The COPDX Plan guidelines5 developed by the Australian Lung Foundation and the Thoracic Society of Australia and New Zealand provide an appropriate framework for diagnosis and management. The key recommendations are: Confirm diagnosis, Optimise function, Prevent deterioration, Develop a self-management plan and manage eXacerbations.
C—Confirm diagnosis and assess severity
|• Breathlessness || |
|• Cough |
|• Sputum production |
|• Chest tightness |
|• Wheezing |
|• Airway irritability |
|• Fatigue || |
|• Anorexia |
|• Weight loss |
Consider the diagnosis of COPD in all smokers and ex-smokers older than 35 years. The diagnosis of COPD rests on the demonstration of airflow obstruction.
The sensitivity of the physical examination for detecting mild to moderate COPD is poor.
The signs vary according to the nature of the disease and the presence of infection. Signs may be completely absent in the early stages of COPD: chronic bronchitis may present only with wheezing, while dyspnoea is a feature of associated airflow obstruction.
reduced chest expansion
diminished breath sounds ± wheeze
‘pink puffer’—always breathless
‘blue bloater’—oedematous and central cyanosis
signs of respiratory failure
signs of cor pulmonale
The diagnosis is usually clinical with a history of increasing dyspnoea and sputum production in a lifetime smoker with no features of asthma. It is imprudent to make a diagnosis of chronic bronchitis and emphysema in the absence of cigarette smoking unless there is a family history suggestive of alpha1-antitrypsin deficiency.6
At diagnosis, up to 50% of lung function may have been lost.
Spirometry remains the gold standard for diagnosing, assessing and monitoring COPD. Post-bronchodilator forced expiratory ratio (FER) <0.7 is required for diagnosis.
COPD Post-bronchodilator FEV1/FVC of <0.70 (<70%) and FEV1 <80% predicted.
The Australian stages of severity based on FEV1% predicted are mild (60–80%), moderate (40–50%) and severe (<40%), while the GOLD1 staging is 1. mild (≥80%), 2. moderate (50–80%), 3. severe (30–50%), 4. very severe (<30%).
This can be normal (even with advanced disease) but characteristic changes occur late in disease. May exclude lung cancer >1 cm.
The principal goals of therapy are to stop smoking, to optimise function through relief of symptoms with medication and pulmonary rehabilitation, and to prevent or treat aggravating factors and complications.
TABLE 83.1 is a useful consultation checklist mnemonic.7
Table 83.1SMOKES, a consultation checklist for chronic obstructive pulmonary disease7 |Favorite Table|Download (.pdf) Table 83.1 SMOKES, a consultation checklist for chronic obstructive pulmonary disease7
|S = Smoking cessation |
|M = Medication—inhaled bronchodilator, vaccines (influenza, pneumococcus), corticosteroids (if indicated) |
|O = Oxygen—is it needed? |
|K = Komorbidity—cardiac dysfunction, sleep apnoea, osteoporosis, depression, asthma, GORD |
|E = Exercise and rehabilitation |
|S = Surgery—bullectomy, lung volume reduction surgery, single-lung transplantation |
If you smoke, you must stop (persuading the patient to stop smoking is the key to management). The only treatment proven to slow the progression of COPD is smoking cessation.3 Consider smoking cessation medications.
Avoid places with polluted air and other irritants, such as smoke, paint fumes and fine dust.
Go for walks in clean, fresh air.
A warm, dry climate is preferable to a cold, damp place (if prone to infections).
Get adequate rest.
Avoid contact with people who have colds or flu.
Optimal diet—reduce weight if necessary.
Refer to a physiotherapist for chest physiotherapy, breathing exercises and an aerobic physical exercise program.
In the long-term treatment of COPD, bronchodilators are recommended for the relief of wheezing and shortness of breath. Bronchodilation is important to allow ‘lung emptying’ and reduce gas trapping. These include: short-acting β2-agonists (SABAs, e.g. salbutamol, terbutaline) and short-acting anticholinergic drugs (ipratropium bromide); long-acting β2-agonists (LABAs, e.g. eformoterol, salmeterol, indacaterol, vilanterone); long-acting anticholinergic drugs with muscarinic antagonist action (LAMAs, e.g. tiotropium, glycopyrronium, umeclidinium) which block parasympathetic bronchial constriction; and corticosteroids.
The preferred route of administration of bronchodilator is by inhalation, which requires correct device technique.
Inhaled drugs can be administered by MDIs, dry-powder devices or nebulisers. The evidence suggests that an MDI and spacer are as effective as a nebuliser—they are also simpler and cheaper—but the appropriate method depends on patient needs and preference.
