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Chronic obstructive pulmonary disease (COPD) is "characterised by airflow obstruction which is generally progressive, not fully reversible with no obvious change in condition over several months", as defined in the NICE guidelines. (1) It is one of the leading causes of morbidity and mortality worldwide, currently at fifth position (2) with numerous studies suggesting an increase to third position.(3,4) The precise occurrence of COPD is uncertain as the definition of the disease varies as well as inconsistencies within the methods of surveys carried out. However Halbert et al. have reported that at least 3% of the population are affected by COPD with a diagnosis of COPD in 18% of people over 40.(5) Furthermore, in 2005, there were approximately 24,160 COPD related deaths in the UK alone. (2)
COPD is primarily caused by smoking which initiates an inflammatory response in the lungs resulting in the lining of the airways to become inflamed. This results in constriction and excessive narrowing of the smooth muscle. COPD patients typically present with swollen airways which leads to the production of excessive mucus and cilliary dysfunction. (6) As the disease progresses, patients find it difficult to clear secretions, developing a chronic, productive cough, wheezing and dyspnea. (1) Worsening of these symptoms leads to an exacerbation of COPD which is defined by NICE as "a sustained worsening of the patient's symptoms from their usual stable state which is beyond normal day to day variations, and is acute on onset." (1)Patients with an exacerbation experience greater inflammation therefore have an increased number of inflammatory cytokines such as IL-6 and IL-8. Typical symptoms of an exacerbation include increased breathlessness, chronic cough, increased volume of sputum and a change in the colour of sputum. (7)
A diagnosis of COPD is suspected in individuals over 35 that present with one or more of the symptoms and have a risk factor, typically smoking. The patient should also be clinically evaluated for other systemic features of the disease such as weight loss, skeletal muscle wasting and fatigue. (1,8) After clinical evaluation, a diagnosis can be confirmed using spirometry when the FEV1/FVC ratio is less than 70%. Spirometry is fundamental in diagnosing COPD and gives an indication of the extent of damage to the patients lung function. (9) Further assessment should also be carried out when a diagnosis is made including a chest radiograph and a full blood count to determine if the patient has anaemia or polycythaemia. (1)
An exacerbation of COPD is diagnosed depending on the severity of the patient's symptoms and in most cases does not require a full enquiry prior to initiating treatment. However some patients may require further investigations such as a chest x-ray, measurement of arterial blood gases and a full blood count. (1) Arterial blood gases determine the concentration of carbon dioxide and oxygen in the blood as well as the levels of bicarbonate. Furthermore, pulse oximetry and an electrocardiogram (ECG) are undertaken to ensure that the patient is managed appropriately. (1)In addition, a sputum sample is sent for analysis if the patient presents with purulent sputum to determine whether the exacerbation is infective or non-infective. (10)
Initial management of COPD involves smoking cessation in order to reduce acute exacerbations of the disease. Additionally, Lundback et al. have reported the substantial relationship between smoking and the occurrence of COPD suggesting that almost half of all smokers will go on to develop the condition. (3) Therefore, increasing evidence suggests that smoking cessation leads to an improvement in lung function thus resulting in a reduction in the rate of disease progression. (1,3,8,11)
Pharmacological management of COPD initially involves the use of short acting bronchodilators as required which includes the short acting Î²2 agonists (SABA) or anticholinergics. These can be delivered by inhalers or via a nebuliser. (1,12) SABA's such as salbutamol and terbutaline act on Î²2 receptors causing broncholdilation whereas short acting antichlinergics include ipratropium bromide which causes bronchodilation through blockage of muscarinic cholinergic receptors. (13,14) If symptoms persevere then patients can try combined therapy with a SABA and an anticholinergic. This is followed by addition of a long acting bronchodilator such as formoterol or tiotropium if symptoms continue to occur. Following this, in moderate to severe COPD, a study by TORCH has shown the benefit of combined treatment with a long acting Î²2 agonist and an inhaled corticosteroid. (15) However despite such management, theophylline may be required for patients who are still symptomatic. (1,13)
Acute management during an exacerbation of COPD requires an increase in the dose of short acting bronchodilators. In addition, patients are given oral steroids as standard therapy, typically prednisolone (30-40 mg) for up to 14 days. (1)Prednisolone has glucocorticoid activity and exerts its anti-inflammatory effect by combining with steroid receptors in the cytoplasm. This inhibits production of leukocytes and results in suppression of inflammatory mediators such as interleukins and prostaglandins. (13,16) Further management involves the use of antibiotics for patients who present with purulent sputum. Typical antibiotics include an aminopenicillin, a macrolide or a tetracycline depending on the type of micro-organism present. (1)
Evidence for Treatment of the Condition
Oxygen therapy is administered to all patients presenting with an exacerbation of COPD in order to keep the patients oxygen saturation (SaO2) above 90%. (1,6) Oxygen therapy is highly beneficial in maintaining sufficient oxygen levels whilst at the same time avoiding respiratory acidosis and an elevation in carbon dioxide levels. (1) The British Thoracic Society advised that oxygen should be commenced at 24-28% at a flow rate of 4l/min before blood gas measurements are available. (19) Durrington et al (20) has reported the increase in incidence of respiratory acidosis amongst COPD patients as a result of higher concentrations of oxygen. Furthermore patients who received higher concentrations of oxygen were more likely to develop further complications in comparison to those who were given lower concentrations. (20) However such complications can be avoided by regular measurement of the patient's arterial blood gases. Adjustments should be made to the concentration of oxygen delivered depending on the patients PaCO2 levels. (20) This patient was given 28% oxygen which increased his SaO2 from 77% to 94% therefore highlighting the benefits of oxygen therapy. Consensus shows that the benefits of oxygen therapy outweigh the risks for most patients. (6,20)
