Treatment

    COPD is treatable at any stage of the illness.  However, to date there is no cure for COPD, and no treatments can completely reverse its destructive effects (Ferrara, 2011).  Without treatment, COPD will gradually worsen, debilitating the lives of those who suffer from it (Higginson, 2010).
    The goals of COPD treatments include smoking cessation, risk reduction, improve exercise tolerance, improved health status and quality of life, and minimization of the frequency and severity of acute exacerbations (Ferrara, 2011; Hudd & Zaiken, 2011).

     A management strategy consisting of combined pharmacotherapy and non-pharmacotherapeutic interventions can effectively improve symptoms, activity levels and quality of life at all levels of disease severity (DE O’Donnell et al., 2008).

    A comprehensive approach to the management of chronic obstructive pulmonary disease (DE O’Donnell et al., 2008).


    AECOPD Acute exacerbation of COPD; LABA Long-acting beta2-agonist; MRC Medical Research Council; PRN As needed; Rx Treatment


     






    Non-pharmacotherapeutic interventions

    There are various treatment options that can help reduce symptoms and prevent complications. The first step in COPD treatment is to quit smoking and learning to avoid lung irritants that can worsen the condition. Diet, Education, Smoking cessation, Vaccinations and Pulmonary rehabilitation (for more detail see Treatment: Nursing Care)

    Natural Remedies (Native remedies, 2012)
    Number of homeopathic remedies can help patients with symptoms of excessive chest mucus:
    • Kali mur is one such ingredient and it is well known for its beneficial effects of the respiratory system and its ability to ease wet coughs.  Kali mur, also known as kalium chloratum, kali muriaticum, or potassium chloride, is naturally found in the mineral sylvine.
    • Similarly, Kali Sulphuricum is excellent at naturally treating phlegm coughs and sinus congestions, as well as reducing inflammation of the mucous membranes.
    • Kali bich also known as potassium dichromate and potassium bichromate. Kali bich works on soothing irritated mucous membranes, especially in the lungs, and helps loosen thick chest mucus.
    Oxygen therapy
    For patients who have more advanced disease, oxygen therapy may be needed during exercise or even activities of daily living (Ferrara, 2011; Hudd & Zaiken, 2011; Higginson, 2010).  Long-term continuous oxygen (15 h/day or more to achieve an oxygen saturation of 90% or greater) offers a survival advantage to patients with stable COPD with severe hypoxemia (DE O’Donnell et al., 2008).

    Surgery
    The most common surgery treatment includes lung volume reduction surgery (LVRS), surgery to remove giant bullae, chest tube insertion for pneumothorax, and lung transplantation (Ferrara, 2011; Higginson, 2010; Martinez, 2010).

    Pharmacotherapy

    Medications to help breathing such as bronchodilators, anticholinergic drugs, mucolytic, corticosteroids, or purified human alpha-1 antitrypsin for deficiency are prescribed.
      
    Recommendations for optimal pharmacotherapy in chronic obstructive pulmonary disease (DE O’Donnell et al., 2008).


     *Refers to the lower dose inhaled corticosteroid/long-acting beta2-agonist (ICS/LABA); AECOPD Acute exacerbation of COPD; LAAC Long-acting anticholinergic; PRN As needed; SABA Short-acting beta2-agonist; SABD Short-acting bronchodilator 




