• Tobacco Smoke:
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Cigarette smoking is by
far the most commonly encountered risk factor for COPD. Cigarette smokers have
a higher prevalence of respiratory symptoms and lung function abnormalities, a
greater annual rate of decline in FEV1, and a greater COPD mortality rate than
nonsmokers. Pipe and cigar smokers have greater COPD morbidity and mortality
rates than nonsmokers, although their rates are lower than those for cigarette
smokers. Other types of tobacco smoking popular in various countries are also
risk factors for COPD. although their risk relative to cigarette smoking has
not been reported. The risk for COPD in smokers is dose-related. Age at
starting to smoke, total pack-years smoked, and current smoking status are
predictive of COPD mortality. Not all smokers develop clinically significant
COPD, which suggests that genetic factors must modify each individual’s risk.
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• Occupational Dusts and Chemicals:
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Occupational exposures
are an underappreciated risk factor for COPD. These exposures include organic
and inorganic dusts and chemical agents and fumes. An analysis of the large US
population-based NHANES III survey of almost 10,000 adults aged 30-75 years,
which included lung function tests, estimated the fraction of COPD attributable
to work
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was 19.2% overall, and
31.1% among never smokers16.These estimates are consistent with a statement
published by the American Thoracic Society that concluded that occupational
exposures account for 10-20% of either symptoms or functional impairment
consistent with COPD.
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• Indoor Air Pollution:
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Wood, animal dung, crop
residues,and coal, typically burned in open fires or poorly functioning stoves,
may lead to very high levels of indoor air pollution.The evidence that indoor
pollution from biomass cooking and heating in poorly ventilated dwellings is an
important risk factor for COPD (especially among women in developing countries)
continues to grow, with case-control studies and other robustly designed
studies now available.
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• Outdoor Air Pollution:
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High levels of urban air
pollutionare harmful to individuals with existing heart or lung disease.The
role of outdoor air pollution in causing COPD is unclear,but appears to be
small when compared with that of cigarette smoking. It has also been difficult
to assess the effects of single pollutants in long-term exposure to atmospheric
pollution. However, air pollution from fossil fuel combustion,primarily from
motor vehicle emissions in cities, is associated with decrements of respiratory
function. The relative effects of short-term, high-peak exposures and
long-term,low-level exposures is a question yet to be resolved.
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2.
Assessment of Symptoms
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Although exceptions
occur, the general patterns of symptom development in COPD is well established.
The main symptoms of patients in
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Stage I: Mild COPD are chronic cough and sputum production. These
symptoms can be present for many years before the development of airflow
limitation and are often ignored or discounted by patients and attributed to
aging or lack of conditioning. As airflow limitation worsens in
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Stage II: Moderate COPD, patients often experience dyspnea, which
may interfere with their daily activities1. Typically, this is the stage at
which they seek medical attention and may be diagnosed with COPD. However, some
patients do not experience cough, sputum production, or dyspnea and do not come
to medical attention until their airflow limitation becomes more severe or
their lung function is worsened acutely by a respiratory tract infection.
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Stage III: Severe COPD: symptoms of cough and sputum production
typically continue, dyspnea worsens, and additional symptoms heralding
complications (such as respiratory failure, right heart failure, weight loss,
and arterial hypoxemia) may develop. It is important to note that, since COPD
may be diagnosed at any stage, any of the symptoms described below may be
present in a patient presenting for the first time.
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Additional features in
severe disease.
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Weight loss and anorexia
are common problems in advanced COPD. They are prognostically important13 and
can also be a sign of other diseases (e.g., tuberculosis, bronchial tumors),
and therefore should always be investigated. Cough syncope occurs due to rapid
increases in intrathoracic pressure
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during attacks of
coughing. Coughing spells may also cause rib fractures, which are sometimes
asymptomatic. Ankle swelling may be the only symptomatic pointer to the
development of cor pulmonale. Finally, psychiatric morbidity, especially
symptoms of depression and/or anxiety, is common in advanced COPD and merits
specific enquiry in the clinical history.
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3.Investigations
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Medical History
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A detailed medical
history of a new patient known or thought to have COPD should assess:
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Physical Examination
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Though an important part
of patient care, a physical examination is rarely diagnostic in COPD. Physical
signs of airflow limitation are usually not present until significant
impairment of lung function has occurred and their detection has a relatively
low sensitivity and specificity.A number of physical signs may be present in
COPD, but their absence does not exclude the diagnosis.
