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CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

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Title: CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)


1
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
  • ABHAY DESHMUKH, MD
  • June 14, 2012

2
OBJECTIVES
  • TO DEFINE COPD AND ITS STAGING
  • TO DISCUSS THE PATHOGENESIS
  • TO UNDERSTAND THE MANAGEMENT PRINCIPLES

3
PROBLEM OF COPD
  • It is the third leading cause of death in the
    United States
  • COPD should be viewed as a systemic disease with
    important pulmonary and extra-pulmonary
    manifestations
  • Dr Nicholas Gross once compared it to defining
    love, everybody knows what it is, but each
    individual describes it differently.
  • Morbidity and mortality 2009 chart book on
    cardiovascular, lung, and blood diseases.
     National Heart, Lung, and Blood
    InstituteBethesda (MD)2009

4
DEFINITION OF COPD
  • Chronic obstructive pulmonary disease (COPD) is a
    preventable and treatable disease with some
    significant extra-pulmonary effects that may
    contribute to the severity in individual
    patients. Its pulmonary component is
    characterized by airflow limitation that is not
    fully reversible. The airflow limitation is
    usually progressive and associated with an
    abnormal inflammatory response of the lungs to
    noxious particles or gases.
  • Global Initiative for Chronic Obstructive Lung
    Disease (GOLD). Global Strategy for Diagnosis,
    Management and Prevention of COPD. GOLD 2010

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6
DIAGNOSIS OF COPD
  • COPD is confirmed when a patient, who has
    symptoms that are compatible with COPD, is found
    to have airflow obstruction (FEV1/FVC ratio less
    than 0.70 and an FEV1 less than 80 percent of
    predicted) and there is no alternative
    explanation for the symptoms and airflow
    obstruction (eg, bronchiectasis, vocal cord
    paralysis, tracheal stenosis)
  • Mohamed Hoesein F.A., Zanen P., Lammers J.W. 
    Lower limit of normal or FEV1/FVC lt 0.70 in
    diagnosing COPD an evidence-based review.
     Respir Med 105. (6) 907-915. 2011

7
  • Chronic bronchitis is defined by a chronic
    productive cough for three months in each of two
    successive years in a patient in whom other
    causes of chronic cough have been excluded.
  • Emphysema is defined by abnormal and permanent
    enlargement of the airspaces that are distal to
    the terminal bronchioles. This is accompanied by
    destruction of the airspace walls, without
    obvious fibrosis.

8
  • Asthma is "a chronic inflammatory disorder of the
    airways in which many cells and cellular elements
    play a role. The chronic inflammation is
    associated with airway responsiveness that leads
    to recurrent episodes of wheezing,
    breathlessness, chest tightness and coughing,
    particularly at night or in the early morning.
    These episodes are usually associated with
    widespread, but variably, airflow obstruction
    within the lung that is often reversible either
    spontaneously or with treatment"

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11
PATHOGENESIS
12
RISK FACTORS
  • Cigarette smoke, containing more than 6000
    molecules and 10 free radicals per puff, can
    initiate an inflammatory response in many ways
  • Tobacco smoke remains the most recognized cause
    for COPD globally
  • There are other exposures that can cause COPD
    related to occupation (various organic and
    inorganic dusts, chemical fumes, smoke), air
    pollution and biomass fuels
  • Cannabis smoke may contribute to COPD
  • Given that only 20 to 30 of individuals who
    smoke appear to develop evidence of COPD, it
    seems clear that there are likely COPD
    susceptibility genes and probably genes that
    might influence severity and response to various
    medications

13
GENES FOR COPD
  • Alfa1-Antitrypsin deficiency- SERPINA1
  • Susceptibility genes for developing COPD or lower
    lung function- EPHX1, GST, MMP12, TGFB1, SERPINE2
  • Nicotine dependence and lung cancer- CHRNA3/5
  • Nakamura H.  Genetics of COPD.  Allergol
    Int 60. (3) 253-258.2011

14
MANAGEMENT OF COPD
15
SMOKING CESSATION
  • Nicotine chewing gum or patch (NRT) has shown to
    increase smoking cessation rates by approximately
    1.5- to 2-fold after 12 months.
  • Bupropion inhibits the neuronal uptake of
    noradrenaline and dopamine. Give 150 mg qday x 3
    days, then 150 mg BID for 7-12 weeks, start
    treatment 1 week before quit date.
  • Varenicline is a partial agonist at nicotinic ?4
    ß2 receptors. Give 0.5 mg qday x 3 days, then
    0.5 mg BID for 4 days, then 1 mg BID for up to 12
    weeks.
  • Counseling has been shown to augment the effects
    of pharmacologic intervention
  • Cahill K., Stead L.F., Lancaster T.  Nicotine
    receptor partial agonists for smoking cessation.
     Cochrane Database Syst Rev 2. 2011

