Emphysema is a pathological increase in the size of airspaces distal to the terminal bronchioles, with destruction of the alveolar walls. The term hyperinflation is used to denote non-pathological over-distension.

Etiology

Diseases of the Airways: Chronic bronchitis, prolonged exposure to irritants and dusts (heavy cigarette smoking), and chronic partial bronchial obstruction.

Conditions associated with Alpha-1-Antitypsin Deficiency:

These predispose the destruction of elastic tissue and collagen. Alpha-1-antitrypsin prevents the breakdown of elastic and collagen by proteases which are liberated from leukocytes. Alpha-1-antitrypsin deficiency may be congenital or acquired. Such persons develop emphysema by the third or fourth decade of life.

Occupational causes

Several occupations which require forced expiratory effort as seen in furnace blowers, goldsmiths and use of wind instruments predispose the development of emphysema in susceptible subjects. Exposure to Cadmium leads to the development of emphysema and pulmonary fibrosis.

Pathology

The lungs are in the inflated position occupying the whole of the pleural cavity. Since the elastic tissue is damaged, the lungs lose their elasticity and they fail to collapse when the chest is opened during autopsy. The diaphragm is depressed and respiratory excursions are diminished. The alveoli are over-distended. The septa rupture and neighboring alveoli coalese to form air cysts. The pulmonary vascular bed is progressively diminished and pulmonary arterial hypertension results. Reduction of alveolar surface area leads to impairment of gas exchange. Right ventricular hypertrophy and cor pulmonale may develop. Emphysematous bullae may rupture to produce spontaneous pneumothorax.

Clinical features

The main symptom is exertional dyspnea. As the condition progresses, even ordinary activity like talking, eating or lying flat may cause dyspnea. The chest is distended in the position of full inspiration. Expansion is diminished and the accessory muscles of respiration are active. Expiration becomes an active process due to loss of elasticity of the lung. Infective episodes occur frequently. Physical examination reveals barrel-shaped chest with diminished expansion, hyper-resonance on percussion, obliteration of cardiac and liver dullness and diminished breath sounds with prolonged expiration. Due to increased intrathoracic pressure, especially during expiration, the neck veins become distended during expiration and collapse during inspiration. The apex beat is felt feebly because of interposition of the distended lung. Right ventricular hyper-trophy produces a heaving impulse in the epigastrium and sub-xiphoid region. Evidence of right ventricular failure may be present.

Radiographic features:

The lungs are hyper-translucent and domes of the diaphragm are lowered. Fluroscopy reveals limitation of respiratory excursions. The normal variation of density of the lung fields during the respiratory cycle is also diminished. Tidal volume, vital capacity, FEV1, MVV and PEFR are diminished. Functional residual capacity and residual volume are increased. In the advanced cases, arterial PO2 (PaO2) is diminished and PaCO2 is increased. Respiratory acidosis may develop.

Course and prognosis:

Once established, emphysema is usually irreversible. Respiratoy infections, respiratory failure, and cor pulmonale may develop as complications. Mild cases are compatible with normal span of life, if the condition is diagnosed early and further deterioration prevented.

Management

All factors that lead to deterioration are avoided. Strict avoidance of cigarette or beedi smoking and avoidance of smoke exhaled by other smokers (passive smoking) are most useful in this regard. The avoidance of dust, allergens, and inclement weather help in preventing its deterioration. Respiratory infections are treated with appropriate antibiotics as in the case of chronic bronchitis. Use of bronchodilators and respiratory physiotherapy help in relieving symptoms and improving lung function.

Special forms of emphysema
 

Compensatory emphysema: This is the condition in which the normal lung tissue undergoes hypertrophy to compensate for extensive damage to the other lung or other parts of the same lung. Being a compensatory phenomenon, this is asymptomatic. The respiratory excursion of the normal lung is increased in this case.

Atrophic emphysema: This condition is the result of senile atrophy of inter-alveolar septa. The total lung volume is not increased.

Bullous emphysema: In this condition air spaces exceeding 1cm in diameter develop either congenitally or as a part of acquired generalized emphysema. With passage of time these bullae enlarge and become giant bullous emphysema. They may rupture to produce pneumothorax.

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