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Inspection.
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• Central cyanosis, or
bluish discoloration of the mucosal membranes, may be present but is difficult
to detect in artificial light and in many racial groups.
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• Common chest wall
abnormalities, which reflect the pulmonary hyperinflation seen in COPD, include
relatively horizontal ribs, “barrel-shaped” chest, and protruding abdomen.
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• Resting respiratory
rate is often increased to more than 20 breaths per minute and breathing can be
relatively shallow.
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• Ankle or lower leg
edema can be a sign of right heart failure.
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Palpation and percussion.
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• These are often
unhelpful in COPD.
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• Detection of the heart
apex beat may be difficult due to
pulmonary
hyperinflation.
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• Hyperinflation also
leads to downward displacement of the liver and an increase in the ability to
palpate this organ without it being enlarged.
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Auscultation.
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• Patients with COPD
often have reduced breath sounds, but this finding is not sufficiently
characteristic to make the diagnosis.
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• The presence of
wheezing during quiet breathing is a useful pointer to airflow limitation.
However, wheezing heard only after forced expiration has not been validated as
a diagnostic test for COPD.
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• Inspiratory crackles
occur in some COPD patients but are of little help diagnostically.
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• Heart sounds are best
heard over the xiphoid area.
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OTHER CRITARIA
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This is usually clinical
(GOLD criteria). There is a history of breathlessness and sputum production in
a lifetime smoker. In the absence of a history of cigarette smoking a working
diagnosis of asthma is usual unless there is a family history of lung disease
suggestive of a deficiency of α1-antitrypsin inhibitor. The patient may have
signs of hyperinflation and typical pursed lip respiration. No individual
clinical feature is diagnostic. Emphysema is often incorrectly diagnosed on
signs of overinflation of the lungs (e.g. loss of liver dullness on
percussion), but this may occur with other diseases such as asthma.
Furthermore, centri-acinar emphysema may be present without signs of
overinflation. Some elderly men (without emphysema) develop a barrel-shaped
chest as a result of osteoporosis of the spine, and a consequent decrease in
height.
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Lung function tests
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show evidence of airflow
limitation. The ratio of the FEV1 to the FVC is reduced and the PEFR is low. In
many patients the airflow limitation is reversible to some extent (usually a
change in FEV1 of < 15%), and the distinction between asthma and COPD can be
difficult. Lung volumes may be normal or increased, and the gas transfer
coefficient of carbon monoxide is low when significant emphysema is present.
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Chest X-ray
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is often normal, even
when the disease is advanced. The classic features are the presence of bullae,
severe overinflation of the lungs with low, flattened diaphragms, and a large retrosternal
air space on the lateral film. There may also be a deficiency of blood vessels
in the periphery of the lung fields compared with relatively easily visible
proximal vessels.
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Haemoglobin level and PCV
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can be elevated as a
result of persistent hypoxaemia (secondary polycythaemia,
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Blood gases
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are often normal. In the
advanced case there is evidence of hypoxaemia and hypercapnia.
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Sputum examination
·
is unnecessary in the
ordinary case as Strep. pneumoniae or H. influenzae are the only common
organisms to produce acute exacerbations. Occasionally Moraxella catarrhalis
may cause infective exacerbations.
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Electrocardiogram.
·
In advanced cor pulmonale
the P wave is taller (P pulmonale) and there may be right bundle branch block
(RSR' complex) and the changes of right ventricular hypertrophy.
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Echocardiogram –
·
performed to assess
cardiac function.
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α1-Antitrypsin levels.
·
The normal range is 2-4
g/L.
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Measurement of Airflow
Limitation (Spirometry)1
·
Spirometry should be
undertaken in all patients who may have COPD. It is needed to make a confident
diagnosis of COPD and to exclude other diagnoses that may present with similar
symptoms. Spirometry should measure the volume of air forcibly exhaled from the
point of maximal inspiration (forced vital capacity, FVC) and the volume of air
exhaled during the first second of this maneuver (forced expiratory volume in
one second, FEV1), and the ratio of these two measurements (FEV1/FVC) should be
calculated. Spirometry measurements are evaluated by comparison with reference
values based on age, height, sex, and race (use appropriate reference values).
