A system of practical medicine. By American authors. Vol. 3 (part 2 of 8)

A system of practical medicine. By American authors. Vol. 3 (part 2 of 8)

When not interfered with by appropriate treatment, these cases run a much more protracted course, and more frequently degenerate into a chronic form, {173} than those of an ordinary catarrhal character. When they are thus allowed to run a protracted course or to continue in a chronic form, they manifest another tendency of great importance--namely, to have the inflammation extend by continuity from the fibrous and muscular structures of the small bronchi into the connective tissue of the pulmonary lobules, inducing sclerosis of the latter tissue and consequent compression or obliteration of the alveoli or air-cells, and permanent contraction of the chest. Much and careful clinical observation has satisfied me that many of the cases now classed by writers as fibrous and inflammatory phthisis began as simple acute or subacute rheumatic bronchitis, which, being renewed at every return of the cold, damp, and changeable part of the year, not only ultimately caused permanent thickening of the bronchial structures, but gradually invaded portions of the connective tissue of the lungs, and induced similar pathological changes in it, constituting the sclerosis just mentioned.

Pseudo-membranous Bronchitis.

This affection has been described by different writers under the additional names of plastic, croupous or croupal, and diphtheritic bronchitis. The extension of the inflammation and membranous exudation to the bronchial tubes in cases of diphtheria and pseudo-membranous tracheitis and laryngitis or croup, is of frequent occurrence. But as a distinct disease limited to the bronchial membrane it is of comparatively rare occurrence.

In 1854, T. B. Peacock noticed in the Transactions of the London Pathological Society 34 cases collected from European sources; Biermer in 1867 increased the number to 58; Kretschy in 1874 added 10, and Chevstok 4 more cases--making in all 72 cases in Europe. In 1879, W. C. Glasgow of St. Louis read to the medical section of the American Medical Association an interesting report on the subject of plastic bronchitis, in which he notices 23 cases which had occurred in this country, accounts of which were obtained from an extensive correspondence with leading physicians in all parts of the United States, as well as from reference to our periodical medical literature.[6] These statistics are certainly sufficient to justify the statement that the disease is of rare occurrence both in this country and in Europe.

[Footnote 6: See Transactions of the American Medical Association, vol. xxx. p. 177, 1879.]

The statistics thus far collected show a much greater prevalence of the disease in males than in females, and that the larger number of cases occur between the ages of fifteen and fifty years, although one case is reported by T. G. Simons of Charleston, S. C., as quoted by Glasgow, at four years of age, and Goumoens one at seventy-two. In a large proportion of the cases reported the disease existed in a chronic form. When acute, and affecting a large portion of the bronchial membrane, it is liable to lead to an early fatal termination from obstruction to the ingress of air to the air-cells of the lungs. But in many cases the disease has extended to only a limited number of the bronchi, and recovery has generally taken place in from two to three weeks.

The symptoms differ from those of ordinary bronchitis in only two important particulars--namely, the more violent and suffocative character of the cough, and the actual appearance of shreds, patches, or casts of pseudo-membrane in the matters raised and ejected by coughing. The latter is the only reliable diagnostic symptom by which it can be certainly differentiated from all other forms of bronchial inflammation. When the membranous exudation is discharged in shreds or small pieces, it may readily escape the attention of the physician, and even considerable casts when expectorated are in some cases so surrounded with mucus and collapsed into a slightly yellowish mass in the central part of the mouthful expectorated, that they might be regarded as only {174} a more muco-purulent part of the mucous secretion. If the whole is thrown into water, however, and agitated a little, the membranous patches and casts will be quickly unfolded in such a manner as to be easily recognized. It is distinguished from mucus by placing it in a solution of acetic acid, which causes it to swell, while mucus contracts in a similar solution. It has the appearance of having been formed in concentric layers, and is sometimes cast-off so complete as to present a continuous representation of one or both primary and several of the secondary bronchial tubes. Under the microscope it has the same fibrillated appearance as other pseudo-membranous formations.

Chronic Bronchitis.

Cases of acute and subacute bronchitis belonging to either of the five varieties just described may be protracted until they assume a chronic form, and other cases of each variety are met with which have been chronic from the beginning. This form of the disease is met with in aged persons more frequently than at an earlier period of life. In children it sometimes follows as a sequel of measles and whooping cough, and in adults is often associated with tuberculosis, emphysema, and cardiac diseases.

ETIOLOGY.--Chronic bronchitis is capable of originating from any and all the causes that have been enumerated as capable of producing the more acute forms of the disease, and consequently prevails most under the same conditions of topography, climate, and social relations.

SYMPTOMATOLOGY.--The symptoms of ordinary chronic catarrhal bronchitis differ from those accompanying the acute form of the disease, chiefly in the absence of general fever and the existence of much less pain or feeling of soreness and oppression in the chest. The patient generally complains of a rather harsh, full cough, usually more severe on first retiring to bed at night and on rising in the morning, but occurring at intervals through the day, and accompanied by a mucous or muco-purulent expectoration varying much in its amount and tenacity. In the great majority of cases occurring in young persons and in the first part of adult life, the expectoration is simply a whitish or slightly opaque mucus, more or less frothy from the intermixture of minute bubbles of air, and easily dislodged, especially in the mornings. In old persons and in cases which have continued a long time, the expectoration often becomes more copious and more decidedly purulent, with slight feverishness at night and some loss of flesh.

In all the cases except those last mentioned the general health of the patient is but little impaired, the appetite and secretions usually remaining nearly natural. Those who pursue indoor occupations or are sedentary in their habits will be prone to constipation and imperfect digestion--more, however, from the circumstances just mentioned than from the effects of the bronchial disease. All cases of chronic bronchitis are subject to temporary aggravation by exposure to a cold and damp atmosphere, whether indoors or out, and are also very susceptible to increase from the inhalation of air containing dust or floating particles of solid matter or of irritating gases.

Cases of ordinary chronic bronchitis rarely prove fatal without the intercurrence of some other disease, and yet there is no natural limit to their duration. In many cases the symptoms almost disappear during the warm months of summer, but return with the first period of cold and wet weather of autumn. Such patients usually find permanent relief by changing their residence to a mild and dry climate.

The symptoms of the rheumatic grade of chronic bronchitis differ from those just described mostly in the more severe paroxysmal character of the {175} cough, with either no expectoration or only a scanty quantity of a glairy, tenacious mucus; in the more soreness or dull pain in the intercostal muscles and attachments of the diaphragm; and in the more marked influence of sudden and severe meteorological changes. Perhaps the most marked and distressing cases of this variety of bronchitis are those we occasionally meet with in old persons whose joints, especially those of the extremities, have long been stiffened and sometimes enlarged from chronic rheumatism, and who are harassed and worn from a harsh, suffocative cough, the worst paroxysms of which are almost always during the latter part of the night and the early morning, accompanied by the expectoration of considerable quantities of a thick, viscid, and very tenacious mucus, which is dislodged with so much difficulty that in the midst of the more violent paroxysms of coughing the action of the stomach is reversed and its contents ejected by vomiting. This is very liable to happen just after breakfast, and to occasion the loss of the morning meal. The condition of these patients is very generally ameliorated during the warm months of summer, but on the whole they emaciate and grow more helpless from year to year, until they die either from exhaustion or the supervention of pulmonary sclerosis (fibroid phthisis), endocarditis, or chronic diarrhoea. There is one grade of rheumatic irritation which is liable to attack the fibrous texture of the smaller bronchi and to give rise to a very persistent form of asthma, which increases with every returning cold season of the year; but as asthma in all of its forms is treated in other parts of this work, I only allude to it in this connection.

