Transcript CHRONIC OBSTRUCTIVE PULOMONARY DISEASE (COPD)

CHRONIC OBSTRUCTIVE
PULOMONARY DISEASE
RON BARAC, DO
INTERNAL MEDICINE LECTURE
SERIES
FEBRUARY 13, 2008
COPD STATISTICS
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An estimated 16 million Americans are diagnosed with
COPD
It is likely that an additional 14 are undiagnosed
True prevalence of COPD may be as high as 30 million
cases
COPD is the fourth leading cause of death in the
United States for people ages 65 to 84, and it is the fifth
leading cause of death for people ages 45 to 64 and
those age 85 and older
The annual cost to the nation for COPD is
approximately $30.4 billion
COPD accounts for:
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13.4 million yearly office visits
634,000 yearly hospitalizations
Percent Change in Age-Adjusted Death
Rates, U.S., 1965-1998
3.0
3.0
2.5
2.5
Coronary
Heart
Disease
Stroke
Other CVD
COPD
All Other
Causes
–59%
–64%
–35%
+163%
–7%
2.0
2.0
1.5
1.5
1.0
1.0
0.5
0.5
0.0 0
1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998
Source: NHLBI/NIH/DHHS
Of the six
leading causes
of death in the
United States,
only COPD has
been increasing
steadily since
1970
Source: Jemal A. et al. JAMA 2005
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COPD Mortality by Gender,
Number Deaths x 1000
U.S., 1980-2000
70
60
Men
50
40
Women
30
20
10
0
1980
1985
1990
1995
2000
Source: US Centers for Disease Control and Prevention, 2002
COPD RISK FACTORS
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Smoking is the primary risk factor:
-80-90% of all COPD deaths are related to smoking
-Female smokers are 13 times more likely to die of COPD than
female non- smokers
-Male smokers are 12 times more likely to die than male
nonsmokers
Second hand smoke
Alpha-1-antitrypsin deficiency
Air pollution
Occupational exposures (involved in 19% of total COPD cases, 31% of
nonsmokers diagnosed with COPD)
History of childhood respiratory infections
Heredity
Atopic dermatitis patients
Risk Factors for COPD
Nutrition
Infections
Socio-economic
status
Aging Populations
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Cigarette smoke
Biomass particles
Particulates
Pathogenesis of
COPD
Host factors
Amplifying mechanisms
LUNG INFLAMMATION
Anti-oxidants
Oxidative
stress
Anti-proteinases
Proteinases
Repair
mechanisms
COPD PATHOLOGY
Source: Peter J. Barnes, MD
Changes in Lung Parenchyma in COPD
Alveolar wall destruction
Loss of elasticity
Destruction of pulmonary
capillary bed
↑ Inflammatory cells
macrophages, CD8+ lymphocytes
Source: Peter J. Barnes, MD
EMPHYSEMA
EMPHYSEMA CXR & CT
CHRONIC BRONCHTIS
COPD
 A clinical diagnosis of COPD should be considered
in any patient who has dyspnea, chronic cough or
sputum production, and/or a history of exposure
to risk factors for the disease.
 The diagnosis should be confirmed by spirometry.
A post-bronchodilator FEV1/FVC < 0.70 confirms
the presence of airflow limitation that is not fully
reversible.
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Diagnosis of COPD
SYMPTOMS
cough
sputum
shortness of breath
EXPOSURE TO RISK
FACTORS
tobacco
occupation
indoor/outdoor pollution
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SPIROMETRY
COPD: Spirometry
 Spirometry should be performed after the
administration of an adequate dose of a shortacting inhaled bronchodilator to minimize
variability.
 A post-bronchodilator FEV1/FVC < 0.70 confirms
the presence of airflow limitation that is not fully
reversible.
 Where possible, values should be compared to
age-related normal values to avoid overdiagnosis
of COPD in the elderly.
