the stomach should not bear the digitalis, as is sometimes the case, or if it fail to act or lose its power, the fluid extract of convallaria, recently introduced as synergistic with foxglove, may be employed as a substitute for it.

Under similar circumstances, if the patient's strength will admit of it, great benefit will sometimes result from a mercurial purge, by which passive congestion of the portal system may be relieved and the upward pressure of an engorged liver in some degree lessened.

4. Atrophic Lobar Emphysema.

This disease differs from the hypertrophic form of emphysema in the circumstance that the bulk of the affected lungs has undergone diminution from waste or atrophy of their tissue. Absolutely, the lungs may contain no more air than they should in health-they may even contain less-but, relatively, there is an increased amount of air in them in consequence of the diminished amount of the lung-tissue. Such relative increase of air in a given area of the lung may be very considerable from the atrophy and destruction of the cellwalls, the alveoli coalescing so as to form cavities, while the individual aircells are not dilated. The entire lung, however, is shrunken, the chest-wall correspondingly depressed and contracted, and the thoracic muscles atrophied. The function of the affected lungs is impaired in consequence of their loss of size and the diminution of the respiratory movements. This is of course especially noticeable when exertion is made, while under other circumstances there may be little or no embarrassment of breathing unless the disease is far advanced and has involved a large amount of both lungs. But, in general, this form of disease causes less distress and is a less formidable affection than hypertrophic emphysema. In some cases a mingling of the two forms is found, as when a person the subject of general atrophic emphysema has a local vesicular dilatation developed at the top and margins of the lungs.

The shrunken state of the lungs in atrophic emphysema prevents the heart from being overlapped, so that the area of cardiac dulness is not lessened, as it is in the hypertrophic form; and as the general waste of the system is attended with a diminution of the amount of blood, dilatation of the right ventricle, and consequent dropsy, are not apt to occur, as they are in hypertrophic emphysema.

ETIOLOGY.-Atrophic emphysema is always due to constitutional causes. It is found chiefly in old persons or in those in whom impaired nutrition has produced the degenerative changes of old age. Hence it is described by some writers as senile emphysema or senile atrophy of the lungs.

SYMPTOMS. Of the general symptoms of atrophic emphysema, apart from those which belong also to the hypertrophic form, the most marked are-first, the lessened size of the thorax; and, second, the character of the dyspnoea, which is not urgent, and is not apt to occur except on making exertion. The blood is lessened in amount from the general impairment of nutrition, and is therefore adapted, so to speak, in quantity to the diminished aerating space. Percussion in general gives exaggerated resonance, from the relative increase of air in the lung and the thinness of the thoracic wall, which thus vibrates more perfectly. In some cases, however, from loss of elasticity in the cartilages of the ribs, the resonance is even diminished. On auscultation there are found somewhat prolonged expiration and, in general, feeble inspiratory murmursigns which belong also, but in greater degree, to true hypertrophic emphysema, from which, however, the atrophic form is to be distinguished by the contraction of the chest that is seen throughout its entire contour.

In some cases of hypertrophic emphysema there may be, it is true, an appearance of partial contraction of the chest-wall, since where the emphy

sema has produced a marked bulging of the upper portion of the thorax the part below may seem by contrast to be contracted. But in the atrophic form of the disease no distension is seen at any part of the chest-wall, the whole surface being more or less sunken and contracted. Even in hypertrophic emphysema with distension of the thorax, when the disease has lasted a long time there may be some degree of wasting of the lung-tissue; but this condition does not constitute true atrophic emphysema, which is such from the beginning without any preceding stage of hypertrophy.

DIAGNOSIS.-The diagnosis of atrophic emphysema is to be made by the physical signs studied in connection with the conformation of the chest. PROGNOSIS. The prognosis of this affection is hopeless as regards a cure, since the organic change is due to the degeneration of age; yet the disease may continue for years without materially or at all affecting the duration of life.

TREATMENT.—The atrophied lungs can never be restored to their integrity; treatment is therefore limited to the use of tonics and nutriment in order to hold in check the process of waste; and to the relief of bronchial catarrh, which is apt to be attended with profuse purulent secretion. The agents best suited to these two purposes have already been considered.

II. INTERLOBULAR OR EXTRA-VESICULAR EMPHYSEMA. INTERLOBULAR or extra-vesicular emphysema is, as has been previously stated, an affection differing anatomically and pathologically from the form of disease already described. In the vesicular form air is present where it normally belongs, but in undue amount; in the interlobular form it is present where it ought not to be-that is, in the meshes of the connective tissue between the lobules, beneath the pleura, and around the bronchial tubes and pulmonary vessels. These situations may be reached by the air through a rupture of the vesicles, and thus in some cases vesicular may be associated with interlobular emphysema, the rupture having occurred from violent cough; or the emphysematous infiltration may be gaseous, as the result of gangrene occurring during life or of decomposition after death.

DIAGNOSIS. The presence of air in the connective tissue of the lungs cannot be determined by any signs or symptoms; if, however, it should be discovered in the subcutaneous tissue of the neck, face, or chest, giving rise to puffiness and crackling of the integument, its presence in the areolar tissue of the lungs may be suspected, especially if there be coexisting vesicular emphysema, the air having passed into the mediastinum and thence into the tissue beneath the skin.

