Chapter XVII: Part 17

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 {251} 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 {252} 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]

[Footnote 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 {253} 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]

[Footnote 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 {254} 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]

[Footnote 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]

[Footnote 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.

{255} 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 {256} 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.

[Footnote 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.

[Footnote 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 {257} 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.

{258}

CONGESTION AND OEDEMA OF THE LUNGS (HYPOSTATIC PNEUMONIA).

BY SAMUEL C. CHEW, M.D.

Congestion and oedema of the lungs are often found together, but they are different morbid conditions, and each may occur independently of the other. It is best, however, to consider them in connection with each other.

DEFINITION.--By congestion of the lungs is meant an active or passive hyperæmia of the pulmonary vessels, which are surcharged with blood.

Oedema of the lungs signifies an effusion of fluid consisting mainly of the serum of the blood into the air-vesicles and, to some extent, into the pulmonary connective tissue. Congestion is at times the determining cause of oedema, but the latter condition may arise from causes not tending to produce the former.

HISTORY AND ETIOLOGY.--As pulmonary congestion and oedema are almost always secondary and dependent affections, their etiology is an essential part of their history, so that these subjects will be best considered together.

Active congestion of the lungs may result from any cause producing an increased afflux of blood to these organs, such as hypertrophy or functional over-action of the heart, or the sudden recession of the blood from the surface and perhaps from other internal organs, such as may take place under the influence of cold. Violent exercise, rapid walking up hill, or even mental excitement, may in some impressible subjects suffice to produce it.

Why vascular congestion should occur in a greater degree and more readily in the lungs than elsewhere from the effect of cold is sufficiently evident when it is considered that the pulmonary capillaries are not supported by surrounding tissue, as those of other parts are. And for the same reason the direct action upon them of cold air or of certain irritant gases, such as ammonia or chlorine, may suffice to cause an undue afflux of blood to them.

How far a neurotic influence exercised reflexively through the vaso-motor system may serve to produce active congestion has not yet been fully determined; but it is probable that the sudden pulmonary congestions which have been known to follow the drinking of a large quantity of cold water when the body is heated may be attributed to such an action.

Passive congestion may be occasioned by a retardation of the blood-flow from the lungs; as, for example, by a hindrance to its onward passage through the left chambers of the heart in consequence of obstructive valvular disease, especially a great degree of mitral or aortic stenosis. So also mitral or aortic incompetency, by allowing the blood to be crowded backward in the pulmonary veins, may interfere with its passage through the lungs, and in this way set up passive hyperæmia.

By some writers mere weakness of the heart is spoken of as a cause of {259} passive congestion of the lungs; but it can hardly be regarded as such apart from influences affecting the blood itself or the tonicity of the pulmonary vessels; for it is to be considered that while weakness of the left chambers of the heart might impede the onward course of the blood received from the lungs, yet at the same time the right chambers, if weakened in a corresponding degree, would send less blood into those organs, and then the conditions of passive hyperæmia would not exist. It is well known, moreover, that cardiac weakness coming on suddenly as in syncope, or gradually as in various asthenic diseases, may be present without the occurrence of any signs of pulmonary congestion. Yet it is not impossible that there may be a disturbance of the balance between the actions of the right and left sides of the heart, and that thus passive congestion of the lungs may result from a relatively greater weakness on the left than on the right side of the heart, so that the left auricle and the pulmonary veins may be obstructed, and backward pressure produced while the right ventricle is still sending blood into the lungs.

It is probable, however, that, in addition to the propulsive power exercised on the blood by the contraction of the heart, another agency affecting its passage through the lungs is the interchange of gases in respiration; and therefore any interference with the reception of oxygen and the elimination of carbonic dioxide may tend to retard the blood-flow, and thus favor stasis or passive congestion. In this way the inhalation of impure air, especially air containing an undue amount of carbonic dioxide, may occasion passive hyperæmia.

Pulmonary oedema is never a primary affection, but is always due to some preceding disease. In the first place, it may, as already stated, take its origin directly from congestion of the lungs, the walls of the obstructed vessels allowing the transudation of serum, which will collect in the air-cells and connective tissue and also in the mucous membrane of the terminal bronchi. In an early stage it may be present in the walls only of the alveoli without being effused into their cavities.

Another cause of pulmonary oedema is obstruction of the circulation of a part of a lung, such as may take place in pneumonia or miliary tuberculosis, the vessels of other parts becoming distended by backward pressure, so that the serum of the blood will exude into the air-cells or interstitial tissue. When this occurs in pneumonia it may be a most alarming and dangerous complication.

