COPD

What is meant by COPD, chronic bronchitis and emphysema?
Chronic bronchitis and emphysema are very common lung diseases that cause the sufferer to cough and become short of breath. These diseases usually occur together, are caused by smoking, with chronic bronchitis 7 times more common than emphysema. These diseases are included under the umbrella term, "chronic obstructive pulmonary disease" (COPD) or "chronic obstructive airway disease" (COAD).

Cigarette smoking is the number one cause for COPD, chronic bronchitis and emphysema.

If you stop smoking, you can reduce your chances of developing COPD or stop COPD from getting any worse. Even with severe disease, stopping smoking helps.

The COPDgene study has shown that women have an increased susceptibility compared to similarly aged men to developing early onset severe COPD when both smoke.

What other risk factors apart from smoking lead to COPD?
In rare cases, environmental dusts or patient/host factors can cause COPD.

Patient/host factors include genetic abnormalities, abnormal lung development and accelerated aging. The commonest genetic disorder in Ireland and the world that leads to COPD is alpha 1 antitrypsin deficiency.

Alpha-1 antitrypsin deficiency
This genetic disorder affects more than 250 000 people in Ireland. Approximately 15 000 patients in Ireland have the severe form of the disease. It is the commonest genetic disorder in both Ireland and the world leading to COPD. Alpha 1 antitrypsin is a protein produced by the liver to protect the lungs. This protein is abnormally produced in this disease leading to its accumulation in the liver.

The Alpha One Foundation in Ireland provides free testing for this genetic disorder in conjunction with HSE Ireland. You can access more information using the website www.alpha1.ie

There is also information accessible through the helpline 01 809 3871 or by email [email protected]

All patients with COPD or chronic respiratory symptoms should be tested. Due to its genetic nature, all patients with a positive family history of alpha 1 antitrypsin deficiency should be screened for the disease.

Alpha-1 antitrypsin deficiency is managed through routine COPD management along with management of separate extrapulmonary complications like liver disease when it occurs. Currently alpha 1 augmentation treatment is only available for severe alpha 1 antitrypsin deficiency, mainly the ZZ phenotype.

Clinical Presentation of COPD.
COPD presents with chronic breathlessness, chronic cough or frequent sputum production. Patients usually admit to a history of smoking. COPD requires pulmonary function testing to make the diagnosis. Spirometry is required to show a post bronchodilator FEV1/FVC ratio less than 0.70 which confirms fixed airflow obstruction.

COPD has recently refined their GOLD ABCD criteria to help assessment of COPD.

An exacerbation of COPD is when a patient has acute worsening of their respiratory symptoms that requires additional therapy. Increased breathlessness is a key factor which defines an exacerbation of COPD. Patients may also report increased cough or wheeze associated with increased sputum volume or sputum purulence.

Exacerbations of COPD
Exacerbations are key moments in the course of a patient’s COPD. All therapies are directed at reducing this crisis event. The main risk factor is seasonal spike in respiratory viruses during the winter months in Ireland. Note respiratory virus infections can also then lead to secondary bacterial infections. Pollution, symptomatic variability and comorbidities can also lead to an exacerbation.

It is important to recognize that active smoking perpetuates chronic bronchitis which has the potential to less remission in between COPD exacerbations.

Exacerbations of COPD can last from 1 week to a month. Occasionally up to 1/5 COPD patients have not recovered to their baseline after an exacerbation.

Management of COPD
Smoking cessation is the single most effective and cost-effective treatment for COPD. It is important that patients understand this as approximately 80% of COPD patients relapse after the 1st year of quitting cigarettes.

Inhaler therapies remain the main pharmacologic agent in the COPD armamentarium.

All COPD patients should receive both the annual influenza vaccine and the pneumococcal vaccine PCV13 and PPSV23.

Pulmonary rehabilitation is a highly effective therapy which should be recommended to all patients.

Patients with severe resting chronic hypoxemia will benefit from long term oxygen therapy (LTOT). New evidence now shows that patients with exercise-induced moderate desaturation should have their individual factors considered first before prescribing oxygen therapy.

Pharmacologic options in stable COPD
Symptomatic COPD patients should be first started on either a single or dual long-acting bronchodilator inhaler. Long-acting muscarinic antagonists inhalers(LAMA) are preferred to long-acting beta-agonist inhalers (LABA) for monotherapy.

New evidence now shows that an inhaler with dual bronchodilation (LAMA/LABA) is superior to a LABA inhaler combined with an inhaled corticosteroid (ICS) in reducing exacerbations in COPD.

Despite this treatment can be escalated to triple therapy or combining a LAMA LABA and ICS if exacerbation still occurs frequently despite dual bronchodilation.

Patients with recurrent exacerbations despite maximal inhalers should have prophylactic macrolide therapy. Azithromycin 250mg daily or Azithromycin Monday/Wednesday/Friday has been shown to reduce frequency of exacerbations annually in ex-smokers.

Long-term NIV is not routinely recommended for hypercapnic COPD patients (CO2 retaining patients). If trialled in selected patients to improve symptoms or exercise tolerance, careful surveillance of benefits should be done with short term follow-up of symptoms and arterial blood gases.

Pulmonary rehabilitation in COPD
Pulmonary rehabilitation is multidisciplinary intervention tailored to each COPD patient’s capabilities. It has been shown to improve chronic symptoms, quality of life and activities of daily living.

Unfortunately, pulmonary rehabilitation just as a single short-term intervention does not lead to sustained benefits. Benefits wane with time. It is important to foster home-based exercises in combination with infrequent hospital based sessions to maintain the progress and benefits achieved after pulmonary rehabilitation.

Importance in treating co-morbid diseases in COPD
COPD is frequently associated with extra-pulmonary comorbidities. The leading cause of admissions among patients with COPD apart from exacerbations are due to myocardial infarctions, strokes and cancers. This is likely due to common risk factors smoking and aging which are implicated in all these disease processes. New evidence has shown a 6-fold increase in stroke within 7 weeks of an exacerbation of COPD. Studies have confirmed COPD is linked with atherosclerosis which leads to Increased ischaemic heart disease and myocardial infarctions and angina;

Increased carotid atherosclerosis and strokes

Increased peripheral artery disease

It is crucial than as part of managing COPD, the co-morbid diseases are optimised including optimising patient’s vascular care with good diet and exercise, cholesterol modification and consideration for statin and antiplatelet therapy.

Asthma-COPD overlap syndrome (ACOS)
ACOS has become clinically relevant as inhaled corticosteroid inhalers are falling out of favour.

In patients with evidence of bronchodilator reversibility, atopy, early-onset respiratory symptoms, and eosinophilia the concomitant diagnosis of asthma should be considered. In patients with ACOS, it is imperative that inhaled corticosteroid therapy is maintained.

Future guidelines will likely move toward identifying treatable pathways like Th2 inflammation or eosinophilic inflammation, rather than disease labels as ACOS or COPD.