The existence of interlobular emphysema is not, in general, of serious sig nificance, as the air commonly disappears from the subcutaneous tissue in a few days; whence it may be inferred that it likewise disappears from the connective tissue of the lung, the opening which had admitted it there having become closed. If present in large amount in the lung-substance, it may, however, increase the difficult breathing of an emphysematous subject by compressing a number of the air-vesicles. Or, again, if the interstitial emphysema be subpleural, the bulla may burst, and the air, escaping into the cavity of the chest, may occasion pneumothorax, or even hydro-pneumothorax, from the resulting inflammation. Such an occurrence is, however, very

uncommon.

Even when the diagnosis of interlobular emphysema is established, no treatment is needed or practicable.

COLLAPSE OF THE LUNG (ATELECTASIS).

BY SAMUEL C. CHEW, M. D.

DEFINITION. The term atelectasis is derived from areas, incomplete, and Extats, expansion, and designates a condition in which the lung has failed to expand or has returned in part or throughout its whole extent to the state of non-expansion which is normal in foetal life. In the former case the state is one of congenital atelectasis, and is of course met with only in the new-born; in the latter it is acquired atelectasis, or collapse of the lung, a portion or portions of the organ which have once been expanded having the air excluded from their alveoli, so that these collapse and return to the pre-natal state. To this condition of acquired atelectasis the term apneumatosis, from a negative, and par@ots, filling with air, was applied by Fuchs in 1849, and it has since been adopted by Graily Hewitt.

HISTORY.-For a long time this affection was regarded as a peculiar form of pneumonia, for the reason that at post-mortem examinations patches of collapsed lung-tissue were found which appeared to have undergone solidification. Inasmuch as the condition was most frequently met with in young children, and the supposed solidification was often limited to certain lobules of the lung with intervening healthier spaces, it was described as the lobular pneumonia of children.

The secondary nature of the affection, and the fact that it is very generally preceded by bronchitis, and sometimes by catarrhal pneumonia, were pointed out by Barthez and Rilliet in 1838. Some other important distinctions between this affection and general or lobar pneumonia had been referred to by various writers, but it was not until 1844 that its true nature was satisfactorily elucidated by Bailly and Legendre, who showed, by blowing air into the lungs after death, that the lobules supposed to be hepatized were not really solidified by exudation, but had simply collapsed for want of air.

ETIOLOGY.-The congenital atelectasis of new-born children may be due to original feebleness, to protraction of labor interfering with the blood-supply through the cord, or to obstruction of the air-passages by mucus or other substances. In any case, it is the result of non-expansion of the chest, so that the lungs are not unfolded. This constitutes atelectasis in the strict

sense.

Acquired atelectasis, apneumatosis or collapse of the lung, is an affection most frequent in early infancy, though not limited to that period of life, since bronchitis with defective innervation and great impairment of strength, the essential factors in the production of the disease, may occur at any period of life.

It is probably in almost every case secondary to bronchitis, and due to the occlusion of the smaller bronchi by the presence of mucus allowing the egress, but impeding the ingress, of air, so that the lobules to which they lead are gradually evacuated of air, and thus finally collapse.

Obstruction of a bronchial tube by a foreign body or by the pressure of a

morbid growth within the lung may produce collapse of the lobules to which such tube leads, a smaller or larger part of the lung being involved in proportion to the size of the obstructed bronchus. Such cases are, however, very rare, and they more closely resemble the condition brought about by the pressure of a pleural effusion giving rise to the state of carnification, which is, in effect, an atelectasis involving the greater part or the whole of a lung, and not limited to certain lobules nor taking place lobule by lobule.

The principal cause of lobular collapse is no doubt bronchial catarrh, the action of which is aided by impairment of the general strength and of muscular respiratory power; for the natural elasticity of the lung-tissue would favor the exit and oppose the entrance of air unless it were counterbalanced by muscular action in inspiration. If, then, this inspiratory action is lessened, the requisite amount of air will not enter the alveoli, and that which they already contain will be in part driven out, and perhaps in part absorbed into the blood, by the pressure to which it is subjected. Deficient innervation and lower vital power are thus important elements in determining collapse, which is most common in very young infants or in those who, though somewhat older, have had their nutrition impaired by malhygienic influences or by other diseases.

The mechanism of the production of lobular collapse by the presence of mucus in the bronchial tubes has been well explained by the classical observations and experiments of Gairdner and of Hutchinson. They showed that the physical result of collapse is in part due to the force of expiration being greater than that of inspiration, and in part to the anatomical formation of the bronchial tree. As to the former of these causes, it was shown by the experiments of Hutchinson, already alluded to in the article on EMPHYSEMA, that the force of expiration capable of being applied for the overcoming of obstruction in the bronchial tubes is greater than that of inspiration-in opposition to the teaching of Laennec, who regarded the inspiratory as the greater force. Repeated efforts to clear the bronchial tubes of accumulated secretion by the forced expiration of coughing must therefore remove air from the alveoli in greater amount than it can be returned to them by inspiration, and so they must ultimately be evacuated of their contents and consequently collapse.

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

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

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. 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 ale 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

1 1 Reynolds's Syst. Med., vol. iii. p. 872.