During an exacerbation of COPD, increased doses of short acting bronchodilators are given to patients in order to reduce breathlessness. Studies have shown that bronchodilator treatment greatly improves lung function during an exacerbation therefore maximum bronchodilation is given to patients as initial treatment as indicated in various guidelines. (1,8,21) In patients with an acute exacerbation of COPD nebulisers are generally used to deliver an increased dose of bronchodilators to the airways. (13) Furthermore, studies suggest that using combined bronchodilator therapy with a Î² agonist and an anticholinergic has improved effectiveness in COPD patients. (22) One study by Chan et al. has shown the advantages of combined ipratropium bromide with salbutamol via a nebuliser. From the results it was evident that there was enhanced bronchodilation with combined treatment which lasted longer compared to when salbutamol was given alone. (22,23) This is further compounded by Balter et al. who has further shown that the addition of ipratropium bromide to salbutamol has long term benefits for COPD patients. (24) Numerous studies have shown that addition of an anticholinergic such as ipratropium to a Î²2 agonist results in reduced adverse effects compared to an increased dose of Î²2 agonists when given alone. (22-25)
Despite this, one study by Moayyedi et al. compared the effect of combined therapy with salbutamol and ipratropium against salbutamol which was given alone to patients with an exacerbation of COPD. It was found that there was no further advantage with the addition of an anticholinergic. (25) Additionally, the results demonstrate that ipratropium bromide administered alone had the same effects as salbutamol or combined treatment. Furthermore this study concluded that addition of ipratropium bromide to bronchodilator treatment increases costs of therapy and side effects for patients. Further to this the authors suggest that nebulised ipratropium should only be added to therapy if the patient doesn't respond to a Î²2 agonist. However this trial did not have an adequate sample size in order to identify any progress in lung function by means of spirometry testing, when ipratropium bromide was added to therapy. (25) NICE guidelines also suggest that other factors such as an improvement in symptoms and duration of symptoms should be taken into consideration when assessing the efficacy of bronchodilators. (1)
In spite of the contrasting evidence regarding the efficacy of combined treatment with ipratropium and salbutamol, the vast majority of studies suggest that combined bronchodilator therapy is far more effective than either agent given alone. (22-24)The patient in this case was given Combivent nebulisers (salbutamol sulphate and ipratropium bromide) which is consistent with NICE guidelines and highly effective for acute exacerbations of COPD based on evidence from numerous studies.
Systemic corticosteroids are also used in the management of COPD exacerbations with standard therapy comprising of prednisolone 30-40 mg daily for 7-14 days. (1,13) Jadwiga et al. has reported that patients who receive oral steroids upon an exacerbation have a reduced recovery time. (7) This was further replicated by Davies et al. who reported that patients treated with prednisolone have a shorter duration of time in hospital compared to the patients on placebo. (26)Furthermore, studies have shown that oral prednisolone reduces the incidence of further exacerbations in COPD patients. (7) Studies have reported that a short term course of oral corticosteroids is as effective as prolonged treatment, with the further benefits of preventing the adverse effects associated with their long term use. (7) Niewoehner et al. (27) carried out a trial to evaluate the efficacy of oral corticosteroids in the treatment of COPD exacerbations. From the results it was evident that steroids were beneficial in decreasing the incidence of unsuccessful treatment at 30 and 90 days, however long term therapy with oral steroids showed no greater benefits. (27,28) In addition to this, studies reveal that patients on oral steroids have greater mobility and have improved overall health compared to patients in whom steroids were not indicated. (26) From another trial, it was observed that spirometry measurements also improved in patients who were treated with oral prednisolone. (29)
However steroids are associated with many adverse effects and studies report the increased incidence of hyperglycaemia in patients with diabetes mellitus (28) Furthermore some studies report that only a minority of patients are responsive to oral steroid treatment with only 10-15% of patients showing an improvement in spirometry measurements. Additionally, studies suggest that patients susceptible to recurrent exacerbations, who receive multiple courses of oral prednisolone are at an increased risk of developing osteoporosis. (30) Although treatment with oral prednisolone is recommended in the guidelines for an acute exacerbation of COPD, there is still insufficient evidence supporting its use in exacerbations of COPD and many studies conducted are inconsistent regarding doses of prednisolone used and the duration of treatment. (29,30)
This patient was treated with 40 mg oral prednisolone daily which is in accordance with NICE guidelines.(1) In addition, numerous studies provide evidence on the beneficial effects of treatment with oral steroids in reducing exacerbation frequencies in COPD patients. Although some studies show that only a minority of patients have improved spirometry measurements with steroid therapy, in the vast majority of them patients have shown improvements in overall health and recovery time from exacerbations. (26-30)