The Global Initiative for Chronic Obstructive Lung Disease (GOLD) by nyf51324

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									                                    Clinical Perspectives




          The Global Initiative for
            Chronic Obstructive
           Lung Disease (GOLD)
                                                                  by Dennis R. Wissing, PhD, RRT, CPFT




    C            hronic obstructive pul-
    monary disease (COPD) continues
    to be a leading cause of chronic
    morbidity and mortality in the
                                           Chronic Obstructive Pulmonary
                                           Disease.” The report was published
                                           in 2001 1 ; subsequent updates
                                           followed in 2003 and 2004, with an
                                                                                    variety of inhaled irritants and
                                                                                    gases. 1 Due to the progressive
                                                                                    nature of COPD, it can be classified
                                                                                    based on severity. Table 2 is an
    United States.1 While the incidence    additional update expected in            adapted summary of the classifica-
    of many chronic diseases such as       2006. The GOLD executive sum-            tions as discussed in the GOLD
    heart disease is stabilizing, the      maries may be viewed at www.             report.
    number of patients with COPD           goldcopd.org.                               The hallmark of COPD is
    continues to rise. COPD is                The goals of the GOLD stan-           sputum production, cough, and
    projected to rank fifth as a world-    dards are COPD prevention and            dyspnea. These symptoms often
    wide burden of disease during the      education of caregivers on effective     develop before clinical documenta-
    next decade.2 Despite COPD’s high      diagnosis and management of              tion of airflow limitation by spirom-
    prevalence, the disease is often       COPD. The standards are based on         etry. The airflow limitation associ-
    underappreciated, misdiagnosed,        four components of care of the           ated with COPD is a result of a
    and mismanaged. A paradigm shift       patient with COPD (see Table 1).         mixture of central and small airway
    in the diagnosis, treatment, and       This article is a brief summary of the   disease, specifically inflammation
    management of COPD is on the           2004 GOLD executive summary.             of the bronchioles.
    horizon due to the Global Initiative                                               A clear, globally accepted defini-
    for Chronic Obstructive Lung           Definition of COPD                       tion of COPD remains controver-
    Disease (GOLD). GOLD is a coop-           Traditionally, COPD is viewed as      sial; however, focusing on the
    erative effort by the U.S. National    a disease syndrome composed of           inflammator y changes, air way
    Heart, Lung, and Blood Institute       varying degrees of chronic bronchi-      remodeling, and the partial
    (NHLBI) and the World Health           tis and emphysema. The GOLD              reversibility of the disease affords
    Organization (WHO).                    standards no longer include these        the respiratory therapist with new
      During the late 1990s, the           diseases in the definition of COPD.      direction in management and treat-
    GOLD program gathered a panel of       Rather, COPD is defined as a             ment.
    experts from all over the world to     disease state characterized by
    produce an extensive report titled,    airflow limitation with a partially      Burden of COPD
    “GOLD Workshop Report, Global          reversible component. Airflow limi-         The burden of COPD worldwide
    Strategy for the Diagnosis, Man-       tation is progressive and results        is expected to increase during the
    agement, and Prevention of             from an inflammatory response to a       next two decades due to an increase