PATHOLOGY AND MORBID ANATOMY OF BRONCHITIS.--The special pathology of inflammation involving the mucous membrane and other structures of the bronchi does not differ from that of similar grades of inflammation in any other structures of the body. It consists essentially of an increase or disturbance of those properties of living organized matter which regulate the molecular movements constituting nutrition, disintegration, secretion, and cell-evolution to such a degree as to cause accumulation of blood in the capillaries, followed by exudation and increased cell-proliferation, which may organize into plastic material or pseudo-membrane or degenerate into pus, according to the coincident circumstances and condition of the patient.

Consequently, the anatomical changes resulting from acute catarrhal bronchitis are, in the early stage, more or less intense congestion of blood in the vessels, causing redness and tumefaction of the membrane, soon followed by an increased flow of mucus, with increase or proliferation of mucous corpuscles and epithelium-cells, while leucocytes or white corpuscles are seen permeating the capillary walls and penetrating the submucous tissue or mingling with the increased epithelium upon the surface. These several inflammatory products are seen adhering to the surface of the inflamed membrane and in the smaller tubes, often so filling their calibre as to greatly interfere with the ingress and egress of air through them, and of course adding to the dyspnoea that characterizes the capillary form of bronchitis. During the latter stage of the disease pus-corpuscles are seen freely intermingled with the mucus, and, owing to the exfoliation of much of the epithelium, the surface of the mucous membrane often appears irregular, abraded, or ulcerated.

When the inflammation has been protracted into a chronic form, the vessels appear less congested, but the cell-proliferations continue both in the mucous and submucous structures, causing thickening and increased density, with a still more purulent quality of secretion. The bronchial glands are also {176} sometimes found enlarged, and either softened, colored with pigment, or, more rarely, calcified.

In addition to the foregoing changes, in many cases of the capillary form of bronchitis some lobules of the lungs are found collapsed from the complete occlusion of the bronchi leading to them by the accumulation of tenacious mucus with other inflammatory products. And in the same cases the air-cells in other parts of the lungs, more frequently the upper and anterior parts, are enlarged from over-distension, constituting a degree of emphysema.

In very chronic cases, especially of the rheumatic variety, considerable hypertrophy of the connective tissue of the bronchi has been found, and in other cases atrophy of the same tissue, the latter generally accompanied by more or less dilatation of the tubes.

In pseudo-membranous or croupous bronchitis the bronchial tubes are found lined, and in some cases filled, with a plastic exudate. Usually, only a limited number of the bronchi are affected. The tube-casts that may be expelled are generally in the form of balls, which may be unrolled, and which will then be found to be fragments or complete cylindrical casts of the tubes. They are, when expelled, usually yellowish and often sanious. When washed they are white. There are frequently points of enlargement along the casts which are caused either by the presence of air-bubbles within them, or by a more rapid exudation from that point on the bronchus. The largest casts are usually solid and laminated in structure; the smaller ones more frequently are hollow, containing a greater or less number of air-bubbles; the smallest consist of a single solid thread. Under the microscope the casts seem to be composed of a structureless or fibrinous substance holding numerous mucus and pus-cells, more or less numerous globules of fat, and occasional epithelial cells; seldom red blood-corpuscles, although these may be numerous on the surface. The casts are usually moderately compact, firm, and elastic. Toward the end of the disease, however, they may be less firm. In some cases toward the close of life epithelial cells are abundant in them, but in other cases on post-mortem examination the epithelial lining of the bronchi is found nearly or quite entire. The mucous membrane may be much reddened, or, on the other hand paler than normal. The submucous tissues are also sometimes involved in the swelling, and occasionally infiltrated with serum.[7]

[Footnote 7: For a representation of one of the most complete specimens of pseudo-membranous casts from the bronchi the reader is referred to the paper of Glasgow in the Transactions of the American Medical Association, already referred to.]

DIAGNOSIS.--The principal diseases from which acute inflammation of any part of the bronchial mucous membrane needs to be differentiated are pneumonia, pleurisy, laryngitis, tracheitis, and asthma, while it is still more important to keep a clear line of diagnosis between the chronic grades of bronchial inflammation and the earlier stages of pulmonary phthisis and of emphysema. From nearly all the diseases named it is separated by negative evidence or the absence of symptoms and physical signs characteristic of those affections. It neither presents the rusty expectoration or high temperature or fine crepitant râle of pneumonia, nor the acute pains or short stifled cough or friction-sounds of pleurisy in the early stage, and still less is there in the middle and later stages any of the dulness on percussion that characterizes the corresponding stages of the other two diseases. In true asthma the active symptoms are distinctly paroxysmal, without fever or increase of temperature, and the respiration during the paroxysms is slow, with marked prolongation of the expiratory act; while in bronchitis, both catarrhal and capillary, the symptoms are continuous, the temperature increased, and the respirations more frequent than natural. All grades of bronchitis are easily distinguished from laryngitis and tracheitis by auscultation, which enables us {177} to trace all the morbid sounds to the chest in the former, and to the front part of the neck in the two latter.

The great advantage of recognizing pulmonary tuberculosis and other forms of phthisis in the early stage of the disease makes the diagnosis between it and chronic bronchitis a matter of primary importance. This can be readily done by all practitioners who have acquired a reasonable degree of skill in the practice of auscultation and percussion. In all forms and stages of pulmonary phthisis, whether from primary tubercular deposits, pneumonic exudation followed by caseous degeneration, or from interstitial fibroid sclerosis, there is increased vocal fremitus and diminished resonance on percussion; neither of which is present in any grade of uncomplicated bronchitis. It is true that in the advanced stage of some very severe cases of capillary bronchitis there occurs sufficient pulmonary oedema to increase the vocal fremitus and diminish the resonance over some parts of the chest; but the accompanying symptoms and immediately preceding history of such cases are sufficient to separate them from any stage of phthisis. The same remark is applicable to those rare cases in which an attack of pseudo-membranous bronchitis results in the complete occlusion of one or more of the bronchi and the permanent collapse of the pulmonary lobules to which the occluded tubes lead. If in addition to the plain difference in the physical signs already mentioned we remember that in all the forms of phthisis there is progressive loss of flesh, some increase of temperature and acceleration of pulse, with a contraction of the upper and anterior part of the chest, while none of these changes result from bronchitis alone, there should be no difficulty in keeping the line of diagnosis clear between these two diseases. And yet there is probably no more frequent or important error committed in diagnosis than that of mistaking the early stage of pulmonary phthisis for bronchitis. This may arise in part from the fact that bronchitis often supervenes and continues coincidently with phthisis. But the practitioner should remember that whenever there is increased vocal fremitus and diminished resonance in any given case there is some altered condition of the lung-structure, and consequently some form of disease besides bronchitis, however plain the ordinary symptoms of the latter may be at the same time.

From pulmonary emphysema, chronic bronchitis is distinguished chiefly by the abnormally-increased resonance on percussion in the former, especially over the upper and anterior parts of the chest, and the peculiar depression of the spaces above the clavicles and between the ribs at the beginning of the inspiratory act, and their return to over-fulness near its close; while none of these changes accompany any grade of simple bronchial inflammation.