16
PULMONARY REHABILITATION
  • Pulmonary rehabilitation is an important
    nonpharmacologic therapeutic in COPD, yet it
    remains underutilized.
  • Typical components include patient assessment,
    exercise training, education, nutritional
    intervention, and psychosocial support.
  • Has positive impacts on health-related quality of
    life, reduced symptoms, improved peripheral
    muscle strength, exercise endurance, reduced
    number of hospital days, and improved
    psychosocial status, reduction in
    hospitalizations and emergency room visits
  • Pulmonary rehabilitation joint ACCP/AACVPR
    evidence-based clinical practice guidelines.
     Chest 131. (Suppl 5) 4S-42S.2007

17
OXYGEN THERAPY
  • Oxygen therapy is well established to increase
    survival and is indicated for patients with an
    arterial oxygen tension (PaO2) of less than 55 mm
    Hg.
  • Goal is to maintain saturations greater than 90
    during rest, sleep, and exertion.
  • Anthonisen N.R.  Long-term oxygen therapy.  Ann
    Intern Med 99. (4) 519-527.1983

18
PHARMACOLOGIC MANAGEMENT
  • Given that airflow obstruction is the primary
    concern in COPD, it follows that short-acting and
    long-acting bronchodilators form the cornerstone
    of pharmacologic management.
  • Inhaled short-acting ß2 agonists such as
    albuterol have a more rapid onset of effect and
    shorter duration of action than short-acting
    anticholinergic agents such as ipratropium and
    thus are more often prescribed as rescue
    medications to relieve acute bronchospasm.

19
  • Patients that have persistent symptoms and
    require daily use of short-acting agents are
    recommended to switch to long-acting (12 hours)
    bronchodilators such as salmeterol and the
    long-acting antimuscurinic agent (LAMA),
    tiotropium (24 hours).
  • Several studies have identified the long-acting
    ß2 agonists (LABAs) to be effective in reducing
    symptoms, and improving lung function and
    health-related quality of life in patients with
    COPD.
  • Optimizing treatment of chronic obstructive
    pulmonary disease an assessment of current
    therapies.  Am J Med 120. (8 Suppl 1) S4-S13.
    2007

20
  • Given the importance of inflammation in the
    pathogenesis of COPD, inhaled corticosteroids
    (ICS) are typically the next line of therapy
    recommended for patients.
  • ICS should be added to bronchodilators and should
    not be used as monotherapy in COPD.
  • ICS given to patients with stable COPD for longer
    than 6 months led to about 30 reduction in the
    total number of exacerbations.
  • The effects of inhaled corticosteroids in chronic
    obstructive pulmonary disease a systematic
    review of randomized placebo-controlled trials.
     Am J Med 113. (1) 59-65.2002

21
  • For patients not optimally controlled in terms of
    symptoms with frequent use of rescue inhalers and
    with evidence of frequent exacerbations,
    combination therapy with ICS and either LABAs or
    LAMAs are recommended.
  • In a study of 782 patients with COPD, fluticasone
    propionate/salmeterol 250/50 µg significantly
    reduced the annual rate of moderate to severe
    exacerbations by 30.5 compared with salmeterol
    alone (Plt.001)
  • The most common side effects seen with ICS
    include skin bruising, oropharyngeal candidiasis,
    and voice alterations.
  • Effect of fluticasone propionate/salmeterol
    (250/50 microg) or salmeterol (50 microg) on COPD
    exacerbations.  Respir Med 102. (8)
    1099-1108.2008

22
  • Triple therapy comprising fluticasone/salmeterol/t
    iotropium in those with very advanced disease was
    superior to the use of the fluticasone/salmeterol
    or tiotropium/salmeterol in terms of improvements
    in symptoms and reduced rescue medication
    requirements
  • Due to its narrow therapeutic index and potential
    side effects, theophylline has been relegated to
    a third-tier option for COPD
  • Gaebel K., McIvor R.A., Xie F., et al  Triple
    therapy for the management of COPD a review.
     COPD 8. (3) 206-243. 2011

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24
Management of Acute COPD exacerbations
25
Diagnostic Evaluation of Patients with Suspected
COPD Exacerbation Perform routinely Pulse
oximetry Hypoxemia Perform if
hospitalized Arterial blood gas Hypercarbia,
Hypoxemia Chest radiography Alternate sources
of dyspnea Complete blood count Anemia,
Leukocytosis, Polycythemia Electrocardiography
Cardiac arrhythmias, Cardiac ischemia Metabolic
panel Electrolyte disturbances, Hypo- or
hyperglycemia Metabolic acid-base
changes Consider performing, especially if
patient is not responding to conventional
exacerbation treatment Brain natriuretic peptide
CHF (one third of dyspnea in chronic lung disease
may be attributable to CHF), Cardiac enzyme
measurement Cardiac ischemia (myocardial
infarction is underdiagnosed in patients with
COPD)
26
MANAGEMENT OF ACUTE EXACERBATION
  • Acute exacerbations of COPD are associated with
    in-hospital mortality rates of about 10
  • Nebulized formulations of rapidly acting
    bronchodilators should be used aggressively.
  • Supplemental oxygen should be given to maintain
    the PaO2 above 60 mm Hg and the SaO2 above 90
  • Up to 50 to 80 of exacerbations may be
    associated with pathogens known to colonize the
    respiratory tract, including various viruses and
    Haemophilus influenzae, Streptococcus pneumoniae,
    and Moraxella catarrhalis.
  • The more significant the symptoms of cough,
    sputum, and dyspnea and the more purulent the
    sputum, the more likely patients will benefit
    from empiric antibiotic therapy.

