New GOLD guidelines were published in 2011 including a fundamental change: Symptoms and not just airflow limitation have now to be taken into account to guide the management of chronic obstructive pulmonary disease (COPD). The rationale behind this change is that airflow limitation, which is linked to the frequency of exacerbations and measure future risks, has poor correlation with the daily impact of the disease upon the individual patient, and therefore serves as little practical use on its own. The major goal of COPD management is thus now two folded:
- Reduce symptoms (measured by the modified Medical Research Council (mMRC) dyspnoea scale and/or COPD Assessment Tool (CAT))
- Reduce future risk (measured by the severity of airflow limitation and/or exacerbation history in the previous 12 months)
The new guidelines also emphasise the importance of comorbidities, which have to be assessed and treated as part of these goals.
COPD and chronic asthma might sometimes be difficult to differentiate. As a general rule (though not exclusively), asthma tend to develop earlier in life, while COPD symptoms are slowly progressive and tend to develop in people with history of tobacco smoking or other smoke exposure.
Once the diagnosis of COPD is done, patients are now divided into four groups (A, B, C and D) according to their symptom/risk profile (see algorithm).
Table 1: Combined severity assessment of COPD based on risk/symptom profile
| SYMPTOMS | |||
| PATIENT GROUP | Less symptoms
mMRC=0-1 CAT<10 |
More symptoms
mMRC≥2 CAT≥10 |
|
| RISK | High risk
GOLD 3-4 (i.e. FEV1<50%) Exacerbations ≥2/year |
C | D |
| Low risk
GOLD 1-2 (i.e. FEV1≥50%) Exacerbations ≤1/year |
A | B | |
The patient group determines the pharmacotherapy strategy recommended for stable COPD.
Non-pharmaceutical management
Long-acting bronchodilators, which include long-acting muscarinic antagonist (LAMA) and long-acting beta2-agonist (LABA), are the gold-standard maintenance therapy for the maintenance of COPD, and their mechanism of action is well-known (see box). Long-acting bronchodilators are preferred over short acting formulations. Also note that based on efficacy and tolerability inhaled bronchodilators are preferred to oral bronchodilators, and theophylline is not recommended unless bronchodilators are unavailable/unaffordable for long-term treatment. The phosphodiesterase-4 inhibitor roflumilast may be considered as add on to bronchodilator treatment in patients with chronic bronchitis, severe airflow limitation and frequent exacerbations not controlled by long-acting bronchodilators.
Three pivotal features of non-pharmacological management include:
1) Reduction of exposure to risk factors (principally tobacco smoke)
2) Promotion of exercise
3) Immunisation against influenza and pneumococcal disease
Pharmaceutical management
1) A (low risk, less symptoms)
First line: Short-acting β2-agonist (SABA) prn or short-acting anticholinergic (SAMA) prn
Second line: LAMA or LABA or (SAMA and SABA)
Alternative*: Theophylline
2) B (low risk, more symptoms)
First line: LAMA or LABA
Second line: LAMA and LABA
Alternative*: SAMA and/or SABA
3) C (high risk, less symptom)
First line: (ICS and LABA) or LAMA
Second line: LAMA and LABA
Alternative*: Phosphodiesterase type 4 (PDE4) inhibitors, SAMA and/or SABA, theophylline
4) D (high risk, more symptoms)
First line: (ICS and LABA) or LAMA
Second line: (ICS and LAMA) or (ICS and LABA and LAMA) or (ICS and LABA and PDE4 inhibitor) or (LAMA and LABA) or (LAMA and PDE4 inhibitor)
Alternative*: Carbocysteine, SAMA and/or SABA, theophylline
*Alternative treatment might be administered alone or in combination with other 1st and 2nd line options.
Also see algorithm for a proposed model for the pharmaceutical management of COPD.
| Mechanism of action of bronchodilators
The lungs are innervated by both parasympathetic and sympathetic nerve fibres, which entail the activation of muscarinic and adrenergic receptors, respectively, both located on the airway smooth muscles. Acetylcholine released from the parasympathetic fibres activates the M3 muscarinic receptors, causing bronchoconstriction; conversely, activation of β2-adrenergic receptors by the sympathetic fibres causes bronchodilation. Thus, while both LABAs and LAMAs act by relaxing airway smooth muscles, their mechanisms are complementary: LABAs are functional agonists which activate the sympathetic (bronchodilating) pathway, whereas LAMAs are direct antagonists of a major bronchoconstrictive pathway, acetylcholine. |
1- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis, management and prevention of chronic pulmonary disease, 2011. Available at http://www.goldcopd.org/Guidelines/guidelines-resources.html
2- Gruffydd-Jones K. GOLD guidelines 2011: what are the implications for primary care? Prim Care Respir J 2012; 21(4): 437-441.