PROGNOSIS.--In the ordinary form of acute and chronic bronchitis there is very little tendency to terminate fatally except when it attacks infants or persons infirm from age. And even when it occurs at these extremes of life the fatal terminations are usually caused by the supervention of lobular pneumonia as a complication, and not from the bronchial inflammation alone. Severe cases of capillary bronchitis are more dangerous, and in young children and aged or debilitated persons often prove fatal before the end of the first week of their progress by the direct obstruction to the entrance of air into the air-cells of the lungs. The pseudo-membranous or plastic bronchitis is still more dangerous. It has been estimated that one out of every five dies. But the statistics concerning the number and character of cases are not sufficient to furnish a reliable deduction of the ratio of mortality.

The duration of acute attacks of bronchitis of all varieties from which recovery takes place is from one to three weeks. Uncomplicated cases of chronic bronchitis seldom prove fatal, neither is there any self-limit to their duration. Many cases undergo marked improvement during the warm {178} months of summer, but suffer a renewal of all the more severe symptoms on the return of the cold and wet weather of autumn. In other cases the symptoms continue nearly the same through all the seasons of the year and until an advanced period of life.

TREATMENT.--There are certain leading objects to be accomplished in the treatment of all grades of inflammation affecting the mucous membrane and connective tissue of the bronchial tubes--namely, (a) to diminish or overcome the morbid excitability of the inflamed part; (b) to relieve the vascular hyperæmia or fulness of blood in the vessels, and thereby limit the amount of exudation or morbid secretion and consequent dyspnoea; (c) to counteract or relieve secondary functional disturbances, such as increased heat and dryness of the skin, diminished renal and intestinal activity, and nervous restlessness; (d) to hasten the removal of such plastic exudations as may have caused thickening and induration of the inflamed structures or formed layers or patches of false membrane on the bronchial surface, and to lessen the tendency to establish a stage of purulent degeneration or suppurative action in the inflamed part; (e) to regulate diet, drinks, exercise, and clothing in such a way as to sustain healthy nutrition and prevent the further action of predisposing and exciting causes.

The first three objects to be accomplished belong more particularly to the early stage of acute and subacute attacks, but are present in some degree throughout the whole course of the disease; while the last two belong to the latter stages of the acute and to all stages of the chronic grades of the inflammation. While the foregoing indications to be fulfilled or objects to be accomplished are present in all the various grades and stages of inflammation of the bronchi, the particular means for accomplishing them will be modified by the age and previous physical condition of the patient, the nature of the predisposing and exciting causes, the extent of the disease, and the stage of its advancement; or, in other words, the nature and extent of the pathological changes already accomplished. For instance: the same remedial agents that would be most efficient in relieving the morbid excitability and the vascular fulness of the first stage of acute inflammation in a young or middle-aged and previously healthy, vigorous subject might be positively injurious, or even fatal, if used in the same stage of inflammation in a subject previously anæmic and feeble or debilitated from age or from causes capable of impairing the quality of the blood and favoring a typhoid condition of the system. Consequently, the practitioner who not only sees clearly the objects most desirable to accomplish, but who most judiciously selects and adjusts the means or agents he uses to the special conditions of each patient, will meet with the highest degree of clinical success.

In the first stage of acute attacks involving the bronchi of both lungs in vigorous adult persons, and especially if the inflammation extends into the smaller tubes, causing much dyspnoea and dry râles, there is no single remedy that will so certainly and speedily check the intense engorgement of vessels in the bronchial membranes, and thereby gain time for the action of other remedies, as one prompt and liberal abstraction of blood by venesection. In cases of a little less severity, and in children, the application of from two to twelve leeches to the upper and anterior part of the chest, the number being regulated by the age of the patient, will be a good substitute for the venesection. And in case leeches are not at hand extensive dry cupping over both the anterior and posterior parts of the chest may be applied with much benefit. Immediately after the venesection, leeching, or cupping, and without these in cases of only ordinary severity, the whole chest may be enveloped in an emollient poultice or in folded napkins wet in warm water and covered with oiled silk. At the same time the following combination may be given internally: {179}

No. 1. Rx. Liquoris ammonii acetatis, (60.0 c.c.) fluidounce ij; Tincturæ opii camphoratæ, (75.0 c.c.) fluidounce iiss; Vini antimonii, (15.0 c.c.) fluidounce ss; Tincturæ veratri viridis, (6.0 c.c.) fluidrachm iss.

M.--Sig. Give to an adult 4 cubic centimeters or 1 teaspoonful in a tablespoonful of water every two, three, or four hours, according to the severity of the case. The same may be given to children, the dose being properly adjusted to the age of the child.

If the tongue be coated, the bowels inactive, and urine high-colored, from 6 to 30 centigrams (grs. j-v) of calomel, according to the age of the patient, may be given, and followed in four or five hours by a saline laxative sufficient to procure two or three evacuations from the bowels. Under the influence of these remedies the high fever and great sense of soreness and oppression in the chest which exist in the first stage of the more acute cases in previously healthy subjects rapidly diminish, giving place to more moist râles, easier breathing, and some expectoration. As soon as such amelioration of symptoms has been obtained, the mixture containing veratrum viride should be discontinued, and the following formula substituted in its place:

No. 2. Rx. Syrupi scillæ comp. (45.0 c.c.) fluidounce iss; Tincturæ sanguinariæ, (15.0 c.c.) ounce ss; Tincturæ opii camphoratæ, (60.0 c.c.) fluidounce ij.

M.--Sig. Give to an adult 4 cubic centimeters in a little additional water every three or four hours.

If the patient suffers much from severe sore pain in the head, aggravated by coughing, or from nervous restlessness, the addition of bromide of potassium, 16 grams (drachm iv), to the above formula will render it more efficient in relieving these symptoms and in promoting rest. Under such quieting and expectorant influences, aided by a mild laxative when needed, the cough, soreness, and oppression in the chest, and all other active symptoms, diminish from day to day, and convalescence ensues in from seven to nine days.

If after the first three or four days the temperature rises in the evening and the cough becomes more troublesome, interfering with rest during the first part of the night, followed by some sweating in the early morning, a single dose composed of sulphate of quinia from 3 to 6 decigrams (gr. v-x), pulverized sanguinaria-root 3 centigrams (gr. ½), and codeine 16 milligrams (gr. ¼) given between six and eight o'clock each evening for three or four evenings, will often contribute to the rest of the patient and hasten the establishment of convalescence.

Cases are sometimes met with, especially in patients debilitated by previous ill-health or age, in which the fever subsides after the first three or four days, leaving the patient with a feeling of unusual weakness, a deep harassing cough, copious muco-purulent expectoration, and little or no appetite. In such cases tonics and the more stimulating class of expectorants are indicated. A mixture of equal parts of the syrup of Prunus virginiana, syrup of senega, and camphorated tincture of opium, given in doses of 4 cubic centimeters or one teaspoonful every four or six hours, and 13 centigrams (gr. ij) of quinia three times a day, will often cause a rapid improvement in all the symptoms. In some of the cases last described there is added to the other symptoms a troublesome nausea and disposition to vomit with the paroxysms of coughing, in which I have found the following formula a good substitute for the mixture containing the prunus virginiana and senega:

No. 3. Rx. Acidi carbolici, (0.50 grams) gr. viij; Glycerinæ, (30.0 c.c.) fluidounce j; Tincturæ opii camphoratæ, (60.0 c.c.) fluidounce ij; Aquæ, (60.0 c.c.) fluidounce ij.

