COPD is a progressive illness that requires a

multidisciplinary approach to management.

Our Drug review discusses its diagnosis and

the available treatment options, followed by

sources of further information.

Chronic obstructive pulmonary disease (COPD) isa progressive illness defined as airway obstruction

that is not fully reversible. It is usually the result ofcigarette smoking or occupational exposure leadingto chronic inflammation in the airways; however, 5per cent of those diagnosed with COPD are neversmokers.1

It produces a significant disease burden both in pri-mary and secondary care, with a prevalence of 900 000diagnosed cases and an estimated two million undiag-nosed cases in the UK.2 COPD is a major cause of mor-bidity and mortality, with around 25 000 deaths peryear, and costs of more than £800 million to the NHSand 24 million lost working days per annum.3 It is themost common reason for hospital admission with res-piratory disease.4

DiagnosisDiagnosis requires a combination of history, physicalexamination and confirmation of airway obstructionon postbronchodilator spirometry. There is no singlediagnostic test: COPD should be considered inpatients over the age of 35 who have a risk factor

22 Prescriber 19 March 2013 www.prescriber.co.uk

Drug review COPD

Current approaches to diagnosis

and management of COPD Sonia Parmar BSc, MRCP and Phil Raines MA, MRCP

SP

L

(smoker/exsmoker) and who present with exertionalbreathlessness, chronic cough, regular sputum pro-duction or frequent winter ‘bronchitis’ or wheeze.Examination may be normal or may reveal signs of ahyperinflated chest, wheeze or decreased air entry, useof accessory muscles or pursed lip breathing, hypoxiaor cyanosis.

The MRC dyspnoea scale helps grade breathless-ness according to the level of exertion required toelicit it (see Table 1).

InvestigationsPostbronchodilator spirometry should be assessed asthis allows airflow obstruction to be quantified, as perthe Global Initiative for COPD (GOLD) guidelines,and helps to differentiate from asthma.6 Asthma maybe present if there is a >400ml response to bron-chodilators, if serial peak flow measurements show sig-nificant (20 per cent) diurnal or day-to-day variabilityor if the forced expiratory volume in one second(FEV1) and FEV1/forced vital capacity (FVC) ratioreturn to normal with drug therapy. Asthma tends topresent at a younger age, with more variable day-to-day symptoms and nocturnal symptoms.7

Airway obstruction is defined as a reduced post-bronchodilator FEV1/FVC ratio <70 per cent andFEV1 <80 per cent predicted (see Table 2). Disabilityand quality of life in COPD can be poorly representedby the FEV1 but this gives some idea of severity andprognosis. Spirometry values must be compared withthe predicted normal values, which depend on thepatient’s age, height and sex.

Other investigations to consider include:• chest X-ray to exclude an alternative diagnosis, egmalignancy• alpha-1 antitrypsin level if young age, strong familyhistory or little smoking history• body mass index (BMI) • haemoglobin to exclude anaemia/polycythaemia• serial peak flow monitoring to exclude asthma • ECG if there are signs of right-heart failure• sputum culture if expectorating large amounts ofsputum.

The BODE index (BMI, airflow Obstruction,Dyspnoea, Exercise capacity) helps to make an assess-ment of clinical outcomes including exacerbations,hospital admissions and mortality in patients with sta-ble COPD (see Table 3). Here, exercise capacity ismeasured objectively using the six-minute walk test.

ManagementManagement of an individual patient’s COPD shouldbe guided by the symptoms and disability that they

experience. Patients with COPD should be involvedin informed decisions about their care to encourageadherence and help educate patients about their con-dition. COPD is a multisystem disease; it can lead toright heart failure (cor pulmonale), peripheral musclewasting and mood or cognitive changes that shouldalso be addressed.10

The management of COPD is likely to be sharedbetween healthcare professionals in both primary andsecondary care. Most patients with mild and moderatesymptoms and those who are not having frequent exac-erbations may be managed predominately in primarycare.11 Increasingly, patients with more severe diseasemay also be followed up in the community but there maybe a need for ready access to secondary-care services.

