The second mechanical cause to which Gairdner refers is found in the shape of the bronchial tubes, which taper in size as they advance toward the air-cells. The mucus contained within a tube may in consequence of this shape act as a ball-valve, being displaced forward in the direction of the greater diameter by the expiratory efforts, thus allowing the exit of air, the entrance of which will be impeded because inspiratory action will at once close the valve. This valve-action of a plug of mucus is well illustrated and proved by the experiments of Mendelssohn and Traube. In one of these a shot was introduced into the left bronchus of a dog, and in two days the left lung was found collapsed and the right one in a state of supplementary emphysema. The collapsed lung was afterward distended by inflation. In a like manner pledgets of mucus may establish an air-pump action that will empty the cells to which the obstructed tubes lead and cause them to collapse. It is, moreover, not improbable that a portion of the contained air is absorbed by the blood-vessels, as is maintained by Fuchs.
As a predisposing cause age has a remarkable influence in producing atelectasis, the condition being much more frequent under five or six years of age than after that time. This is explained by two considerations: The first is the greater prevalence of catarrhal affections of the air-passages in young children than in other subjects; the second is the fact that the chest-walls in a child are more pliable and less firm and resistant than those of an adult, so that when the diaphragm descends in inspiration a portion of the chest-wall may sink in, and the lung immediately beneath such portion will not expand to meet the costal wall as it does in older persons. According to Graily Hewitt, the part at which the chest-wall is most depressed is "at the junction of the cartilages with the ribs, and the ribs which more especially exhibit this want of power to resist the atmospheric pressure are those just above and below the nipple, the fourth to the seventh inclusive."1
1 Reynolds's Syst. Med., vol. iii. p. 872.
The principal cause of collapse involving an entire lobe or the whole lung is the presence of liquid in the thorax in the form either of inflammatory serous effusion, empyema, or hydrothorax. The admission of air into the cavity of the chest by perforation of the lung or by a penetrating wound of the thorax may also lead to the same result by allowing atmospheric pressure on the lung. In such cases the lung may again expand on the absorption or withdrawal of the liquid or air, but it sometimes remains permanently compressed and carnified.
SYMPTOMS.—It is probable that atelectasis in very limited degree may exist without being discovered or suspected, the amount of lung involved being insufficient to interfere by its loss of function with respiration or to give rise to appreciable symptoms.
In congenital atelectasis the symptoms are obvious from the moment of birth, and all point to obstructed or imperfect respiration; but they vary in degree. Should expansion of the chest not take place at all, the heart, which at first may be felt feebly beating, will soon stop, and death will occur. In other cases, in which the atelectasis is not absolute, but yet expansion is not accomplished sufficiently for respiration to be kept up, the infant is more or less cyanotic, especially about the lips and face and at the extremities. The movements of the thorax are slight in degree, and the cry is weak and suppressed, and at last inaudible. In such cases death usually occurs in a few hours, but sometimes life is protracted for several days. The symptoms then are like those of acquired atelectasis or collapse of the lung.
In this condition—which, as already stated, is generally the result of bronchitis occurring in debilitated children—the symptoms show malaëration of the blood. Sometimes they are gradually developed, and sometimes they occur quite suddenly, according to the rapidity with which the collapse spreads through the lung and the number of lobules involved in it.
The signs of bronchitis are present before the occurrence of collapse, and are more or less mingled with those pointing to the collapsed state. The hurried respiration so often met with in bronchitis is increased by the collapse of any considerable numbers of lobules in the lung. The evidences of imperfect oxygenation of the blood, which in children are often apparent in bronchitis, are greatly augmented on the occurrence of collapse, the breathing becoming more rapid and oppressed, the working of the alæ nasi increased, and the dusky hue of the surface spreading and becoming deeper. The character of the respiration is modified in a very remarkable way, as pointed out by George A. Rees of London, in consequence of the pliable and yielding condition of the chest-walls in early childhood. When the upper part of the chest is elevated in inspiration and the diaphragm descends, the space thus produced cannot be filled by the lungs in consequence of their partially collapsed state; and for this reason the intercostal spaces and the lower end of the sternum are sunken by the atmospheric pressure at each inspiratory act. This character of breathing may also be observed in older subjects of collapse as regards the depression of the intercostal spaces, though in less degree than in children, in consequence of the greater rigidity of the thorax after childhood.
As collapse of the lung in very limited degree may be unattended with general symptoms, so likewise it may have no positive auscultatory signs. A moderately extensive tract of the lungs must be affected in order to produce these to an appreciable extent. This amount cannot be stated exactly, but, according to Gerhardt, it is from an eighth to a sixth of one lung.2
2 Ziemssen's Cyclop., vol. v. p. 332.