{180} M.--Sig. Give 4 cubic centimeters (fluidrachm j) or 1 teaspoonful before each mealtime and at bedtime, giving the quinia a little after the meals.

If more anodyne influence is required to procure rest at night, 16 milligrams (gr. ¼) of codeine may be added to the teaspoonful of carbolic acid mixture given at bedtime. If, as sometimes happens in cases of acute bronchitis, both of the catarrhal and capillary varieties, the inflammation invades some of the lobules of the lungs, as indicated by undue rise of temperature, greater expansion of the wings of the nose during inspiration, with short expiration, and diminished resonance with fine crepitation over limited portions of the chest, I have found the most certain and speedy relief to follow the application of a blister over the seat of the pneumonia and the internal use of the following formula:

No. 4. Rx. Ammonii chloridi, (12.00 grams) drachm iij; Antimonii et potassii tartratis, (0.13 grams) gr. ij; Morphiæ sulphatis, (0.20 grams) gr. iij; Extract, glycyrrhizæ fluidi, (30.0 c.c.) fluidounce j; Syrupi, (90.0 c.c.) fluidounce iij.

M.--Sig. Give to adults 4 cubic centimeters (fluidrachm j) or 1 teaspoonful, mixed with a tablespoonful of water, every three or four hours until some relief is obtained, and then at longer intervals. For children the doses must be diminished in proportion to the diminution of age. Quinine and laxatives may be used in these cases under the same indications as in uncomplicated bronchitis.

In the severe attacks of capillary bronchitis in young children many writers recommend emetics, and subsequently nauseating doses of antimony or ipecacuanha. But I have not seen sufficient benefit result from emetic doses of these agents to compensate for the early prostration, and sometimes continued gastric irritability, which they induce. I prefer the proper application of leeches at the very beginning, followed by emollient applications to the chest, and the same remedies internally as already mentioned, aided, perhaps, by an earlier use of quinine and digitalis if the cardiac action becomes weak and frequent. In all this class of cases, however, much caution should be exercised in regard to the use of opiates, either alone or in combination with other remedial agents, lest their narcotizing influence should diminish the force and frequency of the respiratory movements too much, and encourage the accumulation of the inflammatory products in the smaller bronchi to such a degree as to produce apnoea or death by the exclusion of air from the alveoli or air-cells of the lungs. And yet just enough of these quieting agents to diminish excitability and allay excessive restlessness is as desirable in children as in adults.

In the plastic or pseudo-membranous form of bronchitis it is an object of much importance, in the first stage, to limit the amount of plastic exudation, and later to hasten the loosening and disintegration or discharge of such layers of false membrane as may have formed on the bronchial mucous surface. For these purposes alterative doses of calomel may be given alternately with the doses of the formula containing the liquor ammonii acetatis already given (see Formula No. 1) during the first twenty-four hours, and subsequently pretty full doses of the iodides of sodium or potassium or of the bicarbonates. In acute cases in children, when the symptoms indicate that the false membrane is loosening and the dyspnoea is great, an emetic that will induce prompt and free vomiting may hasten its expulsion and afford much relief.

In the cases which have been described as rheumatic bronchitis of the more acute or active grade I have seen the most prompt and satisfactory degree of relief follow the administration of the following combination of remedies in the early stage: {181}

No. 5. Rx. Sodii salicylatis, (25.00 grams) drachm vj; Glycerinæ, (15.00 c.c.) fluidrachm iv; Vini colchici radicis, (25.00 c.c.) fluidrachm vj; Syrupi scillæ compositi, (45.00 c.c.) fluidounce iss; Tincturæ opii camphoratæ, (60.00 c.c.) fluidounce ij.

M.--Sig. Give 4 cubic centimeters (fluidrachm j) every three or four hours in a little additional water.

In several cases in which this grade of inflammation was located chiefly in the smaller bronchi, causing very distressing and persistent dyspnoea, I have found an equal mixture of the wine of colchicum-root and the acetated tincture of opium, given in doses of 25 to 30 minims every three hours at first, to afford more relief than any other remedies I could use; and after some degree of relief had been obtained, by lengthening the interval between the doses to four or six hours and continuing it a few days, all the symptoms were removed. When the disease occurs in old persons, accompanied by severe paroxysms of coughing and only a scanty and very viscid mucous expectoration, much benefit may sometimes be derived from the use of the carbonated alkalies, such as the carbonate of ammonium or bicarbonate of sodium, dissolved in an equal mixture of the fluid extract of the Phytolacca decandra, liquor ammonii acetatis, and camphorated tincture of opium, in such proportions that the patient will get 3 decigrams (gr. v) of carbonate of ammonium in each dose of the mixture.

It is proper to remark that there are many mild attacks of bronchitis, caused by exposure to sudden and severe meteorological changes, which if seen during the first twenty-four hours can be speedily arrested by a hot or stimulating foot-bath and a full dose of the compound powder of opium and ipecacuanha (Dover's powder), taken in the evening, and followed the next morning by a saline laxative and two or three moderate doses of quinine during the day. Similar results can also be obtained in some cases by the use of any agents that will allay irritability and at the same time produce a free or copious elimination from the skin and kidneys. An efficient diaphoretic dose of pilocarpine, or a full warm bath, followed by two or three moderate doses of quinine, will succeed well if employed in the initial stage of the disease. Unfortunately, but few cases come under the care of the physician until after this stage is past.

TREATMENT OF CHRONIC BRONCHITIS.--Most of the cases of chronic bronchitis are treated satisfactorily by a more moderate use of the same remedial agents that have been recommended in the acute and subacute grades of the disease, aided by a judicious regulation of diet, dress, and exercise. In the great majority of cases of the ordinary chronic catarrhal variety of bronchitis the formula already given, numbered 4, or the one numbered 2, if given to adults in doses of 4 cubic centimeters (fluidrachm j) before each meal and at bedtime, mixed with a tablespoonful of water, will afford the necessary relief without confining the patient to the house. If the bowels become constipated while using either of these prescriptions, the evil may be obviated by taking one of the following pills every evening:

No. 6. Rx. Extract. hyoscyami, (2.00 grams) gr. xxx; Ferri sulphatis, (2.00 grams) gr. xxx; Pulveris aloës, (2.00 grams) gr. xxx; Pilulæ hydrargyri, (2.00 grams) gr. xxx.

M. et ft. pil. No. XXX. If one pill taken every evening does not prove sufficient to prompt one natural intestinal evacuation each morning, another can be taken after breakfast. The patient should adhere to a plain, nutritious, and easily digestible diet, avoiding the use of all varieties of alcoholic drinks, wear good warm underclothes of flannel all the time, and take moderate daily outdoor exercise so long as the strength will permit.