Stopping smoking This is the most important intervention for patientsat any stage of disease and should be encouraged atevery opportunity using a combination of medica-tion – nicotine replacement therapy/varenicline(Champix)/bupropion (Zyban) – and support.Ongoing smoking leads to a more rapid decline inlung function over time, which can worsen symptomsand survival.12

ImmunisationAll patients with COPD should be offered a pneumo-coccal vaccination and annual influenza vaccinations.A study comparing vaccinated to unvaccinated peoplewith chronic lung disease over three influenza seasonsdemonstrated a 52 per cent reduction in hospitalisa-tions for both pneumonia and influenza and a 70 percent reduction in risk for death.

A similar study for pneumococcal vaccine foundreductions of 43 and 29 per cent respectively and there

www.prescriber.co.uk Prescriber 19 March 2013 23

COPD

Table 1. MRC Breathlessness Scale (after reference 5)

1 not troubled by breathlessness except on

strenuous exercise

2 short of breath when hurrying or walking up a

slight hill

3 walks slower than most people on the level,

or stops for breath when walking at own

pace

4 stops for breath after walking about 100m

or after a few minutes on level ground

5 too breathless to leave the house, or

breathless when dressing or undressing

Grade Degree of breathlessness related to

activities

seemed to be a synergistic effect when both vaccineswere given together.13

Self-managementSelf-management plans in COPD are important toenable patients to modify their lifestyle and respondappropriately to the first signs of an exacerbation.Recognising exacerbations early and prompt use of arescue pack of oral steroids, inhaled short-acting beta2-agonists (SABAs) and/or antibiotics may lead toreduced hospital admissions.14 However, the patientshould be advised to seek medical attention shouldthey fail to respond.

Management of anxiety and depressionCOPD leads to disabling and distressing symptoms thatcan lead to a patient becoming socially isolated andprevented from undertaking activities they may haveenjoyed. This can lead to anxiety or depression, whichoften has similar symptoms to their COPD and may beoverlooked but can have a significant effect on theirquality of life. This may exacerbate the pre-existingsymptoms as the patient is less able to cope with theirsymptoms and also worsens the psychosocial impactof COPD.15,16

Studies show that patients with COPD have a 2.5times greater risk of suffering from depression,which worsens as the severity of COPD progressesand leads to more hospital admissions.17 Treatmentof these problems should include psychological andpsychosocial interventions before antidepressantsare considered.

Pharmacological therapyStepwise maintenance therapy according to FEV1 isoutlined in Figure 1.

Inhaled therapyAlthough COPD is characterised by irreversible airflowobstruction, bronchodilators are the mainstay of phar-macological therapy.18 Beta2-agonists act directly tocause bronchodilatation on bronchial smooth musclewhereas anticholinergics inhibit resting bronchial tone.

As well as improving breathlessness through directbronchodilator effects, both classes of drugs also

appear to reduce hyperinflation, explaining why clin-ical benefits may be seen without significant changesin the FEV1.

Short-acting bronchodilators SABAs, eg salbutamol, and short-acting muscarinicantagonists (SAMAs), eg ipratropium, are the mostcommonly employed bronchodilators in COPD andcan be used on a regular or as-required basis. Theeffect of short-acting bronchodilators on airway calibrecan last for up to four hours.

As-required short-acting bronchodilators shouldbe the initial treatment for the relief of breathlessnessand exercise limitation in COPD.

Long-acting bronchodilators The duration of action of tiotropium(Spiriva)means that it can be used once daily.Clinical evidence favours the use of long-acting mus-carinic antagonists (LAMAs) in preference toSAMAs and this is cost effective as well as more likelyto improve treatment adherence due to the use ofa once-daily therapy. The UPLIFT (UnderstandingPotential Long-term Impacts on Function withTiotropium) trial demonstrated that tiotropiumdecreased exacerbations, reduced hospitalisationsand improved quality of life.19 It also showed a pos-itive outcome on mortality.

Adverse effects appear to be dry mouth thoughthere has been some concern of cardiovascular riskparticularly when using the Respimat device inpatients with known arrhythmias.20 The device shouldbe used with caution in patients with a history ofarrhythmia, and all patients should be reminded notto exceed the stated dose.21

Newer LAMAs include aclidinium (EkliraGenuair), which is twice-daily administration, andglycopyrronium (Seebri), which is once-daily.