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Additional Investigations
·
For patients diagnosed
with Stage II: Moderate COPD and beyond, the following additional
investigations may be considered.
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Bronchodilator
reversibility testing.
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Despite earlier hopes,
neither bronchodilator nor oral glucocorticosteroid reversibility testing
predicts disease progression, whether judged by decline in FEV1, deterioration
of health status,or frequency of exacerbations in patients with a clinical
diagnosis of COPD and abnormal spirometry. Small changes in FEV1 (e.g., <
400 ml) after administration of a bronchodilator do not reliably predict the
patient’s response to treatment (e.g., change in exercise capacity). Minor
variations in initial airway caliber can lead to different classification of
reversibility status depending on the day of testing, and the lower the
pre-bronchodilator FEV1, the greater the chance of a patient being classified
as reversible even when the 200 ml volume criterion is included.
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Differential Diagnosis
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In some patients with
chronic asthma, a clear distinction from COPD is not possible using current
imaging and physiological testing techniques, and it is assumed that asthma and
COPD coexist in these patients. In these cases, current management is similar
to that of asthma. Other potential diagnoses are usually easier to distinguish
from COPD.
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·
Figure 5.1-7.
Differential Diagnosis of COPD
·
Diagnosis
Suggestive Features
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COPD
Onset in mid-life.
·
Symptoms slowly progressive.
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Long history of tobacco smoking.
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Dyspnea during exercise.
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Largely irreversible airflow limitation.
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Asthma
Onset early in life (often childhood).
·
Symptoms vary from day to day.
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Symptoms at night/early morning.
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Allergy, rhinitis, and/or eczema also present.
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Family history of asthma.
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Largely reversible airflow limitation.
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Congestive Heart
Failure Fine basilar crackles on
auscultation.
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Chest X-ray shows dilated heart,
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pulmonary edema.
·
Pulmonary
function tests indicate
·
volume restriction, not airflow limitation.
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Bronchiectasis
Large volumes of purulent sputum.
·
Commonly associated with bacterial infection.
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Coarse crackles/clubbing on auscultation.
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Chest X-ray/CT shows bronchial dilation,
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bronchial
wall thickening.
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Tuberculosis
Onset all ages
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Chest X-ray shows lung infiltrate.
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Microbiological confirmation.
·
High local prevalence of tuberculosis.
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Obliterative
Bronchiolitis Onset in younger age,
nonsmokers.
·
May have history of rheumatoid arthritis or
·
fume
exposure.
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CT on expiration shows hypodense areas.
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Diffuse
Panbronchiolitis Most patients
are male and nonsmokers.
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Almost
all have chronic sinusitis.
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Chest X-ray and HRCT show diffuse small
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Centrilobular nodular opacities and
·
hyperinflation.
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·
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Stages of COPD
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The impact of COPD on an
individual patient depends not just on the degree of airflow limitation, but
also on the severity of symptoms (especially breathlessness and decreased
exercise capacity). There is only an imperfect relationship between the degree
of airflow limitation and the presence of symptoms. Spirometric
staging,therefore, is a pragmatic approach aimed at practical implementation
and should only be regarded as an educational tool and a general indication to
the initial approach to management.
·
·
Stage I: Mild COPD - Characterized by mild airflow limitation (FEV1/FVC <
0.70; FEV1 ≥ 80% predicted).Symptoms of chronic cough and sputum production
may be present, but not always. At this stage, the individual is usually
unaware that his or her lung function is abnormal.
·
·
Stage II: Moderate COPD - Characterized by worsening airflow limitation (FEV1/FVC
< 0.70; 50% ≤ FEV1 < 80% predicted), with shortness of breath typically
developing on exertion and cough and sputum production sometimes also present.
This is the stage at which patients typically seek medical attention because of
chronic respiratory symptoms or an exacerbation of their disease.
·
·
Stage III: Severe COPD - Characterized by further worsening of airflow limitation
(FEV1/FVC < 0.70; 30% ≤ FEV1 < 50% predicted), greater shortness of breath,reduced
exercise capacity, fatigue, and repeated exacerbations that almost always have
an impact on patients’ quality of life.