Still another and very frequent cause of pulmonary oedema is Bright's disease in its different forms, in which the oedema occurs as a part of the general dropsy incident to these affections. In acute congestive nephritis it may come on very rapidly, constituting acute pulmonary oedema. Hertz remarks that an acute oedema may take place in the course of an acute nephritis, as has been reported by Lebert, but that such an occurrence is not frequent.[1] The writer of this article has himself seen several cases of acute pulmonary oedema occurring as a part of the dropsy of scarlet fever.

[Footnote 1: _Ziemssen's Cyclop._, v. p. 279.]

More frequently it is met with in chronic albuminuria, and varies in amount from time to time, as dropsical effusions elsewhere do in this condition.

Attacks of asthmatic dyspnoea are not uncommon in the course of Bright's disease, especially in cases of chronic contracted kidney. They are described as uræmic asthma, and are referred by some writers to the action of the depraved blood on the centres of respiration. This explanation may be correct in some cases, but it seems likely that they are due in part to dropsical oedema of the bronchial mucous membrane, the connective tissue, or the air-cells. A weakened condition of the heart, such as is apt to occur {260} in advanced periods of Bright's disease, has probably some share in determining the oedema.

In any case of oedema, according to its situation, whether it is in the connective tissue, the bronchial mucous membrane, or the air-cells, and according also to the amount in which it is effused, it will interfere more or less with breathing. If there be interstitial infiltration with swelling of the bronchial mucous membrane, lessening the calibre of the tubes, there may be merely some embarrassment of respiration; but if the effusion invade any considerable number of the air-cells, urgent dyspnoea will be produced. Oedema is generally most abundant at the lower part of the lungs, and is not uncommonly associated with pleural effusion, the two conditions being due to the same cause; and then the interference with respiration is greater and more perilous.

SYMPTOMS.--It is possible that a slight degree of pulmonary congestion may exist when the circulation is hurried without the occurrence of any other symptoms except moderate acceleration of the breathing. Under such circumstances, however, the existence of congestion cannot be proved. When it is brought about in greater degree, either by over-action of the heart or sudden recession of blood from other parts, the earliest and most prominent symptoms are a sense of oppression in the chest and quickened, laborious respiration, which may rapidly increase until the dyspnoea becomes most urgent and distressing. The heart's action grows more hurried, the pulsations in the carotid and temporal arteries are strongly felt, and the face is deeply flushed. Cough is always present, at first dry in character and afterward accompanied with expectoration of frothy mucus, which may be tinged with blood or may be even mingled with a considerable amount of bright-red blood.

The different appearances of the expectoration are probably due to the fact that in some cases the distended pulmonary capillaries allow the transudation of blood-corpuscles, and in others they are actually ruptured by the strain, so that pure blood escapes from them.

If the congestion is due to weakened action of the heart, with remora of the venous circulation, and is passive in character, the symptoms may be less acutely developed and less urgent than they are in the active form; indeed, in some cases in which very considerable portions of the lung are involved there may be no excessive dyspnoea while the patient is quiet, in consequence of the organism having become gradually accustomed to the imperfect respiration.

As the congestion increases, however, and the lungs become more affected, the signs of malaëration are more conspicuous. Dyspnoea is more oppressive, the face and surface generally, especially the lips and extremities, become cyanotic and cold, and the patient perishes from apnoea and from coma occasioned by oedema of the brain or medulla or stasis of blood in the cerebral veins, the respiratory centres being paralyzed. With the occurrence of somnolence the efforts to free the air-passages from fluid by coughing and expectoration grow less and less as the sensibility is obtunded.

When the congestion is not very extensive the amount of air in the lungs is not lessened sufficiently to materially affect the percussion note, which may remain resonant, though it may have a somewhat tympanitic quality. The vesicular murmur is still heard, but it is rather rough in character. When the general symptoms indicate a graver degree of congestion there will be corresponding changes in the physical signs; resonance will be lessened, or even replaced by dulness, in consequence of the filling of the alveoli with serum or blood; and the respiratory murmur will be completely masked by coarse and fine mucous râles. If the dulness is very marked, bronchial breathing and bronchophony may be observed. Elsewhere in parts not {261} involved in the congestion exaggerated or puerile breathing may be heard from the supplementary action that takes place there.