The usefulness of a bronchodilator for an individual can only be assessed by a therapeutic trial, accepting either objective improvement in lung function or improvement in symptom control as endpoints.
Short-acting bronchodilator therapy
Most studies suggest that short-acting β2-agonists and ipratropium bromide are equally efficacious in patients with COPD. If patients do not respond adequately to one of these bronchodilators then it is appropriate to consider a trial of a combination of the two classes of bronchodilator with objective monitoring of response.
Use the following by inhalation:6
salbutamol 100–200 mcg, up to 4 times daily
terbutaline 500 mcg, up to 4 times daily
or (with and without)
ipratropium bromide 40–80 mcg, up to 4 times daily
For patients unable to use an MDI or a spacer, a nebuliser should be used, with the following doses:
salbutamol or terbutaline 2.5 to 5 mg
ipratropium bromide 250 to 500 mcg by nebuliser, up to 4 times a day
Long-acting bronchodilator therapy
Long-acting β2-agonists can be used in patients who remain symptomatic despite treatment with combinations of short-acting bronchodilators and those with frequent exacerbations. Used regularly they can be effective and may be more convenient than using short-acting bronchodilators.8 Long-acting anticholinergic therapy2 with tiotropium bromide (taken by inhalation) has been proven to reduce the frequency of exacerbations with COPD compared with short-acting anticholinergic drugs. The choice of drug can be determined by the patient’s response to a trial of the drug, the drug’s adverse effects and cost including PBS listing.
For treatment with long-acting bronchodilator by inhalation, see TABLE 83.2.
Table 83.2Long-acting bronchodilators7 |Favorite Table|Download (.pdf) Table 83.2 Long-acting bronchodilators7
|eformoterol ||12 mcg twice daily |
|salmeterol ||50 mcg twice daily |
|indacaterol ||150–300 mcg daily |
|olodaterol ||5 mcg daily |
|aclidinium ||322 mcg twice daily |
|tiotropium ||18 mcg daily |
|glycopyrronium ||50 mcg daily |
|umeclidinium ||62.5 mcg daily |
Only 10% of patients with stable COPD benefit in the short term from inhaled corticosteroids (ICS). There are no distinguishing clinical features to predict in advance which patients may respond. The aim of treatment is to reduce exacerbation rates and slow the decline of the disease. The effect of ICS on mortality is uncertain, and there is some evidence that ICS use may increase rates of pneumonia. Note that asthma can possibly coexist with COPD. Benefits are not seen in patients who continue to smoke.
If corticosteroids are to be used, usual practice is ICS/LABA combination inhalers (fluticasone/salmeterol, fluticasone/vilanterol or budesonide/eformoterol), which are available on the PBS for use in symptomatic patients with moderate to severe COPD (FEV1<50% predicted).9
In this group, tiotropium combined with an ICS/LABA combination inhaler (triple therapy) is more beneficial than the individual treatments alone.9 Combining LAMA and LABA provides a modest additive effect.10
Guidelines for prescription include:
documented but limited evidence of responsiveness to inhaled corticosteroids, including functional status
those with an FEV1 ≤50% predicted
two or more exacerbations requiring oral steroids in 12 months
There is no role for ICS monotherapy in the treatment of COPD. Oral corticosteroids are not recommended for maintenance therapy in COPD, although they may be needed in patients with severe COPD where corticosteroids cannot be withdrawn following an acute exacerbation. A stepwise approach to management is outlined in FIGURE 83.2.
Stepwise approach to management of COPD.
Reducing risk factors for COPD is a priority, and smoking is the most important and prime target if this continues to be a problem. Stopping is the only measure that slows the progression of COPD. Reinforce patient education programs, and avoid exposure to passive smoke as far as possible.
Annual influenza vaccination
Influenza vaccination reduces the risk of exacerbations, hospitalisation and death. It should be given in early autumn to all patients with COPD.
Vaccination (23vPPV) to prevent invasive bacteraemic pneumococcal pneumonia is recommended, with a booster at 5 years.11
Long-term oxygen therapy (LTOT) reduces mortality in COPD. Long-term continuous therapy given for at least 15 hours a day (as close as possible to 24 hours a day) prolongs life in hypoxaemic patients—those who have PaO2 consistently <55 mm Hg (7.3 KPa; SpO2 88%) when breathing air. At assessment for ongoing therapy, the patient’s condition must be stable and the patient must have stopped smoking at least 1 month previously. Flow should be set at the lowest rate needed to maintain a resting PaO2 of 60 mm Hg. A flow rate of 0.5–2.0 L/min is usually sufficient. Best used for at least 18 hours a day.6 There is no clear-cut evidence about the effectiveness of intermittent ambulatory domiciliary oxygen therapy, but patients with hypoxaemia during sleep may require nocturnal oxygen therapy.