Inhaled combination therapySince beta2-agonists, anticholinergic drugs andinhaled corticosteroids (ICS) affect airway calibre andlung function through different mechanisms, combin-ing drugs of these classes may give synergistic benefitsin patients with FEV1 less than 50 per cent predicted.The TORCH (TOwards a Revolution in COPDHealth) study showed that combination therapy (ICS+ LABA) reduced the rate of decline of lung function,as assessed by FEV1, the exacerbation rate and theoverall quality of life.22

Full effective doses in COPD are Seretide 500Accuhaler (fluticasone/salmeterol) one puff twicedaily or Symbicort Turbohaler 200/6 (budesonide/

24 Prescriber 19 March 2013 www.prescriber.co.uk

COPD

Table 2. GOLD classification of airway obstruction8

<70% ≥80% mild

<70% 50–79% moderate

<70% 30–49% severe

<70% <30% very severe

FEV1/FVC ratio FEV1 Severity (GOLD classification)

formoterol) two puffs twice daily. There is some evi-dence of a small increased risk of pneumonia whenusing some inhaled steroids, though this should notpreclude their use.19,23

Inhaler devicesDrug delivery devices are as important as the drugsthemselves; incorrect use of the device will limit effec-tiveness of therapy. For the most part this involves useof handheld inhalers (metered-dose inhalers or drypowder inhalers) with or without spacers as required.It is important to regularly assess inhaler technique tocheck that the inhaler is being used appropriately. Aprior study in elderly patients showed those whoacquired adequate technique with a particular devicedemonstrated inadequate technique when assessed amonth later.24

Nebulisers can be considered if the patient is stillbreathless despite maximal inhaler therapy andshould only be continued if there is improvementin the patient’s symptoms, quality of life or lungfunction.

Nebulised therapyThere is no clear evidence of benefit of nebulisedover inhaled therapy; nebulised medication is costly,takes time to administer and may restrict patients’activity and increase the risk of side-effects, therebyreducing quality of life. It should not be used as areplacement for inhaled therapy where operation ofthe inhaler is impaired, although a nebuliser can beoperated by carers. A small subgroup of patients maybenefit from home nebulised therapy on a trialbasis.25

Oral therapyMucolytic therapy, eg carbocisteine (Mucodyne), maybe prescribed if a patient with COPD has a chronicproductive cough as it increases expectoration of spu-tum by reducing its viscosity. There may also be anantioxidant effect. It can be continued if there is symp-tomatic benefit.26

The role of theophylline in COPD remains contro-versial and it should only be used after a trial of short-acting and long-acting bronchodilators, or in patientswho are unable to use inhaled therapy. It is believedto have effect on relaxing airway smooth muscle,increasing mucociliary clearance and strengtheningthe diaphragm.27 However, it carries risks for inter -actions with other medications and potential toxicity;there is therefore a need to review for interactions andmonitor plasma levels.

Long-term steroids are not recommended as theyhave little effect against neutrophils, which are pre-dominant in COPD;28 if they are used, however, osteo-porosis prevention is recommended in all patientsaged over 65. Antitussives and prophylactic antibioticsare not recommended as there is insufficient evidencefor their use.

Newer medicationsIndacaterol (Onbrez Breezhaler) is an ultra LABA thatis licensed as part of maintenance treatment of mod-erate-severe COPD and can be used once a day. Studiesshow a benefit in postdose FEV1 when compared withplacebo and tiotropium.29 Common side-effectsinclude peripheral oedema and paraesthesia, and cau-tion should be used in patients with epilepsy.30

Roflumilast (Daxas) is a selective long-acting phos-phodiesterase-4 (PDE-4) inhibitor with anti-inflamma-tory effects. It is currently licensed as an adjunct tobronchodilators for the maintenance treatment ofpatients with moderate-severe COPD associated withfrequent exacerbations. Studies have shown a statisti-cally significant improvement in the rate of moderateor severe exacerbations with roflumilast when com-pared with placebo. It also improved pre- and post-bronchodilator FEV1 when compared with usualinhaler therapy.31

