Management of the patient with chronic obstructive airway disease (COPD) in a primary health care context

Chronic obstructive airway disease (COPD) is a progressive lung disease characterised by airflow obstruction that is not fully reversible and is associated with abnormal inflammatory responses of the lung to noxious particles or gases. The global prevalence of COPD is between 7–19%, with variations in different regions of the world, and a predominance in men and people aged over 40 years.1 In Cape Town, South Africa, the prevalence of COPD is 22.2% for men and 16.7% for women.1 Mintz et al. have determined that 21% of patients aged 30 years or more with more than 10 years of smoking history seen in primary care settings are likely to have COPD.2 The Global Burden of Disease Study 2010 reported a prevalence estimate of 8.9%3 and it is expected that it will be the 6th cause of death in the world with an increase in economic and social burden.4 Risk factors


Introduction
Chronic obstructive airway disease (COPD) is a progressive lung disease characterised by airflow obstruction that is not fully reversible and is associated with abnormal inflammatory responses of the lung to noxious particles or gases. The global prevalence of COPD is between 7-19%, with variations in different regions of the world, and a predominance in men and people aged over 40 years. 1 In Cape Town, South Africa, the prevalence of COPD is 22.2% for men and 16.7% for women. 1 Mintz et al. have determined that 21% of patients aged 30 years or more with more than 10 years of smoking history seen in primary care settings are likely to have COPD. 2 The Global Burden of Disease Study 2010 reported a prevalence estimate of 8.9% 3 and it is expected that it will be the 6th cause of death in the world with an increase in economic and social burden. 4

Risk factors
Tobacco use is the most important cause and contributing factor for COPD progression. Occupational exposures from gold mining, coal mining and cotton textile dust, indoor air pollution from burning wood and other biomass fuels, and poorly burning stoves also play a causative role. In addition, infections such as childhood respiratory infections and pulmonary TB, airway hypersensitivity, α1-antitrypsin deficiency, and demographic factors such as age, family history of atopy and low socioeconomic status, all contribute to the development of COPD.

Clinical presentation
The two subtypes of COPD -chronic bronchitis and emphysema -often coexist with their pathologic and clinical features (Table 1). 5 The onset of COPD is insidious, with chronic cough, expectoration, and exertional dyspnoea. A high index of suspicion should be considered in every patient with risk factors of the disease. 4   Table 2).  criteria. (Table 3) Table 3. COPD severity grading -GOLD criteria Very severe COPD (GOLD 4) < 0.7 < 30% of predicted or FEV 1 < 50% with respiratory failure or right-sided heart failure • Chest x-ray is done to exclude other conditions or identify comorbidities.

Radiographic signs of hyperinflation are:
• Increased anteroposterior diameter, increased retrosternal airspace, reduced cardiac silhouette with a vertical heart, flattening of the diaphragms, (better demonstrated on lateral chest x-ray), enlarged central pulmonary arteries and reduced peripheral vascular markings.
• Chest CT scan can demonstrate emphysema, cystic and bullous lesions.
• Echocardiogram is recommended if the physical examination findings are suggestive of cor pulmonale.
• Full blood count may show polycythaemia due to hypoxia or anaemia • Eosinophil count > 100 cells/uL in recurrent exacerbations determines need for inhaled corticosteroid 4 • Blood gases may reveal hypoxia if peripheral oxygen saturation is < 92% or respiratory failure if PCO2 > 45 • Serum α 1 -antitrypsin level is indicated in patients aged ≤ 45 years with minimal or no smoking history, positive family history of COPD and lower lobe emphysema.

Differential diagnosis
The differential diagnosis of a patient with dyspnoea and persistent productive cough includes the following conditions:

• Asthma
Begins in childhood and is usually episodic. There may be personal or family history of allergy, eczema or rhinitis. The episodes are characterised by wheezing and the airway obstruction is reversible with bronchodilators.

• Bronchiectasis
This may be difficult to differentiate from chronic bronchitis. The sputum is copious with occasional haemoptysis. There may be past history of pneumonia, pertussis, tuberculosis and nontuberculous mycobacterium infection. Chest x-ray finding of tram tracking (parallel narrow lines) radiating from the hilum and cystic spaces are suggestive of bronchiectasis. A high-resolution chest CT will show bronchial dilatation and bronchial wall thickening to confirm the diagnosis.

• Pneumonia
Usually presents with fever, chills and pleuritic chest pain. Chest percussion is dull and auscultation may reveal crackles or bronchial breath sounds. The area of infiltration is confirmed by chest x-ray.

• Tuberculosis
Usually manifests with chronic productive cough, fever, night sweats and weight loss. Chest x-ray may reveal infiltrates, cavitation or fibrosis. A positive sputum Acid Fast Bacilli (AFB), GeneXpert or culture confirms the diagnosis.

• Congestive heart failure
Usually presents with orthopnoea and basilar crackles may be heard on auscultation. Brain natriuretic peptide level is elevated, chest x-ray shows cardiomegaly with increased pulmonary vascular congestion, and echocardiogram confirms the diagnosis.

• Lung cancer
Patients with lung cancer may present with cough, haemoptysis, dyspnoea, chest pain, weight loss and night sweats. This needs to be considered as smoking is a risk factor for lung cancer and COPD. The physical examination and chest x-ray or chest CT findings will suggest further diagnostic investigations (bronchoscopy, lung/pleural biopsy, thoracenthesis) towards tissue pathology diagnosis of lung cancer.

Management
The management of COPD is based on the GOLD grade and exacerbation history (Table 4). Tobacco use must be explored and discussed with patients at all visits and if necessary motivational interviewing to stop tobacco use must be initiated as early as possible. 4 There are management interventions that prolong survival 5 ( Table 5). All other management interventions provide symptom relief with no mortality benefit.
The progress of COPD is fraught with gradual decrease in FEV 1 and episodes of acute exacerbations. Acute exacerbation of COPD is defined as sustained worsening of dyspnoea, cough, or sputum production of acute onset leading to increased use of medications. The most common trigger is viral or bacterial upper respiratory infection. Other causes include irritants from air pollution, pulmonary embolism, myocardial infarction, anaemia, and congestive heart failure.
The investigations in the setting of acute exacerbation of COPD include FBC, chest x-ray, ECG and pulse oximetry and/or arterial blood gas. Spirometry is not recommended in acute exacerbation as this may be difficult to perform and may not be accurate.
The management of acute exacerbation of COPD includes the following: • The airway should be secured and ventilation assisted in patients with altered level of consciousness.    • Oxygen is administered to maintain the SaO 2 between 88-92% for CO 2 retainers.
• Systemic corticosteroids: Oral prednisone 40 mg daily, for 5-7 days without tapering. Alternatively, IV methylprednisolone 125 mg 12 hourly could be used but this has increased risk of side effects.
• Antibiotics: These are indicated for exacerbations with increased sputum production plus either increased dyspnoea or increased sputum purulence. The choice of antibiotics is based on patient risk factors and local antibiotic resistance patterns as follows 5

Prognosis
The prognosis of COPD is variable, depending on genetic predisposition, environmental exposures, comorbidities and acute exacerbations. The single best prognostic predictor is the level of dyspnoea. The BODE index is a 10-point measure of four factors (body mass index, obstruction, dyspnoea and exercise capacity) used to predict mortality in COPD ( Table 6). The probability that the patient will die from COPD increases as the BODE index score increases.

Follow-up
Patients with COPD should be followed up regularly to monitor disease progression or development of complications. Stable COPD patients can be followed up at three to six monthly intervals while patients with severe frequent exacerbations or recently discharged from hospitalisation should be followed up at two to four weekly intervals.