{182} In addition to the several remedies that have been mentioned as applicable to the treatment of the different varieties of acute and subacute bronchitis, there are many others that have been found more or less beneficial in the treatment of chronic cases. Among the more important of these are the iodide of potassium and sodium, the grindelia robusta, eucalyptus globulus, oenothera biennis, cimicifuga racemosa, asclepias tuberosa, balsams copaiba and tolu, gum benzoin, turpentine, cod-liver oil, and the hypophosphites of sodium, calcium, and iron; and a still larger number that have been used for inhalation. As a general rule, when the cough is harsh and the expectoration scanty, with the predominance of dry râles, such remedies as the muriate and iodide of ammonium and the iodides of potassium and sodium, given in conjunction with small doses of antimony and some mild anodyne, will produce the best effects. On the other hand, if the expectoration is abundant and of a muco-purulent character, the balsamic and terebinthinate remedies, given in connection with such tonics as the lacto-phosphate of calcium, phosphate of iron, sulphate of quinia and strychnia with codia, hyoscyamia, or lupulin, at night to procure rest, will afford the greatest relief. In some of these cases I have obtained very good effects from a combination of two parts of the syrup of iodide of calcium with one of the fluid extract of hops, given in doses of 4 cubic centimeters (fluidrachm j) each morning, noon, tea-time, and bedtime.

When chronic bronchitis is complicated with pharyngitis and laryngo-tracheitis, much palliative influence may be obtained by judiciously-directed inhalations, either in the form of vapor or atomization. But when the disease is limited to the bronchi alone, inhalations have much less influence over its progress or in relieving the more distressing symptoms. And unless the nature of the material used is judiciously selected with reference to the particular stage and grade of the disease, the inhalations will be more likely to do harm than good. There are two conditions of the bronchi met with in different cases of chronic bronchial inflammation to which local applications can be made in the form of vapor with much benefit. The first is indicated by an abundant purulent or muco-purulent expectoration, sometimes fetid and at other times not. For such the full deep inhalation of aqueous vapor impregnated with some antiseptic and anodyne will be of great service. One of the best combinations that can be used for this purpose is that of carbolic acid with camphorated tincture of opium in the proportion of 2 grams of the former (gr. xxx) to 90 cubic centimeters (fluidounce iij) of the latter; 4 cubic centimeters (fluidrachm j) of this mixture may be put into 250 cubic centimeters (fluidounce viij) of hot water in an inhaling-bottle and the vapor inhaled freely, five minutes at a time, two or three times each day.

The second condition alluded to is characterized by a persistent, harsh, irritating cough, with little or no expectoration, indicating a sensitive and congested condition of the mucous membrane with diminished secretion. Such cases may generally be much relieved by adding to the antiseptic and anodyne mixture just given some one of the oleo-resin or balsamic preparations, of which perhaps none are more efficient than that which is known in the shops as oil of Scotch pine. Four cubic centimeters (fluidrachm j) of this may be added directly to the quantity of the other ingredients already given, and then used in the same manner. The combination thus used appears to allay the morbid sensitiveness and speedily establishes a better secretory action.

There is another important class of cases met with most frequently in persons of both sexes between twelve and twenty years of age. They present a narrow, imperfectly-developed chest, with so sensitive a condition of the bronchial membrane that every trifling exposure to cold and damp air renews the vascular hyperæmia and cough, until both become permanent and the morbid process extends into the connective tissue of the pulmonary lobules, {183} establishing what some call interstitial pneumonia and others fibroid phthisis. In the earlier stage of all this class of cases the systematic daily practice of full, deep inhalations of pure atmospheric air, coupled with a judicious exercise of the muscles of the chest and arms, will do more to remove all symptoms of bronchial disease and preserve the general health of the patient than all the medicines that have been hitherto devised. There is much evidence in favor of using compressed air for inhalation in these and some other cases of bronchial inflammation. The late F. H. Davis of this city, who during his brief professional career gave much attention to the treatment of diseases of the respiratory organs, and had good opportunities for clinical observation, says, when speaking of the same class of young subjects, that "the inhalation of compressed air for from five to ten minutes once or twice a day produced marked and rapid improvement in all the cases. The size of the chest on full inspiration was increased from one-half inch to one inch in the first month, and a habit of fuller, deeper breathing and a more erect carriage was established."[8] But he adds, with proper emphasis, that the inhalations to be permanently curative must be continued faithfully for many months, and be accompanied by a judicious regulation of all the habits of life.

[Footnote 8: See paper read before the Chicago Society of Physicians and Surgeons, April, 1877, on "The Respiration of Compressed and Rarefied Air in Pulmonary Diseases."]

Every physician of much practical experience knows, however, that, in defiance of all the remedies and methods of treatment hitherto devised, there are many cases of chronic bronchial inflammation which will continue, and be aggravated at every returning cold season of the year, so long as the patient lives in a climate characterized by a predominance of cold and damp air with frequent and extreme thermometric changes. And yet a large proportion of these, by changing their residence to a mild and comparatively dry climate, either greatly improve or entirely recover. Consequently, in all the more severe and persistent cases such a change is of paramount importance, and should be made whenever the pecuniary circumstances of the patient will permit. Probably the best districts in our own country to which the class of patients under consideration can resort are the southern half of California, the more moderately elevated places in New Mexico and the western part of Texas, Mobile in Alabama, Aiken in South Carolina, and most of the interior parts of Georgia and Florida. My own observations lead me to the conclusion that the unfortunate invalid, suffering from any grade of chronic bronchial inflammation, can find in some of the regions named all the relief that could be gained in the most celebrated health-resorts on the other side of the Atlantic. But adherence to strictly temperate and judicious habits of life, with regular daily outdoor exercise, is essential to the welfare of the invalid in whatever climate he may choose to reside.

In the foregoing pages I have said nothing concerning the management of those cases of asthma, emphysema, interstitial pneumonia, etc. which often occur either as complications during the progress of bronchial inflammations or as sequelæ, simply because they will all be fully considered in the articles embracing those topics in other parts of this work.

{184}

BRONCHIAL ASTHMA.

BY W. H. GEDDINGS, M.D.

SYNONYMS.--Asthma convulsivum (Willis); Spasmus bronchialis (Romberg); Asthma nervosum; Krampf der bronchien.

DEFINITION.--A violent form of paroxysmal dyspnoea, not dependent upon structural lesion; characterized by wheezing respiration, with great prolongation of the expiration, and by the absence of all symptoms of the disease during the intervals between the attacks.

HISTORY.--Derived from the Greek [Greek: asthmatnô] to gasp for breath, the term asthma was employed by the older writers to designate a variety of affections of which embarrassed respiration was the most prominent symptom, thus including a great number of diseases which a more extended knowledge of pathology has since distributed among other nosological groups. By the earlier authors simple embarrassment of breathing was designated as dyspnoea; if attended with wheezing it was called asthma; while those forms in which the difficulty in respiration was so great as to prevent the patient from lying down were appropriately styled orthopnoea (Celsus). Ignorant to a great extent of pathological anatomy and unprovided with the improved methods of physical diagnosis which we now possess, they described as asthma not only the dyspnoea due to cardiac and pulmonary diseases, but also that occasioned by affections of the pleura and greater vessels. Covering such an extensive range of territory, it was found necessary to subdivide the disease into a number of varieties, each author classifying them according to his conception of the cause, seat, and nature of the trouble. Some of these--e.g. a. dyspepticum--still find a place in medical literature, but the vast majority of them, having ceased to be of any practical significance, have been discarded, and are now only interesting as examples of the crude and fanciful notions which prevailed in an age during which science rather retrograded than advanced.[1] Of the writers of this period, Willis in the seventeenth century is especially worthy of notice as being the first to describe the nervous character of asthma. Without discarding the accepted forms of the disease, he mentions another variety, characterized by spasmodic action of the muscles of the chest, to which he gave the name asthma convulsivum.