The usual oral dose is 500µg once daily. Commonside-effects include gastrointestinal disturbance, and cau-tion should be used in acute/latent infection, eg tuber-culosis. Use should be avoided in severe depression.30

Pulmonary rehabilitationPulmonary rehabilitation is a multidisciplinary pro-gramme including physical training, disease educationand nutritional, psychological and behavioural inter-vention in order to optimise a patient’s physical andsocial independence.32 Outpatient programmes con-tain a minimum of six weeks and a maximum of 12weeks of interventions. It is offered in moderate tosevere COPD and aims to prevent deconditioning toallow the patient to cope better with their disease. Mostprogrammes are hospital or community based and

Table 3. BODE index; values range from 0 (best) to 10 (worst). A 1-point increase in

the BODE score is associated with a 34 per cent increase in all-cause mortality and a

62 per cent increase in respiratory mortality for COPD patients.9

FEV1 (% predicted) ≥65 50–64 36–49 ≤35

Distance walked in 6 minutes (m) ≥350 250–349 150–249 ≤149

Dyspnoea score (MRC Grade) 0–1 2 3 4

BMI measure >21 ≤21 — —

0 1 2 3

COPD

www.prescriber.co.uk26 Prescriber 19 March 2013

comprise individualised exercise programmes andeducational talks.

Pulmonary rehabilitation should be offered to allpatients who remain functionally disabled (MRCGrade 3 and above) including all those who have hada recent hospital admission for exacerbation.

There is good evidence for the benefits of pul-monary rehabilitation but most programmes requireoptimisation of medical therapy prior to enrolment.Pulmonary rehabilitation is not suitable for patientswho are unable to walk, have unstable angina or whohave had a recent MI.

Pulmonary rehabilitation leads to statistically sig-nificant improvement in quality of life, exercise capac-ity and dyspnoea. There is also a trend in decreasednumber of days in hospital after successful completionof pulmonary rehabilitation compared to the yearbefore,33 though the length of this benefit variesbetween studies. There is also evidence that repeatedpulmonary rehabilitation courses lead to further tem-

porary improvements in breathlessness and exercisecapacity and reduced exacerbations.

Oxygen therapyAs COPD progresses many patients become hypox-aemic and once the PaO2 falls below 8kPa they maystart to develop signs of cor pulmonale, which is a poorprognostic indicator. Some patients become hypox-aemic only on exertion and oxygen can improve exer-cise capacity and reduce disability.

Oxygen should be used with caution in patientswith COPD as some patient’s respiratory drivedepends on their degree of hypoxia and uncontrolledoxygen therapy can result in respiratory depressionand carbon dioxide narcosis.

In stable COPD oxygen can be administered forlong periods during the day and night (long-term oxy-gen therapy, LTOT), as ambulatory oxygen (either aspart of LTOT or on its own to facilitate exercise) or asshort-burst therapy to relieve symptoms.

28 Prescriber 19 March 2013 www.prescriber.co.uk

COPD

Figure 1. Stepwise maintenance therapy according to FEV1; adapted from NICE CG10143

FEV1 ≥50% FEV1 <50%

LABA LAMA

discontinue SAMA

(offer LAMA in

preference to

regular SAMA 4

times a day)

LABA + ICS

in a combination

inhaler

(consider LABA +

LAMA if ICS

declined or not

tolerated)

LABA + ICS

in a combination

inhaler

(consider LABA +

LAMA if ICS

declined or not

tolerated)

LAMA + LABA

+ ICS

in a combination

inhaler

LAMA

discontinue SAMA

(offer LAMA in

preference to

regular SAMA 4

times a day)

Breathlessness

and exercise limitation

Exacerbations or

persistent breathlessness

Persistent exacerbations

or breathlessness

SAMA – short-acting antimuscarinic agent

SABA – short-acting beta-agonist

LABA – long-acting beta-agonist

LAMA – long-acting antimuscarinic agent

ICS – inhaled corticosteroid

FEV1 – forced expiratory volume in 1 second

* SABA (as required) may continue at all stages

offer therapy (strong evidence)

consider therapy (less strong evidence)

SABA or SAMA as required*

Long-term oxygen therapyLTOT has been shown in studies to confer a survivalbenefit when used for more than 15 hours per day.34

LTOT should be prescribed for COPD patients withPaO2 < 7.3kPa when stable, or < 8.0kPa with secondarypolycythaemia, nocturnal hypoxia, pulmonary hyper-tension or concurrent pulmonary fibrosis. Oxygenassessment should be carried out in a specialist unitto decide on oxygen prescription based on arterialblood gases on separate occasions in a patient withoptimal COPD treatment.