Check current smoking status
Smoking cessation clearly reduces the rate of decline of lung function. GPs and pharmacists can help smokers quit. Brief counselling is effective and every smoker should be offered at least this intervention at every visit.
Refer to strategies in CHAPTER 21, including effectiveness of treatment for nicotine dependence.
Current evidence does not support long-term antibiotic use to prevent exacerbations, but they should be used in exacerbations with an increase in cough, dyspnoea, sputum volume or purulence.
No medication has yet been shown to prevent the long-term decline in lung function. Inhaled corticosteroids (ICS) are indicated for patients with a documented response or those who have moderate to severe COPD with frequent exacerbations. ICS use has been observed to be associated with increased rates of pneumonia.
Note: fixed-dose combinations of LABA and ICS (see CHAPTER 82) are used for patient convenience.6
Mucolytic agents may reduce the frequency and duration of exacerbations (evidence level I). Mucolytic therapy should be considered for patients with a chronic cough productive of sputum. Oral mucolytics include potassium iodide, bromhexine, N-acetylcysteine, ambroxol and glyceryl guaiacolate. Compounds containing codeine should be avoided.
Regular use of antitussives in stable COPD is contraindicated.
Regular review with objective measures of function is recommended in anticipation of reducing complications, frequency and severity of exacerbations and admissions to hospital. Regular schedules for follow-up visits are appropriate. Medication review should involve consideration of deprescribing as well as prescribing.
The options are bullectomy, lung volume reduction surgery and transplantation. Patients should be referred for consideration for bullectomy if they have a single large bulla on CT scan associated with breathlessness and an FEV1 <50% predicted. Other lung surgery should be considered in patients with severe COPD who remain breathless with marked restriction of their activities of daily living, despite maximal therapy. Emphysema mainly involving the upper lobes with PaCO2 <55 mm Hg and FEV >20% predicted are some factors required for lung volume reduction surgery.
D—Develop support network and self-management plan5
COPD imposes a considerable handicap on patients and carers, with heavy psychosocial issues including fears about the outcome of the disease.
Respiratory physician referral
Early referral to a respiratory physician is appropriate in order to clarify the diagnosis, consider other therapies, consider long-term home oxygen and facilitate organisation of pulmonary rehabilitation.
One highly effective strategy is pulmonary rehabilitation, which aims to increase patient and carer knowledge and understanding, reduce carer strain and develop positive attitudes toward self-management and exercise. Integrated programs include education, exercise, behaviour modification and support, which are more effective than any separate component.
The support team and multidisciplinary care plans
As the patient’s primary health care provider, the GP is uniquely placed to identify smokers and help them quit, facilitate early diagnosis and coordinate the support team. The support team can enhance the quality of life and reduce morbidity for the COPD patient. The support team can include a nurse/respiratory educator, physiotherapist, occupational therapist, social worker, clinical psychologist, speech pathologist, pharmacist and dietitian.
Government and community support services such as Home Care, home maintenance, exercise programs, Meals on Wheels and support groups can be galvanised to provide support.
Patients should be encouraged to take appropriate responsibility for their own management. The primary care team, supported by Extended Primary Care item numbers, should develop systems to identify those with more severe COPD who might benefit from more focused education and training in self-management skills.
The issues facing the COPD patient include fear, stress, sleep disturbance, anxiety, panic and depression. Proactive management, including optimal care of these problems as they arise, will facilitate coping. Management also focuses on symptom control and maximising the quality of life. These patients have to face palliative care at the end stage and ethical issues have to be handled sensitively.
Referral to in-patient care
The management plan should include the identification of clinical markers indicating more intensive hospital treatment.
Indications for hospitalisation include:5
rapid rate of onset of acute exacerbation with increased dyspnoea, cough or sputum
inability to cope at home
inability to walk between rooms when previously mobile
severe breathlessness leading to inability to eat or sleep
inadequate response to ambulatory treatment
altered mental status suggestive of hypercapnia
significant comorbidity (e.g. cardiac disease)
Diagnosis of an exacerbation is symptomatically the acute onset over minutes to hours of:
Fever may be present, but fever and chest pain are uncommon symptoms. One-third have no identifiable cause, but infections and heavy pollutants can cause the exacerbation. Consider investigating with pulse oximetry, chest X-ray and sputum culture.
Patients should be treated with a bronchodilator, preferably with a large-volume spacer. If nebulisers are used they should be driven by compressed air (to avoid the problem of potentially adverse oxygenation). Systemic glucocorticoids reduce the severity and shorten recovery.