·
·
Stage IV: Very Severe
COPD - Characterized by severe airflow limitation (FEV1/FVC
< 0.70; FEV1 < 30% predicted or FEV1 < 50% predicted plus the presence
of chronic respiratory failure). Respiratory failure is defined as an arterial
partial pressure of O2 (PaO2) less than 8.0 kPa (60 mm Hg), with or without
arterial partial pressure of CO2 (PaCO2) greater than 6.7 kPa (50 mm Hg)
whilebreathing air at sea level. Respiratory failure may alsolead to effects on
the heart such as cor pulmonale (right heart failure). Clinical signs of cor
pulmonale include elevation of the jugular venous pressure and pitting
ankleedema. Patients may have Stage IV: Very Severe COPD even if the FEV1 is
> 30% predicted, whenever these complications are present. At this stage,
quality of life is very appreciably impaired and exacerba-tions may be life
threatening.
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PHARMACOLOGIC TREATMENT
·
·
Pharmacologic therapy is
used to prevent and control symptoms, reduce the frequency and severity of
exacerbations, improve health status, and improve exercise tolerance.
·
·
Drug Category: Bronchodilators
·
These agents act to
decrease muscle tone in both small and large airways in the lungs, thereby
increasing ventilation. Category includes subcutaneous medications,
beta-andrenergics, methylxanthines, and anticholinergics. Bronchodilator
medications are central to symptom management in COPD.
·
Inhaled therapy is
preferred. The choice between _2-agonist, anticholinergic,
·
theophylline, or
combination therapy depends on availability and individual response in terms of
symptom relief and side effects. Bronchodilators are prescribed on an as-needed
or on a regular basis to prevent or reduce symptoms. Long-acting inhaled
bronchodilators are more effective and convenient. Combining bronchodilators
may improve efficacy and decrease the risk of side effects compared to
increasing the dose of a single bronchodilator.
·
·
B2-agonists. The principal action of _2-agonists is to relax airway
smooth muscle by stimulating _2-adrenergic receptors, which increases cyclic
AMP and produces functional antagonism to bronchoconstriction. Oral therapy
·
is slower in onset and
has more side effects than inhaled treatment..
·
Anticholinergics. The
most important effect of anticholinergic medications, such as ipratropium,
oxitropium and tiotropium bromide, in COPD patients appears to be blockage of
acetylcholine’s effect on M3 receptors.
·
Drug Category:
Corticosteroids
·
A recent meta-analysis of
16 controlled trials in stable COPD found that approximately 10% of patients
respond to these drugs. The responders should be identified carefully. An
increase in FEV1 >20% is used as surrogate marker for steroid response. In
acute exacerbation, steroids improve symptoms and lung functions. Inhaled
steroids have fewer adverse effects compared to oral agents. Although
effective, these agents improve expiratory flows less effectively than oral
preparations, even at high doses. These agents may be beneficial in slowing
rate of progression in a subset of patients with COPD who have rapid decline.
·
·
ANTIBIOTICS
·
Patients with COPD are
frequently colonized with potential respiratory pathogens and it is often
difficult to identify conclusively a specific species of bacteria responsible
for a particular clinical event. Bacteria frequently implicated in COPD
exacerbations include Streptococcus pneumoniae, Haemophilus influenzae, and
Moraxella catarrhalis. In addition, Mycoplasma pneumoniae or Chlamydia
pneumoniae are found in 5 to 10% of exacerbations. The choice of antibiotic
should be based on local patterns of antibiotic susceptibility of the above
pathogens, as well as the patient's clinical condition. Most practitioners
treat patients with moderate or severe exacerbations with antibiotics, even in
the absence of data implicating a specific pathogen.
·
·
Prognosis
·
•
The predictors of mortality are aging, continued smoking, accelerated decline
in FEV1, moderate-to-severe airflow obstruction, poor bronchodilator response,
severe hypoxemia, the presence of hypercapnia, development of cor pulmonale,
and overall poor functional capacity.
·
•
The mortality rate is 24% in patients admitted to the ICU with an acute
exacerbation; this doubles for patients aged 65 years or older. FEV1 is a
reliable predictor of mortality from COPD. The mortality rate for patients who
have an FEV1 of less than 0.75 L/s is 30% at 1 year and 95% at 10 years.
·
·
•
The American Thoracic Society (ATS) has recommended the clinical staging of
COPD severity according to lung function. Stage I is FEV1 of equal or more than
50% of the predicted value. Stage II is FEV1 35-49% of the predicted value, and
stage III is FEV1 less than 35% of the predicted value.