Oxygen concentrators are the most convenient andeconomical method of providing domiciliary LTOT.Patients should be warned about risks of fire and explo-sion if they continue to smoke when prescribed oxygen.

Ambulatory oxygenAmbulatory oxygen provides portable oxygen duringexercise and activities of daily living. It can be consid-ered in patients who are noted to have desaturationon exertion and in whom ambulatory oxygen providessome symptomatic benefit or increased exercise toler-ance on a six-minute walk test.

Short-burst oxygen therapyShort-burst oxygen therapy has very little proven ben-efit and is one of the most expensive therapies usedin the NHS. It can be used in patients who do not meetrequirements for LTOT but have episodes of severebreathlessness that cannot be relieved by any othertreatment.35

Palliative careMultidisciplinary palliative care teams should beinvolved early in care planning where a patient’s dis-ease is no longer responsive to curative treatment. Thefocus of palliative care in COPD deals with symptomcontrol and optimising quality of life. Involvement ofpalliative care teams can encourage open communi-cation with patients regarding their disease severityand prognosis and help clarify goals of treatment.

Opioids can be used in end-stage COPD to helpalleviate symptoms of breathlessness that are unre-sponsive to other therapy. Benzodiazepines, tricyclicantidepressants and oxygen can also be used forbreathlessness and to reduce the psychological impactof the condition. Access to a hospice should be avail-able for symptom control and end-of-life care.

Multidisciplinary managementPatients with milder COPD can be managed success-fully in the community by their GP, with the assistanceof trained practice nurses.

More severe cases are increasingly managed by amultidisciplinary team including respiratory special-ists, physiotherapists, smoking-cessation counsellors,and community- and hospital-based specialist nurses.Although evidence for their benefit is lacking, it isthought that such specialist nurses can ensure adherence with treatment and help avoid hospitaladmissions.36

Specialist respiratory physiotherapists can assistin the provision of pulmonary rehabilitation, andthere is some evidence that breathing-retrainingexercises can produce a decrease in symptoms andexacerbation rates.37,38 Advice from dietitians mayhelp to reduce weight loss, an indicator of highermortality.39

www.prescriber.co.uk Prescriber 19 March 2013 29

COPD

Mr A was a 46-year-old gentleman with a 25-pack-year smoking history

who was seen in chest clinic with breathlessness over the preceding

three years. He had been diagnosed with asthma as a child but this had

settled and he was not on any inhalers. On review in clinic his postbron-

chodilator spirometry showed an FEV1 of 1.4 litres (52 per cent pre-

dicted), FVC 2.3 litres (62 per cent predicted), and FEV1:FVC ratio 60 per

cent. He was thought to have COPD given his smoking history and

started on tiotropium and budesonide/ formoterol inhalers. On his next

clinic review he felt much improved. His repeat spirometry showed an

FEV1 of 2.6 litres (98 per cent predicted), FVC 3.5 litres (94 per cent pre-

dicted). The improvement of his spirometry to normal with treatment with

inhaled corticosteroids and bronchodilators implies he has asthma rather

than COPD. Had his spirometry improved, but not to normal, he might

have co-existing asthma and COPD.

Case one: Asthma, not COPD

Ms B was a 62-year-old lady seen in chest clinic with breathlessness and

cough productive of copious sputum over the last two years. She had a 38-

pack-year smoking history. Chest X-ray showed some chronic changes and

postbronchodilatory spirometry showed an obstructive deficit with FEV1

1.6 litres (72 per cent predicted), FVC 2.4 litres (80 per cent predicted) and

FEV1:FVC ratio 68 per cent. She was thought to have COPD and started on

tiotropium, but continued to require courses of antibiotics for recurrent

exacerbations and a fluticasone/salmeterol inhaler was started. Her breath-

lessness improved but repeated sputum cultures were positive for

Haemophilus influenzae and Moraxella catarrhalis. On her next clinic review

a high resolution CT scan was requested, which showed evidence of

bronchiectasis with dilated bronchi. She was successfully managed with

sputum clearance techniques and bronchodilators. A history of cough pro-

ducing large quantities of sputum raises the possibility of bronchiectasis.

