- Prevention of COPD - One of the key interventions in the management of COPD in primary care is the prevention of new cases. COPD is primarily caused by smoking and, therefore, effective smoking cessation services and other stop smoking

British Lung Foundation briefing

National Service Framework for COPD – June 200 initiatives are an important element in reducing the burden this disease has on the NHS

- Early and accurate diagnosis - Damage to the lungs from COPD is irreversible, but there is increasing evidence that appropriate intervention can slow the rate of damage. Early diagnosis is therefore vital for timely intervention and optimum management of the condition

- Pulmonary rehabilitation - Pulmonary rehabilitation results in increased exercise capacity and physical endurance, better emotional function, reduced breathlessness, improved self-esteem and increased independence. Furthermore, patients who have completed a course require fewer GP home visits and reduced hospital bed admissions

- Care provided by a multi-disciplinary care team

- in addition to a GP and practice nurse, COPD patients should have access to a range of healthcare professionals including a respiratory consultant and a physiotherapist or occupational therapist. This team of health professionals should work together to ensure the patient receives the optimum care available to them

- Non-invasive ventilation (NIV) - NIV is an emergency treatment that a patient may receive if taken to hospital because of an exacerbation, it should also be available to treat patients in their own homes where appropriate. NIV is a method of ensuring patients get enough oxygen into their blood. It is not the same as oxygen therapy. NIV involves wearing a mask that covers the nose and is connected to a small machine that pushes oxygen through the mask and into the lungs

Early supported discharge from hospital - These schemes help patients leave hospital earlier after an exacerbation by providing comprehensive at home care from community based healthcare professionals. They are supported through the final days of their recovery and given advice and support in preventing future hospitalisations. Patients indicate that they would prefer to recover in the comfort of their own home where this is possible. By providing this primary care support, hospital beds are released earlier, reducing the burden on the secondary care sector

- Palliative care for COPD patients - Palliative care services tend to be focused towards cancer patients. Serious lung diseases, such as COPD, which are equally debilitating are not thought of in this regard, although patients may suffer for up to 10 years in a state of extreme distress

For further information, please contact:

British Lung Foundation Telephone: 020 7688 5555  Email: parliamentary@blf-uk.org

IMPORTANT UPDATES   TO ABOVE FROM THE BLF.

Calling Health and Social Care Professionals, Managers and Commissioners

The British Lung Foundation would like to invite Health and Social Care Professionals, commissioners and managers to join a virtual forum which aims to:

* Explore what is needed from the forthcoming National Service Framework for COPD in England and discuss how the BLF can support you in its implementation

* Share information and good practice in COPD care  

The forum will be an excellent opportunity for you to network with other professionals across England, and to discuss how you can work with the BLF to ensure that COPD services meet the needs of people living in the communities that you serve.

Click here to join free of charge or contact the COPD project team for more information on 020 7688 5589  

From Pulse

COPD screening backed

23 Feb 07 By Eleanor Goodman GP screening of smokers picks up one-fifth with undiagnosed COPDScreening smokers for COPD identifies up to a fifth who have undiagnosed disease, a new primary care study reveals. The research appears to strengthen the case for GP screening using spirometry, with proposals to be submitted for inclusion in the quality and outcomes framework. Of 818 current or former smokers over the age of 40 screened for COPD, 19 per cent were found to have the disease. A substantial proportion of patients had moderate or severe disease, as measured by the GOLD severity criteria. Researchers classified COPD as mild in 57 per cent of cases, moderate in 37 per cent and severe in 6 per cent. The study, published in February's Primary Care Respiratory Journal, examined spirometry screening results taken in practices in the UK and US. Study leader Dr Robert Halbert, assistant professor of community health sciences at University College Los Angeles in the US, said: 'Earlier diagnosis through targeted case-finding will allow early, aggressive smoking cessation efforts. It may lead to a reduction in the burden of COPD symptoms.'Dr Steve Holmes, chair of the General Practice Airways Group and a GP in Somerset, said the group would be submitting proposals for COPD screening to the QOF review. 'The research is very important and highlights clearly that we have a number of undiagnosed cases with COPD we're not managing early on. That fits in with a lot of the epidemiological research showing we have only picked up about a third of people. It builds on NICE guidance that screening people is a good idea. 'But he said GPs would need new resources if they were to take on screening. 'GP practices definitely have the skills and abilities to do this; the problem may be with resources and time, as this process isn't funded.' Dr Mark Levy, editor of the Primary Care Respiratory Journal and a GP in Middlesex, said: 'It's a good piece of research, but are we really underdiagnosing people or are the criteria incorrect? According to the paper it's being undiagnosed, but that's based on the GOLD criteria.' The GOLD guidelines used a fixed FEV1/FVC value of 0.70 to define airway obstruction, but a discussion paper in the same issue of the journal suggested the lower limit of normal would be a better classification.