4   AARC Tımes      July 2005
                                Clinical Perspectives




                                                                               as host and environmental factors.
Table 1. Four Components of Care of                                            Inflammation with COPD eventu-
the Patient with COPD                                                          ally results in squamous metaplasia
                                                                               of epithelial cells, mucus gland
Component 1       Assess Severity of the Disease and Monitor Disease           metaplasia, and airway closure with
                  Progression                                                  lung hyperinflation. The elastic
Component 2       Reduce Risk Factors Associated with COPD
                                                                               fibers of the lung are destroyed
Component 3       Management of the Patient with Stable COPD
                                                                               along with airspace enlargement
Component 4       Management of Acute COPD Exacerbations
                                                                               (emphysema) due to an imbalance
                                                                               of proteinases and antiproteinases.
in tobacco use and an aging popula-     Pathogenesis, pathology,               Centrilobular changes occur with
tion. 1 Reported prevalence of          and pathophysiology                    dilation and destruction of bronchi-
COPD by countries varies consid-           COPD results from inhaled           oles, primarily in the upper lobes.6
erably due to varying risk factors,     particles and gases causing inflam-    Over the course of the disease,
distribution of population, age vari-   mation, tissue destruction, and        pulmonary vascular changes occur
ation, and different tendencies for     alteration of the destruction and      with thickening of the vessel wall
gene susceptibility among different     repair mechanisms of the lung.         and increased pulmonary vascular
countries.                              COPD pathology includes chronic        resistance.
   In past decades, COPD was seen       inflammation of the central and           Once the patient stops inhaling
predominantly in men. The GOLD          peripheral airways, lung tissue, and   noxious gases (such as cigarette
panel cites recent large population
studies that reported equal occur-      Despite COPD’s high prevalence, the
rence of COPD in men and women.
This is thought to be a result of       disease is often underappreciated,
increasing tobacco use by women
worldwide.                              misdiagnosed, and mismanaged.
Risk factors for COPD                   pulmonary vasculature. In addition,    smoke), the air ways undergo a
   Risk factors for COPD include        there is hypersecretion of mucus,      degree of airway remodeling. The
environmental and genetic factors.      airway narrowing from fibrosis, and    injury-and-repair process results in
The patient’s response to inhaling      destruction of parenchyma (em-         fibrosis and narrowing of the
noxious gases is influenced by the      physema). In addition to chronic       peripheral airways from scar and
amount of exposure along with           inflammation, an unbalance of          collagen tissue. These changes
their genetic susceptibilities. 3,4     proteinases and antiproteinases and    result in a fixed narrowing of the
Other host factors such as varying      oxidative stress also contribute to    airway. Although
levels of airway hyperresponsive-       the development of COPD.
ness among patients with COPD              Inflammation in COPD differs
and altered lung growth during          from that of asthma. For example,
childhood also place the patient at     the principle proinflammatory cell
risk for the disease.5                  associated with COPD is the
   A major factor in the develop-       neutrophil, while with asthma the
ment of COPD is exposure to             predominant cell is the
tobacco smoke. However, the             eosinophil. Proinflam-
patient’s total burden of inhaled       matory mediators also
particles needs to be considered.       differ between the two
Particles from occupational dusts,      diseases.
chemicals, fumes, and indoor and           The decline of lung
outdoor pollution, as well as other     function in COPD is a
inhaled particles contribute to the     result of the interplay
development of COPD.                    between inhaling
                                        noxious gases, as well
                                                                 Student Peggy Rivoire is being instructed in infant intubation
                                                                 by Diana Merendino, MHS, RRT, RPFT, assistant professor of
                                                                 cardiopulmonary science at LSU.
                                                                                         AARC Tımes      July 2005    5
                                       Clinical Perspectives




    Table 2. Classifying COPD                                                            Wheezing and chest tightness can
                                                                                         also be found with mild to very
    Stage 0       At Risk                  Chronic cough, risk factors present.          severe COPD. Noting these symp-
                                           Spirometry is normal.                         toms along with a detailed medical
                                                                                         history, physical examination, and
    Stage 1       Mild COPD                Mild airflow limitation. FEV1/FVC < 70%
                                                                                         spirometry, can assist the health
                                           but FEV1 > 80% predicted. Patient may
                                                                                         care provider such as the physician
                                           not be aware of declining lung function.
                                                                                         or respiratory therapist in develop-
                                                                                         ing an appropriate treatment plan.
    Stage 2       Moderate COPD            Airflow limitation continues. FEV1 /FVC
                                           <70%, FEV1 is 50 to 80% predicted.
                                           May experience productive cough.              Component 2: Reduce Risk Factors —
                                                                                         Eliminating the patient’s exposure
    Stage 3       Severe COPD              FEV1 /FVC <70%. FEV1 30 to 50%                to noxious gases is the primary
                                           predicted. May experience productive          preventive measure for managing
                                           cough.                                        COPD. Noxious gases such as
                                                                                         tobacco smoke, occupational dusts
    Stage 4       Very Severe COPD         FEV1 /FVC <70% and FEV1 <30%                  and chemicals, and air pollution all
                                           predicted. Chronic respiratory failure.       need to be considered when manag-
                                                                                         ing a patient with COPD. The
                                                                                         primary factor to control is tobacco
    airflow limitation is, for the most        apy, counseling, and extensive            smoke, and the respiratory thera-
    part, irreversible, there can be a         patient education.                        pist plays a key role in smoking
    degree of reversibility in COPD.                                                     cessation. Programs include patient
    The reversible component is due to         Component 1:Assess and Monitor Disease    education, counseling, social
    inflammatory cells, mucus, smooth          — Typically, the diagnosis of COPD        support, nicotine replacement
    muscle constriction, and air trap-         is based on a history of inhaling         therapy, behavioral modification,
    ping. This is why smoking cessation        noxious gases and exhibiting airflow      and assistance with relapse.
    is so important for the patient with       limitation with spirometry. Even in
    COPD.                                      the absence of dyspnea, patients with
       Although emphysematous                  a chronic productive cough and a
    changes occur in COPD, the                 history of exposure to noxious gases
    narrowing of the small airways is the      should be evaluated with spirometry.
    predominant cause of airflow limi-         Spirometry remains the gold stan-
    tation and increased airway resis-         dard to diagnose COPD.
    tance. COPD is also associated with           COPD is considered present
    altered gas exchange due to                with an FEV1/FVC (forced expi-
    mismatching of ventilation-to-             ratory volume in first
    perfusion, pulmonary hyperten-             second/forced vital capacity)
    sion, and extrapulmonary effects           less than 70 percent and a post
    such as systemic inflammation and          bronchodilator FEV 1 less
    skeletal muscle dysfunction.7              than 80 percent of
                                               predicted.
    Management of COPD                            Breathlessness is the
      There are four components to the         hallmark symptom of
    management of COPD (see Table 1).          COPD and is often
    Management of mild to moderate             persistent and progres-
    COPD includes disease prevention           sive. Dyspnea is
    and pharmacologic control while the        usually the first symp-
    care of severe to very severe COPD         tom forcing the
    involves a variety of strategies such as   patient to seek
    nutritional support, physical ther-        medical attention.

