COLLAPSE OF THE LUNG (ATELECTASIS).
BY SAMUEL C. CHEW, M.D.
DEFINITION.—The term atelectasis is derived from [Greek: atelês], incomplete, and [Greek: echtasis], 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 [Greek: a] negative, and [Greek: pneumatôsis], 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
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.
Dulness on percussion, varying in degree and extent with the number of affected lobules and their nearness to each other, is a very constant sign of collapse; but it must be kept in mind that if the collapsed lobules are disseminated or central the dulness may be hardly observable. Sometimes there is difficulty in detecting dulness, because from the bilateral character of the bronchitis the collapse of lobules may take place in about equal degree on both sides, so that one side cannot be contrasted with the other. Ordinarily, however, there is a difference in the degree of dulness between the two sides, because the affection is more extensive in one than in the other; and in general the loss of resonance over the collapsed lobules is determinable without comparison of the two sides. Not uncommonly, patches of dulness are found with intervals of comparatively clear resonance.
On auscultation the respiratory sounds are feeble or entirely absent in an area in which a number of adjacent lobules are involved together in collapse.
When a considerable part of a lobe is affected, bronchial breathing may sometimes be heard, but this is in general less marked than the degree of dulness and the amount of condensation would lead the examiner to expect, because the breathing is too feeble to give rise to the vibrations necessary for the production of this sign.
An important indication of lobular collapse is the rapidity with which the signs just described are developed; a part or parts of the lung which had been clear on percussion and normal in respiratory character becoming in a day, or sometimes in a few hours, dull and nearly silent to the ear. This very suddenness with which the physical signs are developed in a case of bronchitis or catarrhal pneumonia in a child points very plainly to the occurrence of collapse of the lung.
PATHOLOGY.—The pathological appearances in collapse of the lung vary according to the extent of tissue involved in the change, and also according to the cause which has induced it. In the disseminated lobular form which is due to bronchitis the collapsed portions are chiefly seen on the surface and at the margins of the lung, and they extend more deeply into the organ as it becomes more involved in the atelectatic condition. On the surface or on a section the collapsed patches are depressed somewhat below the surrounding parts and are of a darker hue, so that they are readily seen as dark-red or purplish spots surrounded by the lighter healthy tissue. The contrast is sometimes enhanced by the fact that the non-collapsed parts are even paler than natural from the vicarious emphysema that has been established in them.
The consistence of the affected part varies in different cases. If the change has occurred without previous congestion, the texture may be somewhat flaccid; but if there has been hyperæmia, the part will be leathery, non-crepitant, and resisting pressure. If no crepitation can be detected the part will sink in water from the complete expulsion of air from the affected lobules. A cut surface is smooth and does not present the granular appearance of a hepatized lung, nor can exudation-matter be pressed or scraped from it.
The collapsed lobules may be made to swell up and resume their normal appearance and rosy color by forcing air with a blowpipe into the bronchus leading to them. This is so generally true, at least, that it has been regarded as a certain test by which to discriminate between atelectasis and pneumonic consolidation when there may be a doubt at a post-mortem examination as to which condition exists. In general, the attempt to inflate will succeed when the air is directed into a collapsed lobule; but the test is of less value than it was once held to be because it has been shown, on the one hand, that lobules which have been collapsed for some time will not always expand under the inflating force, and, on the other, that in recent catarrhal pneumonia the alveoli may for a time still be inflated with air.
Meigs and Pepper, while stating that in general the results of the attempt to produce inflation are altogether different in the two conditions, yet hold, in accordance with Gairdner's teaching, that "partially pneumonic lung may be inflated when the affection is recent and combined, as it frequently is, with bronchitic collapse; while in the latter lesion—i.e. collapse of lobules—in its purest forms complete inflation is often very difficult or impossible after the collapsed state has been of some duration."3
3 Diseases of Children, p. 143, 4th ed.
Nevertheless, the test is of value when applied along with others; for, as stated by J. Lewis Smith, "the inflated pneumonic lung is more solid and resisting when pressed between the thumb and fingers than is the collapsed lung."4
4 Diseases of Children, p. 570, 5th ed.
The chief differences between the two conditions are—1st, the color, which in collapsed lobules is purplish or livid, and in pneumonia reddish-brown; 2d, the microscopic appearance, showing the alveoli filled with cell-proliferation in pneumonia and free from change in collapse; and 3d, the state of the adjacent pleura, which is inflamed and often covered with lymph in pneumonia, while it is entirely healthy in non-complicated collapse.
The bronchial tubes present the appearances met with in bronchitis, being more or less congested, showing a softened state of their lining membrane, and containing liquid mucous secretion and sometimes firmer pledgets which have caused the obstruction.
As regards changes in the heart, extensive atelectasis may prevent closure both of the foramen ovale and of the ductus arteriosus. From the obstruction to the flow of venous blood offered by the collapsed portions of the lungs the right ventricle may become so distended that a portion of its blood may still be forced through the ductus arteriosus, and another portion backward into the auricle and through the foramen ovale, so that both of these channels may be kept pervious.