Need to know - COPD 27 Mar 08Respiratory specialist Professor Wisia Wedzicha answers Dr Steve Brown’s questions on home oxygen, screening and reversibility testing

1. What is the current thinking on screening for COPD in general practice? If we did it, at what age should we start? Take Home Points :

COPD is currently underdiagnosed or diagnosed late, so many patients with mild COPD are missed. A key objective is to diagnose it earlier so we can encourage patients to stop smoking – one of the few interventions that can reduce disease progression. NICE’s 2004 COPD guidelines suggested a diagnosis should be considered in patients over 35 who have any risk factor for COPD, and cigarette smoking is the most important factor1. But we now know that there are other risk factors apart from smoking, including exposure to biomass fuels during cooking, occupational factors such as fumes and coalmining, low birth weight and recurrent infections and reduced lung function in childhood.

2. Should GPs be able to make the diagnosis of COPD just on spirometry findings?   How useful is a chest X-ray?

For the diagnosis of COPD, spirometry is the best way to demonstrate the presence of airflow obstruction. Airflow obstruction is defined as a reduced FEV1:FVC – less than 0.7 after administration of a bronchodilator.

NICE guidelines define COPD as when the FEV1 falls to below 80% predicted, although the WHO GOLD guidelines define mild COPD as an FEV1:FVC ratio less than 0.7 but an FEV1 that is at or above 80%, allowing COPD at an early stage of airflow obstruction to be diagnosed2. So spirometry is also useful to monitor the severity of the condition.
Peak expiratory flow rate may underestimate airflow obstruction in COPD and is not useful for diagnosis. The common symptoms associated with COPD are breathlessness, cough, sputum production and wheeze, but symptoms may appear late in the course of the disease, when lung damage has already occurred.
A chest X-ray is useful to exclude any other pathologies and may show the presence of emphysema, but this ill require confirmation with specialist tests such as CT scanning. We also now recognise that comorbidity – such as cardiovascular disease and diabetes – are important components of COPD and must be evaluated at diagnosis.

3. Do GPs everywhere have to refer for a consultant opinion to decide which COPD patients should have home oxygen? How well has the home oxygen service bedded in?

Home oxygen therapy usually refers to the provision of long-term oxygen therapy (LTOT) at 15 hours per day for patients with evidence of arterial hypoxaemia – that is P_aO2 less than 7.3kPa or between 7.3kPa and 8kPa in the presence of nocturnal hypoxia, pulmonary hypertension or secondary polycythaemia3. So all patients who are potential candidates for LTOT must have a clear diagnosis with arterial blood gas measurements performed.

Oximetry is useful as screening for hypoxaemia, but not accurate enough for LTOT prescription and does not measure arterial carbon dioxide. At present, arterial blood gases can be only performed in respiratory specialist centres or lung function units. It is also important that patients have been optimally treated and any complications of hypoxaemia recognised and managed. So it is to be recommended that at the start of LTOT, all potential patients are reviewed in a respiratory specialist clinic, usually run by a consultant. Some of these patients will also need ambulatory oxygen and this will require further assessment of disability and usage usually by a respiratory nurse or physiotherapist. The evidence for short-burst oxygen therapy (SBOT) is weak, so any patient with progressive breathlessness not responding to therapy should  be referred for a consultant opinion prior to prescription of SBOT.