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Spirometry: Normal and
Patients with COPD
Classification of COPD Severity
by Spirometry
Stage I: Mild
FEV1/FVC < 0.70
FEV1 > 80% predicted
Stage II: Moderate
FEV1/FVC < 0.70
50% < FEV1 < 80% predicted
Stage III: Severe
FEV1/FVC < 0.70
30% < FEV1 < 50% predicted
Stage IV: Very Severe
FEV1/FVC < 0.70
FEV1 < 30% predicted or
FEV1 < 50% predicted plus
chronic respiratory failure
Differential Diagnosis:
COPD and Asthma
COPD
• Onset in mid-life
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Symptoms slowly
progressive
ASTHMA
• Onset early in life (often
childhood)
• Symptoms vary from day to day
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• Long smoking history
• Dyspnea during exercise •
• Largely irreversible airflow
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limitation
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Symptoms at night/early morning
Allergy, rhinitis, and/or eczema
also present
Family history of asthma
Largely reversible airflow
limitation
COPD
ASTHMA
Cigarette smoke
Allergens
Ep cells
Mast cell
CD4+ cell
(Th2)
Eosinophil
Bronchoconstriction
AHR
Reversible
Alv macrophage Ep cells
CD8+ cell
(Tc1)
Neutrophil
Small airway narrowing
Alveolar destruction
Airflow Limitation
Irreversible
Source: Peter J. Barnes, MD
COPD and Co-Morbidities
COPD patients are at increased risk for:
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Myocardial infarction, angina
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Osteoporosis
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Respiratory infection
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Depression
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Diabetes
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Lung cancer
COPD and Co-Morbidities
COPD has significant extrapulmonary
(systemic) effects including:
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Weight loss
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Nutritional abnormalities
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Skeletal muscle dysfunction
GOALS of COPD MANAGEMENT
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Relieve symptoms
Prevent disease progression
Improve exercise tolerance
Improve health status
Prevent and treat complications
Prevent and treat exacerbations
Reduce mortality
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Reduce Risk Factors
 Reduction of total personal exposure to tobacco
smoke, occupational dusts and chemicals, and
indoor and outdoor air pollutants are important
goals to prevent the onset and progression of
COPD.
 Smoking cessation is the single most effective
and cost effective intervention in most people
to reduce the risk of developing COPD and stop
its progression (Evidence A).
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Pharmacotherapy: Bronchodilators
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Bronchodilator medications are central to the
symptomatic management of COPD (Evidence A).
They are given on an as-needed basis or on a regular
basis to prevent or reduce symptoms and
exacerbations.
 The principal bronchodilator treatments are ß2- agonists,
anticholinergics, and methylxanthines used singly or in
combination (Evidence A).
 Regular treatment with long-acting bronchodilators is
more effective and convenient than treatment with
short-acting bronchodilators (Evidence A).
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Pharmacotherapy: Glucocorticosteroids
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The addition of regular treatment with inhaled
glucocorticosteroids to bronchodilator treatment is
appropriate for symptomatic COPD patients with
an FEV1 < 50% predicted (Stage III: Severe COPD
and Stage IV: Very Severe COPD) and repeated
exacerbations (Evidence A).
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An inhaled glucocorticosteroid combined with a
long-acting ß2-agonist is more effective than the
individual components (Evidence A).
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Pharmacotherapy: Glucocorticosteroids
 The dose-response relationships and longterm safety of inhaled glucocorticosteroids
in COPD are not known.
 Chronic treatment with systemic
glucocorticosteroids should be avoided
because of an unfavorable benefit-to-risk
ratio (Evidence A).
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Pharmacotherapy: Vaccines
 In COPD patients influenza vaccines can
reduce serious illness (Evidence A).
 Pneumococcal polysaccharide vaccine is
recommended for COPD patients 65 years
and older and for COPD patients younger
than age 65 with an FEV1 < 40% predicted
(Evidence B).
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Therapy at Each Stage of COPD
I: Mild
II: Moderate
III: Severe
IV: Very Severe
 FEV1/FVC < 70%
 FEV1/FVC < 70%
 FEV1 > 80%
predicted
 FEV1/FVC < 70%
 50% < FEV1 < 80%
predicted
 FEV1/FVC < 70%
 30% < FEV1 < 50%
predicted
 FEV1 < 30% predicted
or FEV1 < 50% predicted
plus chronic respiratory
failure
Active reduction of risk factor(s); influenza vaccination
Add short-acting bronchodilator (when needed)
Add regular treatment with one or more long-acting
bronchodilators (when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Add long term
oxygen if chronic
respiratory failure.
Consider surgical
treatments
Other Pharmacologic Treatments
 Antibiotics: Only used to treat infectious
exacerbations of COPD
 Antioxidant agents: No effect of n-
acetylcysteine on frequency of
exacerbations, except in patients not treated
with inhaled glucocorticosteroids
 Mucolytic agents, Antitussives, Vasodilators:
Not recommended in stable COPD
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Non-Pharmacologic Treatments
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Rehabilitation: All COPD patients benefit from
exercise training programs, improving with
respect to both exercise tolerance and
symptoms of dyspnea and fatigue (Evidence A).
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Oxygen Therapy: The long-term administration
of oxygen (> 15 hours per day) to patients with
chronic respiratory failure has been shown to
increase survival (Evidence A).
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Key Points
An exacerbation of COPD is defined as:
“An event in the natural course of the
disease characterized by a change in the
patient’s baseline dyspnea, cough, and/or
sputum that is beyond normal day-to-day
variations, is acute in onset, and may
warrant a change in regular medication in
a patient with underlying COPD.”
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Key Points
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The most common causes of an exacerbation
are infection of the tracheobronchial tree and
air pollution, but the cause of about one-third of
severe exacerbations cannot be identified
(Evidence B).
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Patients experiencing COPD exacerbations with
clinical signs of airway infection (e.g., increased
sputum purulence) may benefit from antibiotic
treatment (Evidence B).
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