Postbronchodilator spirometry in bronchiectasis often shows airflow

obstruction, but again COPD may also be present.

Case two: Bronchiectasis

Occupational therapy and social service inputRespiratory disability has a high prevalence, being thesecond commonest cause of major disability in elderlypeople and often the level of support provided topatients with COPD is low in comparison.40 This maybe in part due to lack of recognition of the level of dis-ability by medical staff.

It has been noted that disability level is a predic-tor of recurrent hospital admission for COPD andso this is most commonly assessed at the end of aninpatient stay by activities of daily living (ADL) assess-ment or formal occupational therapy (OT) review.41

Patients and carers may be entitled to benefits fordisability and the social service department shouldbe involved early.

Management of exacerbationsAn exacerbation is defined as an acute and sustainedworsening of symptoms compared to the patient’sbaseline. Clinical judgement should be used to deter-mine whether the patient can be managed in the com-munity or requires admission to hospital; the presenceof community-based specialist nurses and/or ‘Hospitalat Home’ schemes in some areas may help to preventadmission.36

In acute exacerbations bronchodilatation can beachieved either with nebulisers or inhalers, providedtechnique is good.42 In the community, oral cortico -steroids should be considered where there is increasedbreathlessness interfering with daily activity and no

contraindication;43 there is no benefit to treatmentduration greater than 14 days.44

Antibiotic therapy (a single antibiotic: a penicillin,macrolide or tetracycline) should be given where thereis a history of increased sputum purulence.45

Specialist interventionsDomiciliary noninvasive ventilationDomiciliary noninvasive ventilation is a method of pro-viding respiratory support in patients with chronichypercapnic respiratory failure who are adequatelytreated but have required ventilatory support duringan exacerbation or become acidotic with LTOT. It canbe provided via a nasal or full-face mask and needsassessment and start-up in a specialist centre.

Surgery Bullectomy can be considered in patients who have asingle large bulla on CT scan and aims to reduce lungcollapse in the surrounding lung caused by the bul-lous. Lung volume-reduction surgery can be consid-ered in patients with predominant upper lobeemphysema who have an FEV1 >20 per cent predictedand are still symptomatic and breathless despite max-imal medical therapy. This aims to reduce poorly func-tioning lung tissue to decrease strain placed on thethoracic muscles.

If more homogeneous emphysema is seen on CTscan or there is evidence of raised pulmonary arterypressures and progressive deterioration, patients canbe considered for lung transplantation.

ConclusionCOPD is diagnosed by the pattern of clinical symptomsand signs in conjunction with quality-assured spirom-etry. Management requires a multidisciplinaryapproach with smoking cessation helping to slow pro-gression and inhaled pharmacological therapy andpulmonary rehabilitation reducing symptoms andexacerbation rates. Specialist interventions, usuallydelivered by secondary care, may be required inselected cases.

Three case studies indicating common pitfalls inthe diagnosis and management of COPD have beenhighlighted in separate boxes.

References1. Behrendt C. CHEST 2005;128:1239–44.2. Healthcare Commission. Clearing the air: a national studyof chronic obstructive pulmonary disease. 2006.3. Britton M. Respir Med 2003;97;71–9.4. Burney P, et al. The burden of COPD in the UK. NHS NationalLibrary for Health: Respiratory Specialist Library, 2006.