                                                                          Dr. Dennis Wissing (right) assists senior student Huratio
                                                                          Williams in instructing patient Mark Randolph.
6    AARC Tımes         July 2005
                                    Clinical Perspectives




    Component 3: Manage Stable COPD           Oral steroidal agents are less         reduction surgery are not recom-
    — A patient with stable COPD           effective in COPD than asthma.            mended at this time.1
    requires assistance with coping with   Use of oral steroids in stable COPD
    the illness, minimizing symptoms,      either on a short-term or a long-         Component 4: Manage Acute Exacerba-
    and improving the quality of life.8    term basis is generally not recom-        tions — Acute exacerbations of
    Patients with COPD can be taught       mended. However, GOLD stan-               COPD symptoms require medical
    treatment strategies so they can       dards recommend a short course of         intervention. The most common
    self-manage their disease.             oral steroids to help identify the rare   cause of acute symptoms is infec-
       Management of stable COPD           patient who may improve with long-        tion.1 Acute exacerbations require
    aids in minimizing or preventing       term oral or inhaled steroids.            assessment of severity of symptoms,
    symptoms. Existing medications            Long-term use of inhaled steroids      blood gas analysis, chest radiogra-
    used in the treatment of COPD          does not alter decline in lung func-      phy, and other appropriate tests.
    have not been shown to slow the        tion associated with COPD. There          Medicated aerosol therapy, oral
    rate of lung function decline.         is evidence supporting the use of         steroids, theophylline, and noninva-
                                                                                     sive positive pressure ventilation
    A paradigm shift in the diagnosis,                                               (NPPV) are recommended for
                                                                                     acute exacerbations of COPD.1
                                                                                        The GOLD standards recom-
    treatment, and management of COPD is                                             mend NPPV for acute exacerba-
                                                                                     tions. However, endotracheal intu-
    on the horizon due to the Global Initiative                                      bation and mechanical ventilation
                                                                                     could be considered in light of the
    for Chronic Obstructive Lung Disease.                                            patient’s likelihood of reversibility
                                                                                     and availability of intensive care
                                                                                     facilities. There is no difference in
    Medications are administered to        inhaled steroids in symptomatic           mortality rates between mechani-
    control the symptoms. Medications      COPD patients with FEV1 less than         cally ventilated patients with
    are adjusted as needed based on the    50 percent of predicted. 1 Other          COPD versus patients mechani-
    severity of the disease. Therapy is    effective pharmacologic treatments        cally ventilated for non-COPD
    usually long-term, and response to     for stable COPD include vaccines          causes.1
    treatment varies from patient to       and alpha-1 antitrypsin augmenta-
    patient.                               tion therapy.
       Short- and long-term beta              Use of antibiotics should be
    agonists are employed to improve       limited to treating infectious exac-
    expiratory flow. Combining bron-       erbations in COPD patients.
    chodilators may be more effective      Mucolytic agents, immunoregula-
    while reducing side effects associ-    tors, vasodilators, respiratory stim-
    ated with increasing the dose of a     ulants, and antitussives are not
    single agent. Combining a short-       recommended in the treatment
    acting beta agonist with an anti-      of stable COPD.1
    cholinergic can result in a greater       No n - p h a r m a c o l o g i c
    change in FEV1 and longer bron-        therapies that are recom-
    chodilator effect then either drug     mended in the manage-
    alone.                                 ment of stable COPD
       Theophylline may be effective in    include pulmonary
    managing stable COPD, but related      rehabilitation, long-
    side effects often limit the use of    term oxygen ther-
    this drug. Physicians tend to rely     apy and bullectomy
    more on medicated aerosols rather      in selected patients.
    than expose the patient to theo-       Lung transplanta-
    phylline-related side effects.         tion or volume
                                                                    Students Sherry Hayes (left) and Heather Kelley are being
                                                                    instructed in the art of intubation by Dennis R. Wissing, PhD,
                                                                    RRT.
8    AARC Tımes       July 2005
       Clinical Perspectives