The physical signs may vary as to their situation with the patient's position as the blood in the congested vessels and the serum in the alveoli and connective tissue gravitate from side to side. But when the change described as hypostatic pneumonia has taken place, and the affected portion of the lung has become condensed in texture, position has little or no influence on the physical signs, which will still remain even when the affected side is kept uppermost.

When oedema of the lungs is produced by serous effusion invading the air-cells, there is some degree of dulness on percussion, especially at the lower part of the chest. Respiratory murmur is feeble or suppressed, and fine moist râles are heard, with an intermixture at times of the true crepitant râle. These signs are generally heard on both sides, but when an area of oedema is due to pneumonia the signs may be present only on the affected side.

COURSE AND TERMINATIONS.--Acute congestion of the lungs depending on over-action of the heart or a sudden recession of blood may cause death in a short time, or may disappear, either spontaneously or under appropriate treatment, almost as suddenly as it has come on. The abatement of the symptoms is generally attended with profuse serous expectoration, and sometimes with hemorrhage, by which the congested vessels are relieved, so that they return to their natural state.

When acute oedema of the lungs is due to Bright's disease in the acute or one of the chronic forms, it is often quickly fatal, though if properly treated it may disappear. When a consequence of chronic renal disease it is apt sooner or later to return. Chronic passive hyperæmia and chronic oedema of the lungs admit of only temporary relief, because they are occasioned by such diseases of the heart or kidneys as are themselves generally incurable; and they are very sure to recur, even though they may be relieved for a time. It is not uncommon in cases of this sort to see the symptoms of chronic oedema suddenly aggravated by the occurrence of an acute attack, which is the immediate cause of death.

PATHOLOGY AND MORBID ANATOMY.--The pathological appearance of a congested lung varies according to the form of the congestion and the manner in which it has been occasioned. Acute congestion may occur very suddenly from some of the causes that have been mentioned, and may disappear with equal rapidity, leaving no traces behind. But sometimes, from the extent of the congestion, respiration is interrupted to such a degree that life is quickly destroyed. In such cases the affected portion of the lung is of a dark color from being engorged with blood, which flows from it if an incision is made. The part is heavier and crepitates less than normal lung-tissue. The bronchial mucous membrane is apt to be hyperæmic, as might be expected from the communication that exists between the pulmonary and bronchial vessels, and the tubes themselves are filled with mucus and sometimes with frothy and bloody serum.

Where the tonicity of the pulmonary vessels has been impaired by sickness, age, or other debilitating influences, passive congestion of the lungs is very likely to ensue if the heart become weakened; and as the effect of gravity will aid in determining the stasis of the blood, the resulting congestion is in life most marked in the lower and posterior regions of the lungs, where the changes are chiefly found after death. As gravity may thus determine the congestion to one part of the lungs, so a change in the patient's position may cause it to disappear from where it was first manifest and to appear in another part which has become most dependent. The condition thus brought about is known as hypostatic congestion. One of the consequences of passive {262} hyperæmia thus induced is a transudation of the serum of the blood into the air-cells and connective tissue of the lungs; and this is one way in which pulmonary oedema may be occasioned. When hypostatic congestion has lasted for some time, it may no longer be affected by changing the patient's position; and when this is the case it may be accompanied by exudation of fibrin into the air-cells and by proliferation of epithelium, thus producing the condition termed hypostatic pneumonia.

All three of these states may be present in one lung at the same time, one portion being passively congested, another oedematous, while the most dependent part may be the seat of hypostatic pneumonia.

The congested parts of the lungs are very dark in color, in some cases almost black; blood flows freely from a section through them, and serum exudes from the alveoli and interstitial tissue when oedema exists. If the altered condition of the lung has lasted for some time, the texture of the affected part may be so firm as to resemble that of the spleen; whence this change is sometimes termed splenization. In this condition dark-red points consisting of extravasated blood may be seen scattered about. If the state already described as hypostatic pneumonia exists, the affected part is still more firm and dense in texture, and presents a granular appearance on section from the exudation of fibrin which has probably taken place, so that it resembles a portion of a lung that has been the seat of an inflammatory process from the first.