30 Prescriber 19 March 2013 www.prescriber.co.uk

COPD

Mr C was a 37-year-old gentleman with an eight-pack-year smoking his-

tory who presented to his GP with symptoms of shortness of breath and

wheeze. His peak expiratory flow rate (PEFR) was 390 litres per minute (62

per cent predicted), and he was started on beclometasone and salbutamol

inhalers for likely asthma. His symptoms failed to improve and serial PEFR

measurements showed no significant change despite regular increases in

his inhaled medication and the addition of oral steroids; he was referred to

a respiratory specialist. He underwent postbronchodilator spirometry,

which revealed FEV1 2.3 litres (56 per cent predicted), FVC 4.5 litres (91

per cent predicted) and FEV1:FVC ratio 51 per cent, suggesting COPD.

Further questioning revealed three family members had died of emphy-

sema at relatively young ages; his alpha-1-antitrypsin level was found to

be low. His oral steroids were stopped gradually and his medications were

altered to include tiotropium for COPD. He was referred to a tertiary centre

specialising in alpha-1-antitrypsin deficiency. The patient’s young age and

relatively low smoking history led to the diagnosis of COPD not being con-

sidered. Alpha-1-antitrypsin deficiency should be considered in patients

who present with COPD at a young age, with minimal smoking history or

strong family history.

Case three: Delayed diagnosis

www.prescriber.co.uk Prescriber 19 March 2013 31

COPD

5. Fletcher CM, et al. BMJ 1959;2:257–66.6. Calverley PM, et al. Thorax 2003;58:659–64.7. British Thoracic Society, Scottish IntercollegiateGuidelines Network. British guideline on the management ofasthma. 2003.8. Global Initiative for Chronic Obstructive Lung Disease(GOLD). Global strategy for the diagnosis, management, and pre-vention of chronic obstructive pulmonary disease. 2008.9. Celli BR, et al. N Engl J Med 2004;350;1005–12.10. Fabbri LM, et al. Lancet 2007;370:797–9.11. Van Wetering CR, et al. Thorax 2010;65:7–13.12. Van der Meer RM, et al. Cochrane Database Syst Rev2003;(2):CD00299.13. Nichol KL, et al. Ann Intern Med 1990;130;397–403.14. Monninkhof EM, et al. Thorax 2003;58:394–8.15. Van Ede L, et al. Thorax 1999;54:688–92.16. Dowson C, et al. New Zealand Medical Journal 2011;114:447–9.17. Van Manen JG, et al. Thorax 2002;57:412–6.18. COPD Guidelines Group of the Standards of CareCommittee of the BTS. (1997). Thorax 1997;52(Supp 5):1–28.19. Tashkin DP, et al. N Engl J Med 2008;359:1543–54.20. Singh S, et al. British Medical Journal 2011;342:d3215.21. MHRA. Drug Safety Update 2011;4(4).22. Calverley PM, et al. N Engl J Med 2007;356:775–89.23. Wedzicha JA, et al. American Journal of Respiratory & CriticalCare Medicine 2008;177:19–26.24. Connolly MJ. Age & Ageing 1995;24:190–2.25. O’Driscoll BR. Thorax 1997;52(Suppl 2):S49–S52.26. Zheng JP, et al. Lancet 2008;371:2013–8.27. Vassallo R, et al. Mayo Clin Proc 1998;73;346–54.

28. Callahan CM, Ann Intern Med 1991;114:216–23.29. Donohue JF. Am J Respir Crit Care Med 2009;10–15.30. BNF 64. September 2012.31. NICE. Roflumilast for the management of severe COPD.TA244. January 2012.32. Salman GF, et al. J Gen Intern Med 2003;18:213–21.33. Ries AL, et al. Chest 1997;112:1363–96.34. Medical Research Council Working Party. Lancet1981;1:681–6.35. Okubadejo AA, et al. Respir Med 1994;88;777–85.36. Gravil JH, et al. Lancet 1998;351:1853–5.37. Christensen EF, et al. Chest 1990;97:645–50.38. Casciari RJ, et al. Chest 1991;79:393–8.39. Landbo C, et al. American Journal of Respiratory & CriticalCare Medicine 1990;160:1856-61.40. Yohannes, et al. Age & Ageing 1998;27:523–5.41. Garrod R, et al. Respir Med 2002;96:725–30.42. Boe J, et al. Eur Respir J 2001;18:228–42.43. NICE. Management of chronic obstructive pulmonary diseasein adults in primary and secondary care. CG101. June 2010. 44. Niewoehner DE, et al. N Engl J Med 1999;340:1941–7.45. Anthonisen NR, et al. Ann Intern Med 1987;106:196–204.