[Footnote 1: "Van Helmont, discarding the ancient doctrine of the four humors, attributed asthma to an error of the Archeus, which he conceived to be enthroned in the stomach and to constitute the source of all diseased as well as of all healthy phenomena. This principle, he supposed, sent forth from the stomach a peculiar fluid, which, when it became diseased, gives rise to a morbid state of the parts to which it was conveyed. He moreover imagined that this fluid sometimes mixed itself with the male semen, and thus formed a compound which, as one of its constituents is the means provided by nature for the propagation of the species, possesses the power of generating a disease of hereditary character. Thus, when this compound was conveyed to the articulations, he affirmed it produced gout, and when it took its direction to the lungs it then occasioned asthma" (Baltimore Med. and Surg. Journ. and Review, Baltimore, 1833, p. 300).]

The improvement in physical diagnosis resulting from the brilliant discoveries of Auenbrugger and Laennec greatly curtailed the domain of asthma. {185} With the aid of auscultation and percussion it was discovered that most of the cases hitherto regarded as asthma were only symptoms of some organic disease. Many distinguished authorities, particularly of the French school, went so far as to declare that there existed no such disease as asthma, and that in every case the dyspnoea and other phenomena described under that name were merely symptoms of some organic affection.

Although very generally received at first, it was not long before this too-sweeping reform encountered opposition from various quarters. Cases were observed with marked asthmatic symptoms in which, after death, the most careful examination failed to reveal the slightest trace of textural lesion. The discovery by Reisseisen of muscular fibres even in the minutest bronchi, and the demonstration of their electric contractility by Longet and Williams, afforded a ready explanation of these cases, and led to the opinion--which has since been generally received--that asthma in the modern acceptation of the term is simply a neurosis. The more recent theories in regard to the nature of asthma will be more fully discussed in the portion of our article devoted to the pathology of the disease.

SYMPTOMS AND COURSE.--The following description of an attack of asthma by Trousseau, who was himself an asthmatic, is perhaps the best that has ever been written: "An individual in perfect health goes to bed feeling as well as usual, and drops off quietly to sleep, but after an hour or two he is suddenly awakened by a most distressing attack of dyspnoea. He feels as though his chest were constricted or compressed, and has a sense of considerable distress; he breathes with difficulty, and his breathing is accompanied by a laryngo-tracheal whistling sound. The dyspnoea and sense of anxiety increasing, he sits up, rests on his hands, with his arms put back, while his face is turgid, occasionally livid, red, or bluish, his eyes prominent, and his skin bedewed with perspiration. He is soon obliged to jump from his bed, and if the room in which he sleeps be not very lofty he hastens to throw his window open in search of air. Fresh air, playing freely about, relieves him. Yet the fit lasts one or two hours or more, and then terminates. The face recovers its natural complexion and ceases to be turgid. The urine, which was at first clear and was passed rather frequently, now diminishes in quantity, becomes redder, and sometimes deposits a sediment. At last the patient lies down and falls to sleep."

The next day the patient may feel well enough to pursue his accustomed avocation, and may remain free from all symptoms of the disease until another attack comes on; but more frequently he is confined to the house, if not to bed, the slightest exertion being sufficient to cause dyspnoea; and during the following night there is a repetition of the paroxysm.

If unchecked by treatment, the disease may continue for days, weeks, and in some instances even for months, the paroxysms often increasing in severity until, as in other nervous affections, it ultimately wears itself out.

There is no regularity in the occurrence of the attacks. In some cases they recur every few days, while in others there may be an interval of weeks or months between the seizures. Even in the same case, although the individual paroxysms of the attack may come on at the same hour, there is, except in rare instances, no regularity in the recurrence of the attack itself; and when it does recur at a certain time it is almost always due to some cause which, as in hay asthma, exerts its influence only at that particular period.

In the great majority of cases asthma comes on without any warning whatsoever, but occasionally it is preceded by certain sensations which to the experienced asthmatic are a sure indication that an attack is impending. With some it is only a feeling of ill-defined discomfort; others complain of various disorders of the digestive system--a sense of dryness of the mouth and pharynx, uncomfortable distension of the epigastrium with eructation of {186} gases from the stomach, and more or less obstinate constipation. A troublesome itching of the skin often precedes the attack. Some experience a feeling of constriction around the throat; a profuse secretion of clear urine is a symptom of this stage. Frequent gaping, frontal and occipital headache, are mentioned; but far more constant than all of these are certain symptoms indicative of a mild grade of acute catarrh of the respiratory organs--coryza, with swelling of the Schneiderian membrane and discharge from the nostrils, sneezing, redness of the conjunctivæ with increased lachrymation, and later, as the irritation extends downward, more or less cough.

The attack almost always comes on after midnight, and, as a rule, between the hours of two and six o'clock in the morning. Salter states that nineteen out of twenty cases occur between two and four A.M. There are, however, occasional exceptions to this rule; sometimes the patient is attacked soon after retiring, and Trousseau cites the case of his mother, who always had her attacks between eight and ten in the forenoon, and also that of a tailor, whose paroxysms invariably came on at three o'clock in the afternoon. Indeed, there is no hour of the twenty-four during which the seizure may not take place. Various attempts have been made to explain why it is that the paroxysms of asthma almost invariably occur during the latter half of the night. Many attribute it to a stasis of blood in the lungs caused by the recumbent posture of the patient, while others claim that it is due to a dulling of reflex impression, the patient during sleep failing to perceive the necessity of breathing. Germain Sée, who discredits both theories, inquires why, if the above explanations are correct, does the attack not come on soon after retiring, as is the case with the dyspnoea of cardiac diseases.

The paroxysm of asthma develops very rapidly, but not so suddenly as is claimed by many authors, several minutes to half an hour or more elapsing before it attains its full height.[2]

[Footnote 2: Germain Sée in Nouveau Dictionnaire de Médecine et de Chirurgie, tome iii. p. 617, Paris, 1865.]

The patient, experiencing an urgent desire for breath, instinctively places himself in the position most favorable for the ready admission of air into the lungs. If in bed he sits up, and, resting on his hands or grasping his knees with them, he so fixes the body that the muscles of respiration may work to the greatest advantage. The shoulders are drawn up and the head thrown back. The expression of the face is one of great anxiety--pale at first, then red, and as the attack increases in severity assumes a dusky, bluish tint; the mouth is partially opened, the nostrils are dilated; the eyes, the conjunctivæ of which are much injected, are prominent, with a wild, staring look; and the forehead is moist with perspiration. Others in their desperate struggle for breath spring from the bed, throw open the window, and, regardless of everything save what they believe to be impending suffocation, recklessly gasp in the cold night air. Sometimes the sufferer prefers to kneel before a table or some other article of furniture, supporting his head with his hands. Whatever posture he assumes, he is actuated by the one impulse of placing himself in the position that will enable him to use to the greatest advantage the muscles of respiration and their auxiliaries. The sterno-cleido-mastoid muscles are contracted to the utmost, and, projecting like hard cords, with the aid of other muscles draw the chest upward. The patient instinctively avoids every unnecessary exertion as having a tendency to aggravate his dyspnoea; he speaks but little, and when questioned usually replies with a motion of the head.

