Chronic obstructive pulmonary disease (COPD)

COPD has become the most popular term to describe patients with chronic bronchitis and emphysema. The distinction between COPD and asthma is blurred as most patients with COPD have some reversible airflow obstruction.

Definitions in COPD:

Chronic bronchitis:

• Cough productive of sputum on most days for at least 3 months of the year for more than 1 year

Emphysema:

• Dilatation and destruction of the lung tissue distal to the terminal bronchioles

Clinical observations in COPD:

It is believed that there are two distinct types of patients, type A and type B:

Type A fighter (pink and puffing):

• The person is very breathless
• Arterial tensions of O₂ and CO₂ are relatively normal
• NO cor pulmonale
• These patients are thought to be suffering, predominantly, from emphysema with little bronchitis

Type B non-fighter (blue and bloated):

• Person does not appear to be breathless
• Marked:
• Arterial hypoxaemia,
• CO₂ retention
• Secondary polycythaemia
• Cor pulmonale

Epidemiology:

• 18% of male and 14% of female smokers
• In the UK, COPD causes approximately 18 million lost working days for men and 2.1 million lost working days for women per year (approximately 7% of all days off sick from work)

Aetiology:

• Smoking is a major factor in the development of COPD
• Is virtually only a disease of smokers
• Climate and air pollution play an important role, with a great increase in mortality from COPD during periods of heavy atmospheric pollution
• Hereditary deficiency of α₁-antitrypsin is responsible for 2% of cases of emphysema

Pathophysiology of chronic bronchitis:

• Hypertrophy of the mucus-secreting glands of the bronchial tree
• The hypertrophy of these mucus glands is evenly distributed throughout the lung and is mainly seen in the larger bronchi
• The number of mucus-secreting goblet cells increases
• This leads to increased mucus production and the regular expectoration of sputum
• The small airways are particularly affected early in the disease, initially without the development of any significant breathlessness. This initial inflammation accounts for the improvement in airway function if smoking is stopped early
• Further progression of the disease leads to progressive squamous cell metaplasia and fibrosis of the bronchial walls
• The consequences of these changes is the development of airflow limitation

Pathophysiology of emphysema:

• Most commonly, distension and damage of lung tissue is concentrated around the respiratory bronchioles, whilst the more distal alveolar ducts and alveoli tend to be well preserved
• Emphysema leads to expiratory airflow limitation and air trapping
• The loss of lung elastic recoil results in an increase in TLC
• The loss of alveoli results in decreased gas transfer

Symptoms of COPD:

• Productive sputum
• Wheeze
• Shortness of breath

Signs of COPD:

In mild disease:

• No signs except wheeze throughout the chest

In severe disease:

• Tachypnoea
• Prolonged expiration
• Use of the accessory muscles
• Intercostal indrawing on inspiration
• Pursing of the lips on expiration
• Poor chest expansion
• Lung hyperinflation

The ‘pink puffer’:

• Always breathless
• Not usually cyanosed

The ‘blue bloater’:

• Oedematous
• Deeply cyanosed
• Hypoventilation
• These patients are likely to have hypercapnia, so the following are present:
• Peripheral vasodilatation
• Bounding pulse
• CO₂ retention tremor

Severe hypercapnia leads to CO₂ narcosis:

• Confusion
• Progressive drowsiness and coma with papilloedema

Complications of COPD:

Respiratory failure:

• Usually defined as one or both of the following:
• P_aO₂ less than 8kPa
• P_aCO₂ of greater than 7kPa

Cor pulmonale:

• Heart disease secondary to disease of the lung
• Pulmonary HT
• Right ventricular hypertrophy
• Right heart failure

Investigations:

Lung function tests:

• Evidence of airflow limitation
• FEV₁ : FRC is reduced
• Low PEFR

CXR:

• Often normal but may show hyperinflation

Hb level and PCV:

• Can be elevated as a result of persistent hypoxaemia (secondary polycythaemia)

Arterial blood gases

Sputum Gram stain and culture

ECG:

• In cor pulmonale, the P wave is taller (P pulmonale)
• May be right bundle branch block (RSR complex)

Echocardiogram

α₁-antitrypsin levels:

• The normal range is 2-4g/L

Treatment:

STOP SMOKING. Even at a late stage of the disease this may slow down the rate of deterioration.

• Bronchodilators (e.g. salbutamol 200μg every 4-6 hours)
• Corticosteroids:
• Initial 2 week trial pf prednisolone 30mg daily
• If lung function improvements, gradually replace with inhaled corticosteroids (e.g. beclomethasone 100-500μg TID)

• Antibiotics:
• Patients should be given a supply of antibiotics to use once their sputum turns yellow or green
• The antibiotics of choice are cefaclor 500mg TID or cefixime 400mg OD
• Diuretics (for all oedematous patients)