Declaration of interestsNone to declare.

Dr Parmar is an ST5 in respiratory medicine, RoyalPreston Hospital, Lancashire, and Dr Raines is consultantin respiratory and general medicine, Whipps CrossUniversity Hospital, London

32 Prescriber 19 March 2013 www.prescriber.co.uk

COPD

For each section, one of the statements is false – which is it?

1a. Asthma may be present if serial peak flow measurementsshow significant (20 per cent) diurnal or day-to-day variability

1b. Airway obstruction is defined as a reduced postbronchodila-tor FEV1/FVC ratio <70 per cent and FEV1 <80 per cent pre-dicted

1c. Disability and quality of life in COPD correlate strongly withFEV1

1d. Measurement of alpha-1 antitrypsin should be considered inpatients who are young, have a strong family history or littlesmoking history

2a. Patients with severe COPD have little to gain from stoppingsmoking

2b. All patients with COPD should be offered pneumococcal andannual influenza vaccinations

2c. Depression in patients with COPD leads to more hospitaladmissions

2d. Patients with severe COPD may be followed up in the com-munity but they need ready access to secondary-care serv-ices

3a. Beta2-agonists and antimuscarinics may confer a clinical ben-efit without significantly changing FEV1

3b. The duration of a short-acting bronchodilator such as salbu-tamol or ipratropium is two hours

3c. In the UPLIFT trial, tiotropium decreased exacerbations,reduced hospitalisations and improved quality of life

3d. Aclidinium is a twice-daily antimuscarinic bronchodilator

4a. Combining beta2-agonists, antimuscarinic drugs and ICS maygive synergistic benefits in patients with FEV1 less than 50 percent predicted

4b. A nebuliser may be considered if a patient is still breathlessdespite maximal inhaler therapy

4c. Theophylline should only be used after a trial of short-actingand long-acting bronchodilators, or in patients who areunable to use inhaled therapy

4d. Indacaterol is a long-acting bronchodilator licensed asmonotherapy for maintenance treatment of mild COPD

5a. Pulmonary rehabilitation should not be offered to patientswho have had a recent hospital admission for exacerbation

5b. LTOT can increase survival when used for more than 15 hoursper day

5c. Short-burst oxygen therapy has very little proven benefit5d. Drugs that may be used to alleviate breathlessness as part of

palliative care include opioids, benzodiazepines and tricyclicantidepressants

6a. Breathing retraining exercises can decrease symptoms andexacerbation rates

6b. Inhalers should not be used for bronchodilatation in acuteexacerbations

6c. Disability level at the end of inpatient stay is a predictor ofrecurrent hospital admission for COPD

6d. Lung volume-reduction surgery can be considered inpatients with predominant upper lobe emphysema whohave an FEV1 >20 per cent predicted and are still sympto-matic and breathless despite maximal medical therapy

CPD: Management of COPDAnswer these questions online at Prescriber.co.uk and receive acertificate of completion for your CPD portfolio. Utilise theLearning into Practice form to record how your learning has contributed to your professional development.

ResourcesGroups and organisationsBritish Lung Foundation. Tel: 020 7688 5555; helpline:03000 030555 (Mon–Fri 10am–6pm); website:www.blf.org.uk.

British Thoracic Society. Tel: 020 7831 8778; e-mail:bts@brit-thoracic.org.uk; website: www.brit-thoracic.org.uk.

Chest, Heart & Stroke Scotland. Tel: 0131 225 6963;helpline: 0845 077 6000 (Mon–Fri 9.30–4pm); e-mail:admin@chss.org.uk; website: www.chss.org.uk.

GuidelinesChronic obstructive pulmonary disease – manage-ment. NHS Clinical Knowledge Summaries.www.cks.nhs.uk/chronic_obstructive_pulmonary_disease.

Management of chronic obstructive pulmonary disease inadults in primary and secondary care. NICE. CG101. June2010.

Roflumilast for the management of severe chronic obstructivepulmonary disease. NICE. TA244. January 2012.