In ordinary respiration the inspiratory movement is twice as long as the expirium, the latter, except in forced expiration, being a purely passive act. In asthma this rule is reversed, the expiratory movement being four or five times as long as the inspirium, and is often so slow that it fills the whole of {187} the pause which usually intervenes between the completion of one respiration and the beginning of another. It is sometimes so slow "that it seems as though the lung would never empty itself." In the desperate struggle for breath the respiratory muscles are exerted to the utmost in futile endeavors to expand the chest; with each inspiration there is an elongation of the thorax, but no lateral movement. The chest moves up and down, but there is no expansion; "the muscles tug at the ribs, but the ribs refuse to rise" (Salter), the walls of the chest remaining immovable.

Notwithstanding the all but tetanic contraction of the diaphragm, there is during each inspiration a sinking in of the epigastrium, and in severe cases also of the spaces above and below the clavicles. During expiration the abdominal muscles, especially the recti, are hard and tense, the pressure thus exerted being sometimes sufficient to expel the contents of the lower bowel and bladder.[3] The transversus is also tightly contracted, and a cross furrow above the umbilicus indicates that the contraction of its upper half is opposed to the contents of the abdomen forced down by the distended lung (Biermer). Although the dyspnoea is great, there is no increase in the frequency of the respirations so long as the patient remains quiet, but, on the contrary, they are often less frequent than in health. This slowing of the respiration is also observed in the dyspnoea from laryngeal stenosis in croup, etc.; but in these cases we do not have the prolonged expiration which is so characteristic of asthma (Biermer). At every breath which the patient takes there is a peculiar wheezing sound which may be heard distinctly all over the room; it is usually heard only during expiration, but some authors (Biermer) claim that it is also audible during inspiration.

[Footnote 3: Bamberger's case, as quoted by Riegel, Ziemssen's Pathologie u. Therapie, Leipzig, 1875, Band iv. 2, S. 282.]

On auscultating the chest it will be found that the ordinary vesicular murmur is either entirely absent, or if heard it is only over very limited areas. In the place of it we have an endless and ever-changing variety of dry sounds, such as whistling, cooing, mewing, snoring, etc., technically styled sibilant or sonorous ronchi. They are usually equally diffused over both lungs, but are sometimes confined to one. The sibilant râles afford an index of the degree of spasm, being in mild cases equally audible during both inspiration and expiration, while in severe attacks they are louder during expiration (Biermer). That the vesicular murmur cannot be heard is due not only to its being masked by the louder ronchi, but also to the absence of the condition necessary for its production, the spasmodic constriction of the bronchial tubes or their plugging with tough, viscid mucus preventing the entrance of sufficient air to produce the sound. Sometimes a hitherto occluded tube becomes pervious, and we have vesicular respiration where a moment before only dry sibilant râles were heard. Usually at the close of the attack, when cough sets in, there are occasional moist râles. These become more frequent as the expectoration becomes more abundant. Frequently, however, the paroxysm terminates much more abruptly, the spasm relaxes, and the air rushing through the tubes gives rise to puerile respiration.

During the paroxysm there is, even in the early stages of asthma, more or less distension of the lungs, measurement of the chest showing that its circumference is four to eight centimeters greater than before the attack (Beau). This transitory emphysema, which must not be confounded with that due to structural changes observed in old cases, disappears with the attack, and the lung returns to its normal condition. This distension causes the exaggerated resonance obtained by percussion which is one of the most constant symptoms. At the base of the lung, especially posteriorly and laterally, there is a peculiar modification of the percussion sound to which Biermer has applied the name Schachtelton, from its resemblance to the note produced by striking {188} an empty pasteboard box. Besides this exaggerated resonance, it will be found that the line of dulness on the right side, which marks the upper border of the liver, is fully two inches lower during the paroxysm than before, and that the area of cardiac dulness is somewhat diminished by the overlapping of the distended lung-tissue (Riegel). Another peculiarity elicited by percussion, and to which Bamberger was the first to direct attention, is that in some rare cases instead of moving vertically the line of hepatic dulness remains unchanged during both acts of respiration.

Toward the close of the attack the congested mucous membrane of the bronchi begins to secrete, and there is more or less cough. The matter expectorated consists at first of little balls of tough, semi-transparent mucus not much larger than a pea. It is exceedingly tenacious, and is raised with great difficulty. Examined under the microscope, the sputum is found to consist "of a great number of corpuscles, some of which are polyhedral in form with rounded angles; they are pale, homogeneous, and slightly granular. At first sight they resemble pus-corpuscles, but they are much larger, less circular in form, and have no nucleus. In addition to these corpuscles there are others which are oval, elongated, fusiform, and sometimes linear in shape, but all of them appear to be of the same nature and possess the same refracting power as the corpuscles first mentioned. They are all of them agglomerated in a sort of viscous matter."[4] The expectoration often contains blood, and in some rare instances profuse hemorrhages have been known to occur. Sometimes the matter has particles of soot and coal-dust intermingled with it, the so-called carbonaceous sputum (Sée). In addition to the cells above described, the sputa contains small yellowish-green masses or threads in which are imbedded the peculiar octahedral crystals which Leyden has ingeniously connected with the etiology of asthma, and to which we shall again have occasion to refer.[5] Ungar has recently also discovered crystals of oxalate of lime in the sputa.

[Footnote 4: Germain Sée, Nouveau Dictionnaire de Médecine et de Chirurgie, pp. 612, 613; also, Salter, Asthma, its Pathology and Treatment, Am. ed., p. 944.]

[Footnote 5: Riegel, in Ziemssen's Handbuch d. Pathologie u. Therapie, vol. iv. 2, pp. 268, 285.]

Laryngoscopic examination reveals more or less congestion of the air-passages. "In ordinary respiration the glottis is widely open during inspiration, and at each expiration the arytenoid cartilages approach each other so as to narrow the glottis; but in the labored respiration of asthma the glottis is fixed in the condition of expiration; that is, the glottis is narrowed, and the air enters and is expired through the same narrow space."[6]

[Footnote 6: Steavenson, Spasmodic Asthma, p. 23.]

The embarrassment of respiration and the pressure of the air in the distended alveolæ by impeding the capillary circulation of the lungs prevent the left auricle from receiving its full supply of blood; hence the pulse is small and weak during the paroxysm, but regains its natural volume as soon as its immediate effects are over. The action of the heart, like every other phenomenon of asthma, is subject to constant variation. At one moment it beats tumultuously, while at the next its action may be so feeble as to cause temporary syncope (Sée). The venous blood, unable to overcome the obstacles to its passage, is forced back into the vessels, causing distension of the cervical veins and the jugular pulse sometimes observed in severe attacks. The bluish hue of the face in bad cases is due to cyanosis resulting from insufficient aëration of the blood. The paroxysm is unattended with fever, the temperature, if altered at all, being rather below than above the normal. Coldness of the face and hands is quite a common symptom in protracted cases.

In addition to the nervous sensations described among the premonitory symptoms, patients have been known to suffer from disturbances of a more {189} serious nature during the paroxysm. In some instances there is complete loss of consciousness, and Riegel[7] states that such cases have been known to have tetanic convulsions of the trunk and extremities.

[Footnote 7: Loc. cit. p. 285.]

