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 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.
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 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 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 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 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 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.
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.
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 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.