    Disability and Lung function impairment is measured by the peak-flow meter. There are 3 zones: green, yellow and red:
    Green (80-100% of best peak flow): SABD Short-acting bronchodilator - PRN; Persistent disability: LAAC Long-acting anticholinergic + SABD Short-acting bronchodilator, or SABA Short-acting beta2-agonist - PRN.
    Yellow (50-80% of best peak flow): LAAC Long-acting anticholinergic + SABA Short-acting beta2-agonist; Persistent disability: LAAC Long-acting anticholinergic + LABA Long-acting beta2-agonist + SABA Short-acting beta2-agonist - PRN; Persistent disability: LAAC Long-acting anticholinergic + Inhaled corticosteroid/long-acting beta2-agonist (ICS/LABA) + SABA Short-acting beta2-agonist - PRN.
    Red (0-50% of best peak flow): LAAC Long-acting anticholinergic + Inhaled corticosteroid/long-acting beta2-agonist (ICS/LABA) + SABA Short-acting beta2-agonist - PRN; Persistent disability: LAAC Long-acting anticholinergic + Inhaled corticosteroid/long-acting beta2-agonist (ICS/LABA) + SABA Short-acting beta2-agonist - PRN + Theophylline.
    Two main classes of bronchodilators are used to treat COPD: β -agonists and anticholinergics. Beta-agonist agents relax airway smooth muscles and improve air-flow.  These agents are also reported to improve ciliary action and mucus clearance.  Beta2-agonists work by stimulating  β-adrenoreceptors, increasing cyclic adenosine monophosphate (cAMP) concentrations and leading to relaxation of the smooth muscles.  Anticholinergics block acetylcholine, a neurotransmitter that activates muscles, thereby inhibiting the bronchoconstrictor effects of acetylcholine and mucus secretion. (Ferrara, 2011; Hudd & Zaiken, 2011; Bostock-Cox, 2010).
    • Short-acting bronchodilators, (eg, Salbutamol /ventolin), both anticholinergics and beta2-agonists, have been shown to improve pulmonary function, dyspnea and exercise performance in patients with moderate to severe COPD (Hudd & Zaiken, 2011).
    • Long-acting beta2-agonists (LABAs),(eg, salmeterol 50 μg twice daily or formoterol 12 μg twice daily) offer more sustained improvements in pulmonary function.  Indicated for moderate to severe COPD.  Inhaled beta2-agonists are generally well-tolerated.  The most common adverse effects include tachycardia, palpitation, irritability, insomnia, muscle cramps and tremor (Hudd & Zaiken, 2011).
    • Long-acting anticholinergics (LAACs) (eg, tiotropium bromide (Spiriva):  onset 30 mins and lasts 24 hours). Tiotropium provides improvements in lung hyperinflation, exercise endurance, exacerbations and health resource utilization in patients with moderate to severe COPD. Apart from occasional dry mouth, inhaled anticholinergic drugs are generally well tolerated (Hudd & Zaiken, 2011).
    • Combined long-acting bronchodilators: The combination of LAAC and LABA bronchodilators may have additive sustained effects on pulmonary function in patients with moderate to severe COPD (Hudd & Zaiken, 2011).
    Corticosteroids in treating COPD patients who suffer from repeated acute exacerbations.
    • Inhaled corticosteroids (ICS) alone: The role for ICS in COPD is controversial (Ferrara, 2011; DE O’Donnell et al., 2008; Hudd & Zaiken, 2011).  However, inhaled corticosteroids are not licensed for use as monotherapy in COPD, and should only be prescribed alongside a long-acting bronchodilator (Bostock-Cox, 2010).
    • ICS/LABA combinations: Two combination ICS and LABA products are currently available in Canada: fluticasone plus salmeterol (Advair), and budesonide plus formoterol (Symbicort). The LABA/ICS combination seemed to have better anti-inflammatory effect than either LABA or ICS by itself (Ferrara, 2011).
    • Oral theophyllines: Relatively weak bronchodilators that offer modest improvements in pulmonary function, dyspnea and exercise performance. 
    • Oral corticosteroids: There is  modest benefit of improvement with oral corticosteroids. Long-term use of low-dose oral steroids is not recommended in COPD due to serious adverse effects associated with maintenance use of systemic corticosteroids (Ferrara, 2011).
    New approved agents
    • Rofiumilast (Daliresp) is a once-daily oral selective PDE4 inhibitor recently approved by the FDA as a treatment at patients with severe COPD with a history of exacerbations (Bostock-Cox, 2010). The exact mechanism is not fully understood, but rofiumilast and its active metabolite roflumilast N-oxide are believed to inhibit in-flammation by increasing cAMP via PDE4 inhibition (Greener, 2011;Hudd & Zaiken, 2011).
    • Indacateroi maleate is the first ultra-long-acting once-daily beta2-adrenoceptor Agonist (Ultra-LABA) for the long-term maintenance therapy (Hudd & Zaiken, 2011).
    Management of acute exacerbation

    Potential preventive strategies for acute exacerbations of chronic obstructive pulmonary disease (AECOPD) (DE O’Donnell et al., 2008). 
     
    Strategies
    Smoking cessation
    Vaccinations
    Influenza (annually)
    Pneumococcal vaccine (every five to 10 years)
    Self-management education
    Regular long-acting bronchodilator therapy (moderate to severe COPD)
    Regular therapy with ICS/LABA combination (moderate to severe COPD with ≥1 AECOPD, on average, per year)
    Oral corticosteroid therapy for AECOPD
    Pulmonary rehabilitation
    (ICS Inhaled corticosteroids; LABA Long-acting beta2-agonist)

    Treatment of acute exacerbation includes: combined, increased doses of inhaled short-acting beta2-agonist (SABA) and an anticholinergic should be used to improve pulmonary function and dyspnea.  Oral or parenteral corticosteroids are recommended in most patients with moderate to severe AECOPD (DE O’Donnell et al., 2008).
    ·         
     Antibiotics are beneficial to treat more severe purulent AECOPD
    Antibiotic treatment recommendations for purulent acute exacerbations of chronic obstructive pulmonary disease.
    Group
    Basic clinical state
    Symptoms and risk factors
    Probable pathogens
    First choice
    Simple exacerbation
    COPD without risk factors
    Increased 
    sputum,
    purulence and dyspnea
    Haemophilus influenzae, Haemophilus,
    Moraxella, Streptococcus pneumoniae
    Amoxicillin, cephalosporins, doxycycline, macrolides, trimethoprim/
    sulfamethoxazole
    Complicated exacerbation
    COPD with risk factors
    As in simple plus at least one of:
    FEV1<50% redicted
    ≥4 exacerbations per year
    Ischemic heart disease, oxygen,
    steroid use
    As in simple plus:
    Klebsiella 
     and other Gram-negatives.
    Pseudomonas species.
    Fluoroquinolone, beta-lactam/beta-lactamase inhibitor
    Repeat prescriptions of the same antibiotic class should be avoided within a three-month interval. FEV1 Forced expiratory volume in 1 s