Management of COPD-related breathlessness and coughing

Dr John L Faul, Consultant Respiratory Physician And Senior Lecturer In Medicine (Ucd), Asthma Research Centre, Bcf Diagnostics, Connolly Hospital Blanchardstown, Dublin 15 | 18 Jul 2013 | 0 Comment(s)

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The following case report highlights the care of a 75-year-old man with chronic cough and breathlessness who failed anti-asthma therapy and was subsequently diagnosed with COPD

Case report


A 75-year-old man came to the hospital because of severe shortness of breath and a daily productive cough. The cough had been present for at least 15 years. Although he had first developed a winter cough, in the prior five years the cough has extended throughout the year. During winter the colour of his sputum changed from white to yellow and then green. During the past year he had taken three courses of antibiotics. He generally coughed white sputum on a daily basis, and the cough was worse in the morning. His shortness of breath has been progressively worsening over 10 years. He reported that he could not climb a flight of stairs and had great difficulty walking while carrying shopping bags. Daily activities such as dressing himself and eating caused shortness of breath. His Medical Research Council (MRC) breathlessness scale was Grade 5.
He had a history of hypertension, hypercholesterolemia, inguinal hernia repair, and a prior deep venous thrombosis, but he did not have childhood asthma. There was no family history of asthma. He had started smoking at age 16 and smoked 20 cigarettes a day for 40 years. He underwent coronary artery bypass grafting 10 years prior. During the past year he had taken eight inhalations each day of both salbutamol and beclomethasone (by metered dose inhaler). He also took atorvastatin, ramipril, and aspirin. He commonly buys a ‘cough bottle’ in his local shop. He reported no allergies. He did not drink alcohol. One year prior he had stopped his ramipril for a period of three months, but this had no effect on the severity of his cough symptoms.
On physical examination his pulse was 92 BPM, his respirations were 22 per minute, his blood pressure was 155/85mmHg, his temperature was 37oC, his oxygen saturation 89% on room air and he appeared pale and diaphoretic. There was no finger clubbing and no palpable neck node. His chest was hyper inflated with poor expansion. There was prolongation of expiration and widespread wheeze.
His vital capacity was 83 per cent predicted; his FEV1 was 0.88 litres (28 per cent predicted). His room air arterial blood gas revealed pH = 7.39, PaO2 = 7.4 kPa, PaCO2 = 6.2 kPa, with 89% saturations. His white cell count was 6.5, haemoglobin 11.0g/dL and his platelet count was 325. His alpha – 1 – antitrypsin level was normal. His chest radiograph was reported normal.
Since there was a history of chronic productive cough coupled with extensive smoking history, a diagnosis of COPD was made. There had been no significant response to anti-asthma therapy and a trial of stopping the ACE inhibitor.
The patient was treated with an inhaled long acting anti-cholinergic (glycopyrronium) and a combination inhalation device, which delivered salmeterol and fluticasone propionate. Six weeks later he returned to the clinic and reported that his cough had reduced in severity and that his exercise capacity had improved. The volume of sputum that he coughed each day was less, he could now climb stairs without difficulty and he was able to shop for groceries without help. His MRC breathlessness scale was improved to Grade 4.
On physical examination his pulse was 92BPM, his respirations were 20 per minute, his blood pressure was 150/80 mmHg, his temperature was 37oC, his oxygen saturation was 91% on room air. His chest examination was unchanged with evidence of wheezing, hyperinflation, and poor expansion. His FEV1 had increased to 1.32 litres (42 per cent predicted). He was referred for pulmonary rehabilitation and vaccinations (pneumococcal and influenza vaccines) were recommended.

Discussion
Chronic obstructive pulmonary disease (COPD) differs from asthma in both diagnosis and treatment. In a patient with chronic cough, the diagnosis of asthma should always be considered because asthma is a common condition and cough is an important asthma symptom (cough-variant asthma). One approach to a patient with chronic cough due to asthma would be to initially treat with a combination of inhaled bronchodilators and inhaled corticosteroids as in this case prior to referral to our clinic. The diagnosis of cough variant asthma is generally established when the cough resolves with anti-asthmatic therapy.
Adults with a chronic cough and sputum production occurring on most days for at least three months and for at least two consecutive years should be given a diagnosis of chronic bronchitis when other respiratory or cardiac causes of chronic productive cough are ruled out. In this case there was no past history of asthma. Finger clubbing and coarse crackles might suggest bronchiectasis, which might be confirmed by high resolution CAT scan of the chest.
The evaluation of patients with chronic cough includes a complete history regarding exposure to respiratory irritants including tobacco smoke and hazardous environments in the home and workplace, because these are important predisposing factors to COPD.