DIAGNOSIS.—Congenital atelectasis, if complete, cannot be mistaken for any other condition occurring at birth, and is sufficiently denoted by the signs already described.
Imperfect expansion of the lungs continuing for some days after birth might suggest patency of the foramen ovale from the purplish hue of the surface common to both conditions. The expansion of the chest and the resonance that it yields on percussion in the cardiac affection will be sufficient to discriminate them except in those cases in which they exist together.
Acquired atelectasis or collapse of the lung may require to be distinguished from bronchitis, from pleural effusion, and from catarrhal pneumonia.
Even uncomplicated bronchitis is in children sometimes accompanied with so much dyspnoea as to cause apprehension that collapse of lobules has taken place, but the absence of percussion dulness, either diffused or in patches, will exclude the supposition.
From pleural effusion collapse of the lung may be distinguished by the fact that the dulness due to pleurisy is generally on one side only, that it is more intense and diffused than that of collapse, and that its line of demarcation may often be made to shift with the position of the patient.
Catarrhal pneumonia is in general distinguishable from collapse by the history, course, and symptoms of the disease, especially the sudden rise of temperature that belongs to pneumonia; as also by the auscultatory signs. The percussion dulness of pneumonia is more extensive than that of collapse, and is accompanied with bronchial breathing; whereas in collapse the respiratory sounds are feeble and mingled with moist râles.
PROGNOSIS.—In congenital atelectasis, if there be no expansion of the lungs within the first few minutes after birth, the prognosis is generally bad. In some apparently hopeless cases, however, the persistent employment of means tending to arouse the respiratory function, and especially of those acting through a reflex influence, is crowned with success. The prognosis varies according to the amount of unexpanded lung; for even when some respiratory efforts have been made, if the air enter only a limited extent of the lungs, the infant will drag on a feeble existence for perhaps a few days, and then perish from apnoea and exhaustion. When the lungs are once fully inflated the danger from congenital atelectasis is past.
In acquired collapse of the lung the prognosis is dependent both upon the number of lobules involved and upon the amount of strength possessed by the patient. A larger amount of disease may be recovered from if the nutrition and nervous system be not much depressed, while a smaller amount may prove fatal in less favorable conditions of the general system. Much also depends upon the extent and duration of the coexisting bronchitis, and the degree to which it has affected the constitutional powers.
TREATMENT.—In the treatment of congenital atelectasis the main endeavor must be directed to arousing the respiratory function; and this is best accomplished by means acting reflexively through the centres of respiration. Sprinkling the chest and back with cold water, the application of cold water to the spine by a sponge or by affusion, or the alternate use of cold and hot water in the same way, will often induce a deep inspiration by which the lungs will be unfolded and respiration perfectly established. If this be not fully accomplished, it is of the utmost importance that the child should be carefully watched as long as the atelectasis continues in any degree, and that the same means should be again resorted to when the failure of respiration is threatened. The temperature of the surface should be maintained by artificial heat and woollen wrappings, as a depression below the normal standard easily takes place, and serves to lower all the vital processes and increase the difficulty of keeping up respiration.
In acquired atelectasis treatment must to a great degree be directed to the superinducing bronchial catarrh. Counter-irritation of the chest may be practised with Stokes's liniment, which consists of equal parts of oil of turpentine, acetic acid, and camphor liniment, or with mustard poultices prepared with special reference to the sensitiveness of a child's skin by mixing the mustard with a double portion of flour or Indian-corn meal. With the same view, dry cups may sometimes be advantageously used.
Expectorants are serviceable by relieving the bronchitis, the best being the syrup or wine of ipecacuanha in the dose of 5 to 10 drops, or the muriate of ammonia in the dose of 1 to 3 grains in simple syrup or syrup of liquorice, every two or three hours.5 These agents may modify the inflammatory state of the bronchial mucous membrane, and thus prevent the extension of the collapse. If bronchial secretion be profuse, the question of the use of emetics becomes very important. When employed judiciously with reference to the real needs of the case, they may be eminently beneficial, acting partly by removing the accumulation in the bronchi which may have occasioned the collapse and may favor its further extension, and partly perhaps by the deep inspiration which precedes emesis serving to expand the collapsed lobules. It must be remembered, however, that there is always a tendency to failure of the vital powers in acquired atelectasis, and that this may be dangerously increased by emetics of a depressing character. The best for the purpose are alum, sulphate of zinc, and ipecacuanha. The repetition of the emetic must be determined by its effect on the breathing and on the patient's strength.
5 One of the following formula may be used:
| Rx. | Syr. ipecac. | drachm i–ij; |
| Syr. prun. virginian. | drachm vj; | |
| Ammon. muriat. | drachm ss; | |
| Aquæ, | ounce j. M. |
Dose, teaspoonful for a child of three to six months.