Future research                                 tive stress in asthma, COPD, and smok-
                                                ers. American Journal of Respiratory and
   GOLD standards call for studies              Critical Care Medicine, 154(4, Pt. 1),
to help us better understand COPD               1055-1060.
at the molecular level and for better           8. Celli, B.R. (1995). Pulmonary rehabilita-
diagnostic techniques and pharma-               tion in patients with COPD. American
cologic agents. Markers for inflam-             Journal of Respiratory and Critical Care
                                                Medicine, 152(3), 861-864.
mation in sputum or exhaled
condensates (lipid mediators, reac-             ADDITIONAL RESOURCES
tive oxygen species, cytokines) may             The AARC web site YourLungHealth.org
help in better managing exacerba-               includes a wealth of information about
tions.1                                         COPD and other lung diseases for both
                                                clinicians and patients. Visit
   Longitudinal studies on COPD                 www.yourlunghealth.org and click on
trends, global survey of costs associ-          “COPD” under the “Diseases and Condi-
ated with the disease, and genetic              tions” area. Also, be sure to check out the
studies could aid in assisting GOLD             “Ask Dr. Tom” portion of the web site,
to achieve one of its major objec-              which features noted lung specialist
                                                Thomas L. Petty, MD, FAARC, answering
tives: prevention of COPD. •                    questions posed by visitors to the site.

Dr. Dennis Wissing is professor of              The AARC online store has two books by
cardiopulmonary science, head of the            Thomas L. Petty, MD, FAARC, on COPD:
department of clinical sciences, and assis-     “Frontline Update in COPD” (thanks to an
tant dean for academic affairs at LSU           educational service from Boehringer Ingel-
Health Sciences Center School of Allied         heim Pharmaceuticals) and “Adventures of
Health Professions in Shreveport, LA.           an Oxy-Phile.” Visit the AARC web site at
                                                www.aarc.org and click on the “Store” tab.
REFERENCES
1. Global Initiative for Chronic Obstructive    On Aug. 24, the AARC will present a
Lung Disease. (2004). Global strategy for       webcast on “Selecting the Most Appro-
the diagnosis, management, and preven-          priate 02 Device for Your Patient.” AARC
tion of chronic obstructive pulmonary           members can participate in this webcast
disease (pp. 1-121). Ghent, Belgium.            and receive CRCE after registering for the
2. Murray, C.J., & Lopez, A.D. (1996).          program and taking a test. For informa-
Evidence-based health policy — Lessons          tion, visit www.aarc.org and click on
from the Global Burden of Disease Study.        “Webcast Central.”
Science, 274(5288), 740-743.
3. Harrison, D.J., Cantlay, A.M., Rae, F., et   The AARC online store has several COPD-
al. (1997). Frequency of glutathione S-         related videotapes or DVDs in the Profes-
transferase M1 deletion in smokers with         sor’s Rounds Series. This program offers 1
emphysema and lung cancer. Human &              CRCE per employee after completing test
Experimental Toxicology, 16(7), 356-360.        within 60 days of purchase. Titles include:
4. Smith, C.A., & Harrison, D.J. (1997).        “Getting Most from Mist: Current/Future
Association between polymorphism in             Aerosol Delivery” (2004 series), “Current
gene for microsomal epoxide hydrolase           State of Pharmacotherapy for Asthma &
and susceptibility to emphysema. Lancet,        COPD” (thanks to an educational grant
350(9078), 630-633.                             from Boehringer Ingelheim and Pfizer
5. Tager, I.B., Segal, M.R., Speizer, F.E., &   Pharmaceuticals), and “Developing a
Weiss, S.T. (1988). The natural history of      Successful Tobacco Cessation Program.”
forced expiratory volumes. Effect of ciga-      Visit the AARC web site at www.aarc.org
rette smoking and respiratory symptoms.         and click on the “Store” tab.
The American Review of Respiratory
Disease, 138(4), 837-849.                       The AARC catalog and online store
6. Leopold, J.G., & Gough, J. (1957). The       feature lung health brochures for patient
centrilobular form of hypertrophic emphy-       education on topics such as “Living Well
sema and its relation to chronic bronchi-       with COPD” and “Quit Smoking Success-
tis. Thorax, 12(3), 219-235.                    fully.” Visit the AARC web site at
7. Rahman, I., Morrison, D., Donaldson,         www.aarc.org and click on the “Store”
K., & MacNee, W. (1996). Systemic oxida-        tab.




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