Ventilatory support may be used if hypercapnia develops or worsens despite optimal drug therapy. Non-invasive ventilatory support may avoid the need for intubation.
Initial therapy by SABA inhalation:
salbutamol 100 mcg MDI, up to 8 to 10 inhalations, repeat as required
terbutaline 500 mcg DPI, 1 to 2 inhalations, repeat as required
ipratropium bromide 20 mcg MDI, up to 4–6 inhalations, repeat as required
If control is inadequate, combine salbutamol or terbutaline with ipratropium bromide.
If a nebuliser is used (which is usually the case upon hospitalisation), use salbutamol 2.5–5 mg, terbutaline 2.5–5 mg or ipratropium bromide 250–500 mcg, as required.
Controlled oxygen delivery—28% via Venturi mask or 2 L/min via nasal prongs should be commenced if the patient is hypoxaemic (oxygen saturation >92% with pulse oximetry). Maintain the arterial oxyhaemoglobin saturation at 90%. It is important to obtain a direct measurement of arterial blood gases to confirm the degree of hypoxaemia and if hypercapnia or acidosis is present.
Note that patients with severe COPD are prone to hypercapnia if they breathe high oxygen concentrations. Supplemental oxygen should be kept to a minimum. If hypercapnia develops assisted ventilation may be required.
Corticosteroids should be used routinely for severe exacerbations. Use:
If oral medication cannot be tolerated, use:
Conversion from IV to oral corticosteroid should occur as soon as practicable.
The duration of oral corticosteroid therapy for exacerbations of COPD is not well established; however, courses of 7 to 14 days are commonly used.
A tapering dose schedule is not required for short courses.
The use of antibiotics for exacerbations is not routinely indicated as many episodes are due to viral infections. Some patients have repeated exacerbations due to bacterial infection (usually Haemophilus influenzae, S. pneumoniae or Moraxella catarrhalis) where antibiotics have been proven to be beneficial, reducing the risk of mortality by 77%.13
The indication for antibiotic treatment is:
amoxycillin 500 mg (o), 8 hourly for 5 days
doxycycline 200 mg (o) as 1 dose on day 1, then 100 mg (o) daily for a further 5 days
azithromycin 500 mg (o) daily for 5 days
A stepwise approach is summarised in FIGURE 83.3.
Management plan for acute exacerbation of COPD
Evidence indicates that regular treatment with long-acting β2-agonists is more effective than treatment with short-acting agents (evidence level I) and is associated with improved quality of life (evidence level II), although they are more costly and do not significantly improve lung function. Current recommended guidelines based on the severity of disease are summarised in TABLE 83.3.
Table 83.3COPD therapy according to severity of disease9,15 |Favorite Table|Download (.pdf) Table 83.3 COPD therapy according to severity of disease9,15
|Stage of COPD ||Treatment |
|0 At risk ||Avoidance of risk factors, esp. smoking |
| ||Influenza and pneumococcal vaccination. ? Haemophilus influenzae vaccination |
|1 Mild ||Add short-acting bronchodilator |
|2 Moderate ||Add long-acting bronchodilators LAMA + LABA |
| ||Consider LABA/ICS and referral |
| ||Add pulmonary rehabilitation |
|3 Severe ||Add inhaled corticosteroids LABA/ICS + LAMA |
|4 Very severe ||Add long-term oxygen (if chronic respiratory failure) |
| ||Consider theophylline (o) or roflumilast |
| ||Consider surgical referral |
The key triad of treatment is: inhaled bronchodilators, smoking cessation and exercise.
The two priorities are improving lung function and reducing exacerbations. LAMA is a cornerstone of COPD treatment.
COPD patients should be referred early for rehabilitation. Contact your respiratory physician or hospital for help.
Pulmonary rehabilitation programs benefit most patients with pulmonary disease.
Rehabilitation teams are interdisciplinary, usually comprising a rehabilitation physician, physiotherapist, occupational therapist, social worker and dietitian.
Patients with COPD commonly present in the fifth decade with productive cough or an acute chest illness.4
Diagnosis can only be established by objective measurement using spirometry with FEV1 being the preferred parameter.
Non-invasive positive pressure ventilation (NPPV) reduces mortality and hospital stay in patients with acute failure; it is also an effective weaning strategy for patients who require intubation.13
The only treatment proven to slow the progression of COPD is smoking cessation.
It is very difficult at times to distinguish COPD from the persistent airflow limitation of chronic asthma in older patients (see TABLE 49.3).
COPD is reportedly ‘massively’ underdiagnosed—screening with good quality spirometry is important.