Respiratory disorders : Obstructive Lung Diseases : COPD
Introduction
COPD is a heterogeneous condition embracing several overlapping pathological processes including chronic bronchitis, chronic bronchilolitis (small airway disease) and emphysema.
COPD is presence of airway obstruction unlike Asthma, which does not change markedly over several months and, is not fully reversible.
Many patients also exhibit a systemic component characterised by impaired nutrition, weight loss and skeletal muscle dysfunction.
Following the marked increase in tobacco consumption in developing countries COPD is gaining global importance; if current trends continue, it will become the fifth leading cause of lost disability-adjusted life years and the third most important cause of death world-wide by 2020.
Risk factors for the development of COPD
Exposures
Tobacco smoke-accounts for 95% of cases in UK
Biomass solid fuel fires
Occupation-coal miners and those who work with cadmium
Outdoor and indoor air pollution
Low socioeconomic status
Low birth weight-may reduce maximally attained lung function in young adult life
Lung growth-insults including childhood infections or maternal smoking may affect growth of lung during childhood, resulting in a lower maximally attained lung function in adult life
Infections-recurrent infection may accelerate decline in FEV1. Persistence of adenovirus in lung tissue may alter local inflammatory response predisposing to lung damage. HIV infection associated with emphysema
Cannabis smoking (controversial)
Host factors
Genetic factors-α1-antiproteinase deficiency
Airway hyper-reactivity
Pathophysiology
An enlargement of mucus-secteting glands and an increased number of goblet cells in the larger airways.
Loss of elastic tissues surrounding the smaller airways, accompanied by inflammation and fibrosis in the airway wall and mucus accumulation within the airway lumen, results in airflow limitation, further increased by enhanced cholinergic tone.
Premature airway closure leads to gas trapping and hyperinflation.
Shortening of expiration during exercise.
Increased V/Q mismatch increase the dead space volume and limits ventilation.
Increased work of breathing due to flattening of the diaphragmatic muscles and an increasingly horizontal alignment of the intercostal muscles.
In the alveolar capillary units the unopposed action of proteases and oxidants results in destruction of the alveoli and the appearance of emphysema.
This result in impaired gas exchange and respiratory failure.
The pathology of emphysema. A. Normal lung. B. Emphysematous lung showing gross loss of the normal surface area available for gas exchange.
Clinical features
Symptoms
Age >40 yrs, h/o persistent cough and sputum production and/or breathlessness.
Chronic severe asthma may be difficult to distinguish from COPD.
Breathlessness: The level should be quantified for future reference; scales such as the modified MRC dyspnoea scale may be of assistance.
Modified MRC dyspnea scale
Signs
Central cyanosis
Finger clubbing is not consistent with COPD
Use of accessory muscle for breathing, barrel shaped chest (hyperinflated), pursed lip breathing, intercostal indrawing during inspiration.
Palpation- Cardiac apex not palpable.
Percussion – Hyperresonant, Loss of cardiac dullness on percussion.
Auscultation- decreased breath sound with prolonged expiration and wheeze. Heart sound loudest in the epigastrium.
Raised JVP and peripheral edema (if Cor Pulmonale).
Investigations
Lung function tests : The diagnosis of COPD requires objective demonstration of airflow obstruction by spirometry- postbronchodilator FEV1 <80% and FEV1/FVC <70%.
Chest X-ray: The classic features are the presence of bullae, severe overinflation of the lungs with low, flattened diaphragms, and a large retrosternal air space on the lateral film. There may also be a deficiency of blood vessels in the periphery of the lung fields compared with relatively easily visible proximal vessels.
Haemoglobin level and PCV can be elevated as a result of persistent hypoxaemia (secondary polycythaemia)
Blood gases are often normal. In the advanced case there is evidence of hypoxaemia and hypercapnia.
Sputum examination is unnecessary in the ordinary case as Strep. pneumoniae or H. influenzae are the only common organisms to produce acute exacerbations.
Electrocardiogram. In advanced cor pulmonale the P wave is taller (P pulmonale) and there may be right bundle branch block (RSR' complex) and the changes of right ventricular hypertrophy.
α1-Antitrypsin levels. The normal range is 2-4 g/L.
Assessment Of Severity Of Airflow Obstruction According To FEV1 As A Percentage Of Predicted Value
Management
Smoking cessation
Bronchodilators
Corticosteroids- they are currently recommended in patients with severe disease (FEV1 < 50%) who report two or more exacerbations requiring antibiotics or oral steroids per year.
Regular use is associated with a small improvement in FEV1, but there is no impact on the accelerated decline in lung function.
Pulmonary rehabilitation- Exercise should be encouraged at all stages and patients reassured that breathlessness, whilst distressing, is not dangerous.
Oxygen therapy- Long-term domiciliary oxygen therapy (LTOT) has been shown to improve survival, prevent progression of pulmonary hypertension, decrease the incidence of secondary polycythaemia, and improve neuropsychological health.
Given via nasal prongs and patients should be instructed to use oxygen for a minimum of 15 hours/day; greater benefits are seen in patients who receive > 20 hours/day.
The aim of therapy is to increase the PaO2 to at least 8 kPa (60 mmHg) or SaO2 at least 90%.
Acute exacerbation of COPD
Characterised by an increase in symptoms like increased cough and sputum production, severe dyspnoea and deterioration in lung function and health status.
May be accompanied by the development of respiratory failure and/or fluid retention and represent an important cause of death.
Presence of cyanosis, peripheral edema or an alteration in consciousness should prompt referral to hospital.
Management
Oxygen therapy- controlled oxygen
Bronchodilators- Nebulised short acting beta 2 agonist + anticholinergic (ipratropium bromide)
Corticosteriod- oral prednisolone reduce the symptoms and improve lung function (30mg for 10 days).
Antibiotic therapy- recommended for patients reporting an increase in sputum purulence, volume and breathlessness (Aminopenicillins or a macrolide).
Prognosis
Inversely related to age and directly related to post-bronchodilator FEV1.
Poor prognostic indicators includes weight loss and pulmonary hypertension.
A recent study has suggested that a composite score comprising the body mass index (B), the degree of airflow obstruction (O), a measurement of dyspnoea (D) and exercise capacity (E) may assist in predicting death from respiratory and other causes.