The new Home Oxygen Service for England and Wales was introduced in February 2006 and some early difficulties were experienced, especially as it was difficult to ascertain exactly who required oxygen provision for SBOT and some patients had bought ambulatory oxygen or had it provided by charities. But the service is running much more smoothly now, helped by increased awareness of the importance of appropriate home oxygen therapy.

4. I have heard that inhaled steroids are not that useful if there is no evidence of reversibility. What’s your view?

We now know that bronchodilator reversibility testing in COPD is too variable to be useful diagnostically and the same reversibility test performed on another occasion gives a different result. We also now know from the ISOLDE study of long-term inhaled steroids in COPD that reversibility did not predict the long-term response to the inhaled steroids4. In addition, a short course of oral steroids also did not predict the response to long-term steroid therapy.

5. When treating acute exacerbations, what dose of oral steroids is best and should the dose reduction be tapered? COPD exacerbations vary in severity and oral steroids will be indicated when they significantly affect the patient’s daily activities. Exacerbations will be more severe in patients with more advanced COPD and these are the patients most likely to need oral steroids. The evidence suggests that the main action of steroids is in the first few days of an exacerbation, and therefore, to minimise side-effects, I use prednisolone 30mg daily for seven to 10 days, without then tapering the dose. Milder exacerbations may just require an increase in inhaled steroid dose.

6. Is there any good evidence that flu or pneumococcal vaccine prevents admissions?

There is good evidence from studies in elderly populations and some from COPD patients that flu vaccination is effective and that it also prevents hospital admission and reduces mortality. But flu vaccination will obviously not protect against other viral triggers of COPD exacerbations such as rhinovirus and respiratory syncytial virus that are also more common in winter.But the evidence for the effectiveness of pneumococcal vaccine is less well documented, though again data from studies in the elderly suggest that hospital admission may be reduced. Few studies have been performed in COPD patients, but there is some evidence that patients with more severe COPD obtain benefit from pneumococcal vaccination.

7. What is the role of respiratory rehabilitation, and what’s your view on community versus hospital provision?

The goal of respiratory – or pulmonary – rehabilitation is to optimise the patient’s physical and social functioning. This is achieved through a multidisciplinary programme, consisting of courses of exercise training and education.The exercise programme needs to be given at least twice a week for a minimum of six weeks, and then patients need to maintain their daily activity. There is strong evidence that pulmonary rehabilitation programmes improve activity, quality of life and reduce the length of hospital stays.Pulmonary rehabilitation programmes can be done in the community and are usually led by physiotherapists or nurses, but the team needs to be multidisciplinary. Patients with severe disease will need supervised programmes with gradual increases in activity, whereas patients with milder disease can follow their exercise programme after initial instruction, either from a healthcare professional or fitness trainer familiar with the needs of patients with respiratory disability.

8. How reliable an indicator of bacterial infection is sputum colour?

It’s broadly correct that patients with purulent sputum – either when stable or at exacerbation – are more likely to have bacterial infection, commonly Haemophilus influenzae or Streptococcus pneumoniae. So if an exacerbation is accompanied by clear sputum, antibiotics are not necessary but they are recommended for exacerbations with increase in sputum production and/or purulent sputum.

9. How rare is alpha-1 antitrypsin deficiency and what tips can help GPs recognise it?

Alpha-1 antitrypsin deficiency is an uncommon cause of COPD – accounting for only about 2% of cases – but it’s important to be aware of the condition as early intervention with smoking cessation can reduce disease progression. COPD in patients with alpha-1 antitrypsin deficiency has a more aggressive natural history and patients may show a fast decline in lung function. Some non-smokers with alpha-1 antitrypsin deficiency may also develop COPD, so seeing COPD in a non-smoker is a clue to the presence of the condition. Alpha-1 antitrypsin deficiency is genetic and other members of the family may be affected and need to be screened. It also causes early onset of COPD and tends to be associated with basal emphysema.