27
Empiric Antibiotics for COPD exacerbations
  • Amoxicillin/clavulanate 875 mg orally twice
    daily for 5 days
  • Levofloxacin (Levaquin) 500 mg daily for 5 days
  • Antibiotics for exacerbations of chronic
    obstructive pulmonary disease.  Cochrane Database
    Syst Rev.  2006(2)CD004403

28
ACUTE EXACERBATION CONTINUED
  • Systemic glucocorticoids have been shown to
    reduce recovery time, reduce hospital time,
    reduce treatment failures, decrease risk of
    relapse and improve airflow limitation.
    Prednisone 30 to 60 mg/d for 7 to 10 days. There
    does not seem to be a difference between
    intravenous versus oral delivery in terms of
    outcomes.
  • Noninvasive positive-pressure ventilation has
    been shown to be able to negate the need for
    intubation and reduce mortality for severe
    exacerbations, and should be started early.
  • Bakri F., Brauer A.L., Sethi S., et al  Systemic
    and mucosal antibody response to Moraxella
    catarrhalis after exacerbations of chronic
    obstructive pulmonary disease.  J Infect
    Dis 185. (5) 632-640. 2002

29
  • Macrolide antibiotics have both antimicrobial and
    anti-inflammatory effects.
  • Recently a prospective double-blind,
    placebo-controlled trial was conducted in which
    1142 patients with a clinical diagnosis of COPD
    on supplemental oxygen and/or having
    exacerbations within the previous year were
    randomized to receive either azithromycin 250 mg
    or placebo daily for 1 year. There was
    significant reduction in time to first
    exacerbation (Plt.0001), rate of acute
    exacerbations (P  .008), and quality-of-life
    scores (Plt.006).
  • Chronic azithromycin decreases the frequency of
    chronic obstructive pulmonary disease
    exacerbations.  Am J Respir Crit Care
    Med 183. A6416. 2011

30
Lung volume reduction surgery versus lung
transplantation
  • Patients with FEV1 less than 20 predicted, and
    either diffusing capacity for carbon monoxide
    less than 20 predicted or homogeneous pattern of
    emphysema on computed tomography, are at high
    risk for death
  • In a carefully selected subgroup of individuals
    with low exercise tolerance post rehabilitation
    and upper lobepredominant emphysema, LVRS offers
    substantial survival, functional, physiologic,
    and quality-of-life benefits
  • Lung transplantation can be considered in
    patients who do not meet criteria for LVRS but
    who are otherwise good candidates
  • Lung transplantation and lung volume reduction
    surgery versus transplantation in chronic
    obstructive pulmonary disease.  Proc Am Thorac
    Soc 5. (4) 447-453.2008

31
Key recommendations for practice
  • Noninvasive positive pressure ventilation
    improves respiratory acidosis and decreases
    respiratory rate, breathlessness, need for
    intubation, mortality, and length of hospital
    stay. A
  • Inhaled bronchodilators (beta agonists, with or
    without anticholinergics) relieve dyspnea and
    improve exercise tolerance in patients with COPD.
    A
  • Short courses of systemic corticosteroids in
    patients with COPD increase the time to
    subsequent exacerbation, decrease the rate of
    treatment failure, shorten hospital stays, and
    improve FEV1 and hypoxemia. A

32
  • Antibiotics should be used in patients with
    moderate or severe COPD exacerbations, especially
    if there is increased sputum purulence or the
    need for hospitalization. B
  • Smoking cessation reduces mortality and future
    exacerbations in patients with COPD. A
  • Long-term oxygen therapy decreases the risk of
    hospitalization and shortens hospital stays in
    severely ill patients with COPD. B

33
References
  • Chronic Obstructive Pulmonary Disease A Concise
    Review. Medical Clinics of North America- Volume
    95, Issue 6 (November 2011).
  • UpToDate 2012.
  • Harrisons Principles of Internal Medicine, 18th
    edition 2012.
  • Management of COPD exacerbations. AFP March 1,
    2010 Volume 81, Number 5.

34
THANK YOU!
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