DIAGNOSIS.--The diagnosis of pulmonary congestion in its different forms, and of pulmonary oedema, is in general not difficult if the symptoms of the causative diseases are carefully observed. Acute pulmonary congestion coming on suddenly, and not preceded by any other affection, needs to be distinguished from the early congestive stage of pneumonia, which it somewhat resembles from the slightly impaired resonance on percussion and the dyspnoea that may occur in both diseases. The chief points of distinction between the two affections are the absence in congestion of initial chill, of pain in the side, and of rise of temperature; all of which are in general present in pneumonia. As the case advances the divergence between the two affections will be wider.

The diagnosis of acute oedema and of chronic congestion and oedema is based upon the physical signs belonging to them, taken in connection with the symptoms of cardiac and renal disease with which they are associated.

Capillary bronchitis bears some resemblance to pulmonary oedema, since in both affections there are moist subcrepitant râles; but in capillary bronchitis there is no such loss of percussion resonance as occurs in pulmonary oedema, and, moreover, fever is not present in oedema, as it is in the inflammatory affection. The character of the expectoration is also different in the two diseases, being thicker and more tenacious in bronchitis and serous or watery in oedema. From hydrothorax, oedema is distinguishable by the shifting line of dulness and by the absence of râles in hydrothorax.

PROGNOSIS.--Acute congestion of the lungs is always a serious affection, and, as already stated, terminates fatally in some cases in a short time. In the majority of instances, however, it disappears spontaneously or under suitable treatment, and the lungs are in general restored to their integrity. It may result in pulmonary hemorrhage, from which recovery may take place, or which may give rise to hemorrhagic infarction, the blood being drawn into the alveoli.

Passive congestion being a secondary affection, its prognosis depends upon the diseases which occasion it.

In pulmonary oedema the prognosis is always very grave. When occurring suddenly as a consequence of acute congestive nephritis, it may wholly {263} disappear under proper treatment, and if the kidney affection is likewise cured there will be no further return of the pulmonary complication. When it comes on in the course of chronic renal disease, it may disappear and recur from time to time, but it is apparently not often the direct cause of death by itself. Sometimes, however, it is associated with cerebral oedema and other conditions which together occasion a fatal termination. When due to pneumonia, oedema adds very much to the gravity of the affection, and may be the immediate cause of death.

TREATMENT.--The treatment of acute pulmonary congestion consists in the use of means to check the undue flow of blood into the engorged lungs. Of these the best, if the patient be seen promptly and the strength of the pulse admit of it, is general bloodletting, by which the mass of the blood is lessened and the action of the heart and pressure within the blood-vessels are lowered, so that both the amount of blood in the hyperæmic vessels and the force with which it reaches them will be diminished.

This measure may be also useful in the way of preventing or checking acute pulmonary oedema by lessening the blood-pressure. Should venesection be thought inadmissible, cups may be applied to the chest in front or behind, and at the same time the volume of the blood may be temporarily lessened by placing ligatures around the thighs, so as to check the flow of blood in the veins near the surface. Revulsion from the congested vessels of the lungs may also be effected by mustard foot-baths or the application of mustard poultices to the chest. Aconite may be serviceable by controlling over-action of the heart, and may be given in the dose of 1 or 2 drops of the tincture of the root at intervals of half an hour until some effect on the circulation is produced.

It is of importance to remove any blood or serum that may be present in the air-cells and smaller bronchi; and for this purpose one of the quickly-acting and non-depressing emetics may be given, such as apomorphia hypodermically or the sulphate of zinc or turpeth mineral by the mouth. Respect must be had to the condition of the patient's strength in ordering an emetic, since if there be much prostration, or if the interference with respiration has seriously depressed the heart, more harm than good might result from its use. Expectorants may somewhat later supplement the action of emetics, or serve to keep up the good effects gotten from them by helping to remove the residual fluids from the air-passages. Among the best of these are the syrup of senega and the carbonate or hydrochlorate of ammonium.

Passive congestion of the lungs, being dependent upon a weakened condition of the circulation, requires the use of means to sustain and reinforce the heart's action. The alcoholic and ammoniacal stimulants are here of great importance, and digitalis may be of sovereign efficacy, especially in cases where the congestion is associated with dilatation and attenuation of the heart. The power possessed by this drug of increasing arterial pressure, and thus producing diuretic action, may render it further serviceable when the congestion is accompanied with oedema, as in this way the serous infiltration may be absorbed and removed. From 10 to 20 drops of the tincture or from 2 to 4 drachms of the infusion of digitalis may be given every two hours until some effect on the pulse or the kidneys is noticed. If the stomach should not bear digitalis well in either of these forms, as is the case with some patients, the alkaloid digitalin in the dose of 1/60 grain may be given. The convallaria recently introduced as synergistic with digitalis may be substituted for it, and in the dose of from 20 minims to 1 drachm of the fluid extract it will be found not uncommonly to be an efficient heart-tonic. Like digitalis, too, it possesses diuretic power from the increased arterial pressure that it occasions.