10. What proportion of COPD patients will need to remain on a low maintenance dose of steroids?

After an exacerbation, most patients recover their lung function to their usual stable state within 14 days. However, some patients can develop more prolonged symptoms and even another or recurrent exacerbation. In this situation, treat first with another course of oral steroids with or without antibiotics as indicated. It is also important to optimise the patient’s usual therapy, which if the patient has more severe disease will consist of combination therapy of long-acting bronchodilators (anti-cholinergics and ß-agonists) and higher dose inhaled steroids. Any other underlying condition such as bronchiectasis needs to be recognised. Most patients will recover at this stage but a very small proportion may be unable to manage without the steroid therapy and will need some low-dose maintenance therapy.

11. Is it worth advising patients with COPD to stop smoking once there is established disease?

Yes. As discussed above, smoking cessation is one of the few interventions that reduces disease progression in COPD. In addition to the effects on reducing FEV1 decline, there is evidence that some therapies such as inhaled steroids may not be so effective in patients who are cigarette smokers. Smoking is also the most important risk factor for lung cancer, and COPD itself is a risk for lung cancer – so this is another important reason why patients should be encouraged to stop smoking. Smoking is also associated with cardiovascular co-morbidity, which is common in COPD. We now know that smokers with COPD are more likely to have airway bacteria in the stable state (colonisation) and this may also enhance disease progression. It is also important that patients prescribe home oxygen therapy do not smoke for safety reasons. Thus there are a number of important reasons that we must strive to stop patients smoking at all stages of COPD.

Professor Wisia Wedzicha is professor of respiratory medicine at the Royal Free and University College Medical School, London

Competing interests: Professor Wedzicha has received funding for research and honoraria for lectures and/or advisory boards from GlaxoSmithKline, Astra Zeneca and Boehringer Ingelheim What I Will Do Now. Dr Brown reflects on the answers to his questions

• I will do more lung function tests on smokers to help with smoking cessation, and explain early if their lung function tests are suboptimal
• I will prescribe up to 10 days of oral steroids for acute exacerbations
• I will not attach too much significance to reversibility testing results
• I will refer more patients for pulmonary rehabilitation
• I will encourage COPD patients to have the flu vaccine and be less concerned if they refuse the pneumococcal vaccine
• I will make short burst oxygen therapy less of a priority

Dr Steve Brown is a GP in Beaconsfield, Buckinghamshirel

Readers' comments.  Ava Aveeno | 25 Mar 08

Alpha-1 Antitrypsin Deficiency is not COPD! The disease is actually a liver deficiency but many GPs will not correctly diagnose the genetic disease. The right name for the genetic condition is Alpha-1 Antitrypsin liver Deficiency. Without knowing the correct name GPs can never treat the genetic condition appropriately for the patients. Alpha-1 antitrypsin (AAT) is a protein (also called “alpha-1 proteinase inhibitor�) produced by the liver to protect the human body from damage caused by the enzyme neutrophil elastase. This enzyme is released by white blood cells during times of inflammation and infection and is necessary in digesting damaged cells and bacteria. When AAT is not available to neutralize this enzyme, healthy body tissues can be damaged such as lungs, liver and skin.
Because AAT is made in the liver there can be a strain on the liver. Sometimes individuals develop liver disease either shortly after birth or occasionally later in life. AAT Deficiency, also referred to as Alpha-1, is an inherited disorder, which results in low or no levels of AAT in the blood.
While the enzyme neutrophil elastase performs valuable and healthy functions like digesting damaged cells and bacteria, removing pollutants and fighting infections, the activities of these substances must be controlled or they can attack normal tissues. Most people have 7 to 10 times more AAT than the person with the alpha-1 deficiency.

           ALPHA-1 ANTITRYPSIN LIVER DEFICIENCY IS NOT COPD!!!

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