INTRODUCTION
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.
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.
Mortality/Morbidity
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.
Sex
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.
PATHOLOGY
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.
Pathological Changes in COPD
Proximal airways (trachea, bronchi more 2 mm internal diameter)
Inflammatory cells: increasing of macrophages, CD8+
(cytotoxic)
T-
lymphocytes, few neutrophils or eosinophils
Structural changes: Goblet cells, enlarged submucosal glands
(both
leading
to mucus hypersecretion), squamous metaplasia of epithelium
Peripheral airways (bronchioles less 2mm )
Inflammatory cells: Macrophages, T lymphocytes (CD8+ more
than CD4+),
B
lymphocytes, lymphoid follicles, fibroblasts, few neutrophils
or
eosinophils
Structural changes: Airway wall thickening, peribronchial
fibrosis, luminal
inflammatory
exudate, airway narrowing (obstructive bronchiolitis)
Increased
inflammatory response and exudate correlated with disease
severity
Lung parenchyma (respiratory bronchioles and alveoli)
Inflammatory cells: Macrophages, CD8+ T lymphocytes
Structural changes: Alveolar wall destruction, apoptosis of
epithelial
and
endothelial cells
•
Centrilobular emphysema: dilatation and destruction of respiratory
bronchioles;
most commonly seen in smokers
•
Panacinar emphysema: destruction of alveolar sacs as well as respiratory
bronchioles;
most commonly seen in alpha-1 antitrypsin deficiency
Pulmonary vasculature
Inflammatory cells: Macrophages, T lymphocytes
Structural changes: Thickening of intima, endothelial cell
dysfunction,
smooth
muscle pulmonary hypertension.
PATHOGENESIS
Inflammatory Cells
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.
Inflammatory Mediators
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).
Oxidative Stress
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.
Protease-Antiprotease Imbalance
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.
PATHOPHYSIOLOGY
Airflow Limitation and Air Trapping
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.
Gas Exchange Abnormalities
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.
Mucus Hypersecretion
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).
Pulmonary Hypertension
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).
Systemic features
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)
CLINICAL PRESENTATION
1. RISK FACTORS
• Genes
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.
• Inhalational
Exposures
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.
• Tobacco
Smoke:
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.
• Occupational
Dusts and Chemicals:
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
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.
• Indoor
Air Pollution:
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.
• Outdoor
Air Pollution:
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.
2. Assessment of
Symptoms
Although
exceptions occur, the general patterns of symptom development in COPD is well
established. The main symptoms of patients in
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
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.
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.
Additional features in severe disease.
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
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.
3.Investigations
Medical History
A
detailed medical history of a new patient known or thought to have COPD should
assess:
Physical Examination
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.
Inspection.
•
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.
•
Common chest wall abnormalities, which reflect the pulmonary hyperinflation
seen in COPD, include relatively horizontal ribs, “barrel-shaped” chest, and
protruding abdomen.
•
Resting respiratory rate is often increased to more than 20 breaths per minute
and breathing can be relatively shallow.
•
Ankle or lower leg edema can be a sign of right heart failure.
Palpation and percussion.
•
These are often unhelpful in COPD.
•
Detection of the heart apex beat may be difficult due to pulmonary hyperinflation.
•
Hyperinflation also leads to downward displacement of the liver and an increase
in the ability to palpate this organ without it being enlarged.
Auscultation.
•
Patients with COPD often have reduced breath sounds, but this finding is not
sufficiently characteristic to make the diagnosis.
•
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.
•
Inspiratory crackles occur in some COPD patients but are of little help
diagnostically.
•
Heart sounds are best heard over the xiphoid area.
OTHER CRITARIA
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.
Lung function tests
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.
Chest X-ray
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.
Haemoglobin
level and PCV
can
be elevated as a result of persistent hypoxaemia (secondary polycythaemia,
Blood gases
are
often normal. In the advanced case there is evidence of hypoxaemia and
hypercapnia.
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.
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.
Echocardiogram –
performed
to assess cardiac function.
α1-Antitrypsin
levels.
The
normal range is 2-4 g/L.
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).
Additional Investigations
For
patients diagnosed with Stage II: Moderate COPD and beyond, the following
additional investigations may be considered.
Bronchodilator
reversibility testing.
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.
Differential Diagnosis
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.
Figure
5.1-7. Differential Diagnosis of COPD
Diagnosis Suggestive
Features
COPD Onset in
mid-life.
Symptoms slowly progressive.
Long history of tobacco smoking.
Dyspnea during exercise.
Largely irreversible airflow limitation.
Asthma Onset early
in life (often childhood).
Symptoms vary from day to day.
Symptoms at night/early morning.
Allergy, rhinitis, and/or eczema also present.
Family history of asthma.
Largely reversible airflow limitation.
Congestive
Heart Failure Fine basilar
crackles on auscultation.
Chest X-ray shows dilated heart,
pulmonary edema.
Pulmonary function tests indicate
volume restriction, not airflow limitation.
Bronchiectasis Large volumes of
purulent sputum.
Commonly associated with bacterial
infection.
Coarse crackles/clubbing on auscultation.
Chest X-ray/CT shows bronchial dilation,
bronchial wall thickening.
Tuberculosis Onset all ages
Chest X-ray shows lung infiltrate.
Microbiological confirmation.
High local prevalence of tuberculosis.
Obliterative
Bronchiolitis Onset in younger age,
nonsmokers.
May have history of rheumatoid arthritis or
fume
exposure.
CT on expiration shows hypodense areas.
Diffuse
Panbronchiolitis Most patients
are male and nonsmokers.
Almost all have chronic sinusitis.
Chest X-ray and HRCT show diffuse small
Centrilobular nodular opacities and
hyperinflation.
Stages of COPD
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.
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.