Or,
| Rx. | Ammon. muriat. | drachm ss–drachm j; |
| Syr. glycyrrhiz. Aquæ, aa | ounce j. M. |
Dose, as above.
Tonics and supporting measures are always called for in the treatment of atelectasis, in view of the fact that the condition is essentially dependent on failure of constitutional strength. Milk, wine-whey, and animal broths are appropriate articles of food; alcoholic stimulants are generally required; and in emergencies, if sudden increase of prostration occur, the carbonate of ammonia in the dose of 1 or 2 grains may be given.
During the whole course of the malady such tonics as quinia or the compound tincture of cinchona or one of the soluble salts of iron may be administered.
Brown Induration of the Lungs.
DEFINITION.—Increased density of certain portions of the lungs, which are of a reddish color, with brown or yellowish-brown spots scattered throughout the indurated tissue.
SYNONYMS.—Pigment induration; Congestive carnification.
HISTORY.—This affection is a form of passive congestion of the lungs, in regard to which it is somewhat uncertain whether the morbid process is simply one of congestion or whether along with this an inflammatory element is likewise present. It is beyond question, however, that the changed condition of the lung is primarily and chiefly congestive, and that it originates from causes which produce congestion.
ETIOLOGY AND MORBID ANATOMY.—The etiology and morbid anatomy of this affection are so closely related that they are best considered together. The most important fact both in the etiology and pathology of brown induration of the lungs is that it is gradually brought about as the consequence of obstruction to the pulmonary circulation from disease of the mitral valve, either constrictive or regurgitant in character. Interference with the return of the blood to the left side of the heart is in this way produced, with consequent stasis in greater or less degree within the pulmonary capillaries.
The most marked changes observed in lungs which have undergone this form of congestion are that they do not collapse when the chest is opened, and that they are more compact and less elastic and crepitant than healthy lungs. On section they present a reddish color interspersed with spots of yellowish- or reddish-brown, which sometimes are of a very dark hue.
Microscopic examination shows an increased size of the capillaries of the lung, which seem to encroach upon the air-cells and thus lessen their capacity. Whether the walls of the alveoli have themselves undergone thickening is a question about which different opinions have been entertained. Rokitansky states that "when stasis has continued for a longer period the walls of the air-cells and the interstitial tissue become swollen, so that the former may become perfectly impermeable to air;"6 and although, in the passage quoted, he is writing of pulmonary congestion in general, and not of this form in particular, yet, as he is describing a stasis which has continued for some time, the observation would seem applicable to the affection under consideration.
6 Path. Anat., vol. iv. p. 59.
Wilson Fox affirms that he has found alveolar thickening in considerable tracts in this affection, with a distinct increase of fibrous tissue in the walls of the alveoli; but this change, he goes on to say, is not uniformly present, and in some places the alveoli are found filled with epithelial products like those of catarrhal pneumonia.
The true explanation of the condition is probably this: that, beginning as a passive congestion, such as might be expected to result from the mitral disease with which it is almost constantly associated, the affection afterward assumes an inflammatory condition of a low type with epithelial proliferation, and in some cases with thickening of the alveolar walls and the interlobular connective tissue. Passive hyperæmia is, however, always the basis of the disease. The brownish spots visible in a section are caused by the leakage of blood from the congested capillaries into the alveoli or interstitial tissue without the occurrence of any large extravasation. The blood thus exuded undergoes pigmentary change, with the production of hæmatoidin, the shades of color varying accordingly as the exudation has been recent or of longer duration.
The failure of the lungs to collapse is due to the encroachment of the dilated capillaries on the air-cells, and perhaps to the thickening of the cell-walls and the partial occupation of the cells themselves by epithelial products.
SYMPTOMS.—The general symptoms and the physical signs of this affection are of the same character as those that occur in other forms of pulmonary congestion. Dyspnoea is felt, especially on making exertion; and this may be attributable in part to the associated cardiac disease as well as to the condition of the lungs. Loss of resonance on percussion and feebleness of respiratory murmur are observable; and when the condensation is great bronchial breathing may be heard.
DIAGNOSIS.—It is evident that there is nothing in these signs distinctive of this particular form of congestion, which is, in fact, not diagnosticable with absolute certainty during life. The probability of its existence may, however, be inferred if along with the above symptoms and signs a presystolic or regurgitant mitral murmur is heard, showing constriction or incompetency of the mitral valve.
PROGNOSIS.—The prognosis of this affection is of course always unfavorable, because the condition depends upon mechanical disease of the heart of an incurable nature. Temporary improvement may, however, sometimes take place under proper treatment.
TREATMENT.—Such treatment must be used as serves to support the weakened heart and hold in check the tendency to dilatation. With this view digitalis or convallaria may be employed, with tonics and alcoholic or ammoniacal stimulants as occasion may require. Counter-irritation over the lungs may be used and expectorants may be given. If dyspnoea be urgent, the preparations of ether, such as Hoffman's anodyne, or the carbonate of ammonia, may be administered.