Treatment
In patients with chronic cough and chronic exposure to respiratory irritants, avoidance should always be recommended, because it is the most effective means to improve or eliminate the cough. Smoking cessation leads to resolution of cough in 90 per cent of patients, however many patients (as in this case report) will continue to have a daily cough, even many years after quitting. While antibiotics are useful in acute exacerbations of chronic bronchitis, long-term prophylactic therapy with antibiotics has no role in COPD. The benefits of postural drainage and chest percussion have not been proven for patients with stable chronic bronchitis, but there are benefits for some patients. For patients presenting with chronic cough, it is recommended that therapy with ACE inhibitors should be discontinued (regardless of the time delay between the onset of cough and the initiation of ACE inhibitor therapy). A diagnosis of ACE inhibitor cough is generally confirmed when the cough resolves (usually within one to four weeks of drug discontinuation). The cough may take up to three months to resolve.

Table 1: Medical Research Council Breathlessness Scale

Severity
COPD severity is generally assessed using spirometry. The current GOLD guidelines suggest patients with airway obstruction (an FEV1/FVC less than 0.7) and a FEV1 less than 50 per cent predicted are classed as Stage III (severe). Subjects with airway obstruction (an FEV1/FVC less than 0.7) and a FEV1 less than 30 per cent or who require long-term (home) oxygen are Stage IV (very severe). ABG analysis or oxygen saturation testing is useful for patients with a FEV1 less than 1.0 litre. In this case report both the low FEV1 and hypercapnia suggest very severe COPD and a poor prognosis. Some signs of severe underlying COPD have an important influence on in-hospital mortality: The number of prior hospitalisations for COPD; the severity of dyspnoea; and a low body mass index.

Disability
The UK’s MRC breathlessness scale (Table 1) is a useful scale that describes a patient’s level of disability due to the severity of their COPD. The scale is entirely subjective and may change up or down over short time periods. Nevertheless scales of this nature help to put a numeric value on a patient’s exercise capacity in the setting of lung disease and such numbers may prove useful when following groups of patients.

Progression
COPD is a progressive disease. In spite of smoking cessation and effective therapies, most patients continue to cough and complain of shortness of breath. The shortness of breath is due to a combination of factors including airflow limitation, chest hyperinflation, ventilation perfusion inequality, cor pulmonale and associated conditions such as hypertension and coronary arterial disease. Bronchodilator therapy (inhaled is preferred) is fundamental to improving symptoms in COPD. Long-acting inhaled bronchodilators reduce exacerbations and improve symptoms and health status. It seems that combinations of different drug classes improves efficacy and may reduce the side effects compared to increasing the dose of a single bronchodilator. While long-term monotherapy with inhaled corticosteroids is effective in asthma, it is not recommended in COPD.
Treatment regimens need to suit the patient and their severity of symptoms and airflow limitation. The presence of co-morbid illness often influences the choices of treatment. Exercise training and formal pulmonary rehabilitation improve symptoms of dyspnoea and fatigue. A formal programme lasts six weeks but the effects can be long lasting, particularly when exercise training is maintained at home. Even with good therapy, patients with COPD commonly continue to have airway obstruction. In the above case report the patient continued to have severe airway obstruction in spite of therapy. Acute exacerbations commonly cause an acute deterioration in symptoms, lung function, and exercise capacity. Patients should be aware that exacerbations are a characteristic feature of COPD and that a change in bronchodilator therapy, the addition of oxygen therapy and or steroids and antibiotics might provide prompt relief of their symptoms.

References on request

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BE, seen mostly in smokers, is characterized by damage to the alveolar walls, causing the formation of large air spaces. These giant bullae, (can grow up to 20cm in diameter) may be removed surgically to improve exercise capacity in certain patients.
Bullous Emphysema

BE, seen mostly in smokers, is characterized by damage to the alveolar walls, causing the formation of large air spaces. These giant bullae, (can grow up to 20cm in diameter) may be removed surgically to improve exercise capacity in certain patients.

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