Passive pulmonary congestion may assume a chronic form in connection with chronic cardiac and renal disease, and without presenting urgent {264} symptoms may cause almost constant embarrassment of respiration in greater or less degree. Under such circumstances the preparations of iron are helpful by enriching the blood and increasing the tone of the heart. One of the best preparations is the mixture of acetate of iron and ammonium,[2] known as Basham's mixture, which combines diuretic with chalybeate action. This may be given in the dose of from 1 to 4 drachms.

[Footnote 2: _U. S. Pharm._, 1882.]

It is of great importance in all cases of passive congestion and of hypostatic pneumonia to change the patient's position from time to time, so as to counteract the influence of gravity and relieve dependent portions of the lungs.

Pulmonary oedema occurring in an acute form in the course of either congestive nephritis or chronic renal disease may seriously imperil life, and therefore it demands prompt and bold treatment. When it results from acute nephritis, it is more immediately dangerous than when dependent on chronic disease of the kidneys; yet in this acute form it may admit of perfect cure if proper remedial measures be at once instituted. Cups may be applied to the loins with the view of relieving the engorged kidneys and enabling them to resume their work of removing fluid from the body. In cases where the strength of the pulse is sufficient, it may even be good practice to abstract blood by the lancet to the amount of six to eight ounces. According to Oppolzer,[3] this treatment may be proper even when somnolence indicates oedema of the brain, provided there be no irregularity of respiration or intermission in the pulse--signs which contraindicate bloodletting.

[Footnote 3: _Ziemssen's Cyclop._, v. p. 285.]

Active diaphoretics are among the best medicinal agents to be employed, their good effects being due to their derivative action and to the large discharge of fluid from the skin which they occasion, thus promoting the removal of what is effused in the lungs. The fluid extract of jaborandi in the dose of from 20 minims to a drachm, or the hypodermic injection of 1/8 to 1/6 grain of nitrate or muriate of pilocarpine, frequently causes prompt and profuse perspiration. The writer is confident that he has seen life saved by the use of this drug when it has been in urgent peril from pulmonary oedema. In the absence of this agent, or along with it, the hot-air bath, which can almost always be extemporized in an efficient form, may serve to promote or increase fluid discharge from the skin. If the patient's strength is sufficient, one of the hydragogue cathartics may be given, and among them the most prompt and active is elaterium in the dose of 1/12 to 1/8 grain every four hours. The action of this drug must be carefully watched and its depressing tendency guarded against by the use of alcoholic stimulants.

When pulmonary oedema results from weakness of the heart, as in dilatation of that organ, or from chronic renal disease, all lowering measures must be avoided. Bloodletting, whether general or local, would still further depress the heart, and by increasing the hyperæmia of chronic Bright's disease would favor the further effusion of serum into the lungs. Dry cupping over the chest before and behind may be serviceable as a revulsive measure. Stimulants and tonics are called for, and digitalis or convallaria is directly indicated from the special power possessed by these agents of improving the cardiac tone and promoting the action of the kidneys by increasing blood-pressure. Digitalis has been thought objectionable when there is much irregularity of respiration, and perhaps it would be safest to postpone its administration until this symptom is relieved by the use of alcohol, ammonia, musk, or other prompt diffusible stimulants.

The writer has had repeated opportunities for observing the value of quinia given hypodermically in checking effusion of serum into the air-passages, and he would strongly recommend its use in the treatment of pulmonary oedema in the form of the hypodermic injection of the solution of hydrobromate of {265} quinia of the strength of 4 grains to 20 minims. Of this solution 10 to 20 minims may be injected at once. If such a solution cannot be obtained, a full dose of 10 to 15 grains of the sulphate of quinia may be given by the mouth.

As in the case of passive congestion of the lungs, so in oedema, advantage may be gained by changing the patient's position from time to time, so as to prevent the constant gravitation of fluid to the same portion of the affected organs.

{266}

HÆMOPTYSIS.

BY WILLIAM CARSON, M.D.

The word means, literally, spitting of blood, from two words, [Greek: haima], blood, and [Greek: ptyô], I spit.