Acute bronchitis in previously healthy subjects is often viral. Bacterial infection with organisms such as Strep. pneumoniae and H. influenzae is a common sequel to viral infections, and is more likely to occur in individuals who are cigarette smokers and in those with chronic bronchitis and emphysema.
The illness begins with an irritating, unproductive cough, together with discomfort behind the sternum. This may be associated with tightness in the chest, wheezing and shortness of breath. The cough becomes productive, the sputum being yellow or green. There is a mild fever and a neutrophil leucocytosis; wheeze with occasional crackles can be heard on auscultation. In otherwise healthy adults the disease improves spontaneously in 4-8 days without the patient becoming seriously ill. Treatment with antibiotics may be given, e.g.
amoxycillin 250 mg three times daily, though it is not known whether this hastens recovery in otherwise healthy individuals.
Chronic bronchitis and emphysema
Chronic bronchitis is defined on the basis of the history as:
• Cough productive of sputum on most days for at least 3 months of the year for more than 1 year Emphysema, on the other hand, is defined pathologically as:
• Dilatation and destruction of the lung tissue distal to the terminal bronchioles
Clinical observations led to the suggestion that there were two distinct types of patient:
THE TYPE A FIGHTER is pink and puffing in that, although very breathless, arterial tensions of oxygen and carbon dioxide are relatively normal and there is no cor pulmonale. These individuals were thought to be suffering predominantly from emphysema with little bronchitis.
THE TYPE B NON-FIGHTER, on the other hand, is blue and bloated, he does not appear to be breathless, but has marked arterial hypoxaemia, carbon dioxide retention, secondary polycythaemia and cor pulmonale. These patients were thought to be suffering predominantly from chronic bronchitis. Although this is an attractive concept and has some clinical usefulness, it is not supported by post-mortem studies that have shown no difference in the degree of mucous gland hyperplasia (i.e. bronchitis) or in the amount ofemphysema in patients with type A compared with type B disease.
Autopsy studies have also shown that substantial numbers of centri-acinar emphysematous spaces are found in the lungs of 50% of British smokers over the age of 60 years and are unrelated to the diagnosis of significant respiratory disease before death.
Alternative terms such as chronic obstructive pulmonary disease (COP D), chronic obstructive lung disease (COLD) or chronic obstructive airways disease (COAD) are unhelpful and should be replaced by the term ‘chronic bronchitis and emphysema’, as both these conditions coexist to a greater or lesser degree in each patient. As the common tests for ‘airway obstruction’, the FEV! and PEFR, actually measure airflow limitation (caused by both loss of elastic recoil and/or narrowing of airways), the term ‘chronic airflow limitation’ is the preferred terminology to describe the functional and physiological problem in chronic bronchitis and emphysema.
EPIDEMIOLOGY AND AETIOLOGY
Chronic bronchitis and emphysema have a prevalence, diagnosed on history, of 17% in men and 8% in women in the age group 40-64 years. In the USA similar prevalence figures have been obtained and many developing countries are showing an increased prevalence. There is no doubt that cigarette smoking is a major factor in the development of chronic bronchitis and emphysema. Not only are these diseases virtually confined to cigarette smokers, they are also related to the number of cigarettes smoked per day. The risk of death from chronic bronchitis and emphysema in patients smoking 30 cigarettes daily is 20 times that of a non-smoker. The bronchitis mortality amongst male doctors in relation to the number of cigarettes smoked.
Climate and air pollution are ofless importance; nevertheless, there is a great increase in mortality from chronic bronchitis and emphysema during periods of heavy atmospheric pollution. The effect of urbanization, social class and occupation may also playa part in aetiology, but these effects are difficult to separate from that of smoking. The socio-economic burden of chronic bronchitis and emphysema is considerable. In the UK chronic bronchitis and emphysema cause approximately 18 million lost working days for men and 2.1 million lost working days for women per year, accounting for some 7% of all days of sickness absence from work. Nevertheless, the number of patients discharged from hospitals in the UK with this disease has been steadily falling; the death rate has also fallen in the last 20 years from 200 to 70 per 100000.
The most consistent pathological finding in chronic bronchitis is hypertrophy of the mucus-secreting glands of the bronchial tree. The hypertrophy of these mucous glands is evenly distributed throughout the lung, and is mainly seen in the larger bronchi. In addition, the number of the mucus-secreting goblet cells increases. This leads to increased mucus production and the regular expectoration of sputum.
In more advanced cases, the bronchi themselves are obviously inflamed and pus is seen in the lumen. Microscopically there is infiltration of the walls of the bronchi and bronchioles with acute and chronic inflammatory cells. The epithelial layer may become ulcerated and, when the ulcers heal, squamous epithelium may replace the columnar cells. The inflammation leads to widespread narrowing in the peripheral airways. The small airways are particularly affected early in the disease, initially without the development of any significant breathlessness. This initial inflammation of the small airways is reversible and 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 physiological consequences of these changes is the development of airflow limitation. If the airway narrowing is combined with emphysema (causing loss of the elastic recoil of the lung) the resulting airflow limitation is even more severe.