The course of an attack of asthma is in most cases quite typical, the paroxysms recurring nightly for an indefinite period, and usually increasing in severity until, as in epilepsy and other nervous diseases, it finally exhausts itself. On awaking from the sleep which usually succeeds the final paroxysm the patient, unless the attack has been very mild and of short duration, feels weak and exhausted, but there is no tendency to the recurrence of the dyspnoea; on the contrary, he may expose himself with perfect impunity to the causes which at other times would be certain to produce an attack. The chest feels stiff and sore, the cough and expectoration diminish, and in a few days disappear, and if the disease has produced no organic lesion the patient returns to his usual state of health.

DURATION.--The duration of asthma, except in young persons and in those rare cases in which the cause can be discovered and removed, is very indefinite, the disease lasting for years, if not for life. As the patient grows older the attacks become less severe, but are more frequent. Sometimes a case which has recurred for years and defied the most energetic treatment will all at once recover of itself.

SEQUELÆ.--Although bronchial asthma is essentially a neurosis, and therefore purely functional in its character, it is rare for it to continue for any great length of time without causing some organic affection of the lungs or heart.

The most common sequel of asthma is emphysema. The bronchial tubes being more or less completely closed, either by contraction of their muscular fibres or by plugs of thick, viscid mucus, the air pent up in the parts beyond the obstruction is subjected to the negative pressure produced by the exaggerated inspiratory act, becomes rarefied, and, in obedience to the diminished resistance induced by the partial vacuum in the thorax, causes distension of the air-cells. This condition continues until, the tubes having again become pervious, the natural elasticity of the lung-tissue, aided by the expiratory muscles, forces out the air and permits them to return to their natural size. This is the transitory emphysema to which we have already alluded. Germain Sée[8] regards it as analogous to the paralytic emphysema which occurs the moment the pneumogastric is divided. With repeated attacks the air-cells lose their elasticity and remain permanently dilated. Owing to the constant distension, the walls of the alveolæ become more and more attenuated, until, finally giving way, two or more of them coalesce, forming one large cell. The symptoms of this condition are the same as those of ordinary vesicular emphysema.

[Footnote 8: Op. cit., p. 637.]

Owing to partial occlusion of the afferent bronchi and the altered conditions of pressure mentioned, the blood accumulates in the capillaries during the paroxysm, the lung-cells do not receive their adequate supply of air, and oxygenation is imperfect. In the early stages of the disease this congestion is only temporary, and disappears with the removal of the obstruction, but in those cases in which the attacks are severe and frequent the vessels lose their contractility and remain permanently congested.

The state of chronic congestion just mentioned is occasionally attended with serous exudation into the interalveolar tissue, which by pressing upon the adjacent air-cells causes their obliteration. This oedema, with the remains of the compressed air-cells and the viscid mucus stagnating in the finer tubes, forms the little islets of carnified tissue known as lobular pneumonia.

The most frequent change observed in the bronchial tubes in old cases of asthma is hypertrophy of their muscular fibres, causing thickening of their {190} walls and diminished calibre. In other cases they are dilated, but this condition is due more to the concomitant bronchial catarrh than to the asthma.

Obstructed in its course through the lungs, the venous blood accumulates in the pulmonary artery, and, pressing back upon the right ventricle, excites it to increased action, which in the course of time leads to hypertrophy of its muscular fibres and dilatation of its cavity.

In the early stages of asthma, the face is usually pale during the intervals between the paroxysms, but when the latter become more frequent the impeded circulation causes stasis in the peripheral vessels. The imperfectly-oxygenated blood gives the face a dusky hue, and in severe cases it may become bluish or even violet-colored. The eyes are prominent, owing to the enlargement of the orbital veins (Sée), and the conjunctivæ congested and watery.[9]

[Footnote 9: For a description of symptoms of the above-mentioned secondary affections the reader is referred to the articles on EMPHYSEMA and HEART DISEASE.]

ETIOLOGY.--Predisposing Causes.--Every one is not liable to asthma, and the fact that out of a large number exposed to its exciting causes only a few are attacked justifies the assumption that there is an inherent tendency to the disease. That this tendency is hereditary in its nature is conceded by every prominent writer on asthma except Lebert, who believes this to be only occasionally the case. Thus, of 35 cases collected by Salter, heredity could be traced in 14, of whom 7 inherited the disease from the father, and the remainder from grandparents and other relations. Ramadge gives an instance in which the disease appeared in four generations: an asthmatic father had four children, three of whom inherited the disease; one of the daughters married, and of her two children one became asthmatic; the other escaped, but the disease reappeared in one of her children.[10]

[Footnote 10: Germain Sée, op. cit., p. 668.]

The hereditary tendency may skip one generation, as is the case with Steavenson,[11] who inherited asthma from his grandfather, his father's generation having been entirely free from the disease. In other cases it may alternate with some other neurosis or with gout or rheumatism; for instance, the children of an asthmatic father may be epileptic or gouty and the grandchildren asthmatic, or the asthmatic tendency may develop in one child of an asthmatic family and the gouty diathesis in another. It is by no means necessary for the hereditary transmission of the disease that the father should be asthmatic when the child is conceived, as there are many cases recorded in which asthma developed in children whose fathers had completely recovered before they contracted marriage and never had any subsequent return of the disease.

[Footnote 11: W. E. Steavenson, Spasmodic Asthma, London, 1882, p. 8.]

All authorities agree that asthma is much more frequent among males than females. Of Théry's cases, 60 were females and 80 males. The more recent statistics of Salter show that the males exceed the females in the proportion of two to one. This undue frequency of a purely nervous disease among males appears at first to be at variance with the generally-received opinion that such affections pertain rather to the female sex; but on investigating the ages at which the attacks first come on it will be found that between the fifteenth and thirtieth years--that is, during the period when sexual function is most active--the proportion is reversed, females being attacked much oftener than males.

Asthma occurs more frequently in childhood than at any subsequent period--a fact which may be explained by the great susceptibility of young children to catarrhal affections of the air-passages and to the frequent occurrence at that age of measles and whooping cough (Salter). Of 225 cases collected by Salter, 71 occurred before the tenth year, and of these, 10 began during the first year, the youngest of them being only fourteen days old at the time of {191} the attack. From ten to twenty it occurs less frequently than at any other period of life, but from that age to the fortieth year there is a steady increase in the number of cases. During the next decade, from forty to fifty, the disease diminishes in frequency, and from that period on the number of cases continues to grow smaller and smaller with advancing years, comparatively few commencing after the fiftieth year.

The following tabular statement, compiled by Salter, shows the comparative frequency of asthma during the various periods of life:

From 1 to 10 years, 71 cases. | From 40 to 50 years, 24 cases. " 10 to 20 " 30 " | " 50 to 60 " 12 " " 20 to 30 " 39 " | " 60 to 70 " 4 " " 30 to 40 " 44 " | " 70 to 80 " 1 "

These figures demonstrate the fallacy of the popular idea that old people are especially liable to asthma. Its prevalence during the later periods of life is due to the fact that while, on the one hand, the affection rarely causes death, on the other it is scarcely ever curable except during childhood, and thus the cases contracted at different ages accumulate and form a large aggregate as life advances.

Those cases occurring in childhood and late in life are likely to be associated with more or less bronchial catarrh, while those which come on when the body has attained its fullest development are almost invariably purely nervous in character.

The period of life at which asthma commences is an important element in the prognosis of the disease, the cases occurring in early childhood being likely to end in recovery, while those coming on later in life are exceedingly protracted in their course and liable to lead to organic diseases of the heart or lungs.

Asthma does not appear to be influenced by the seasons, some authors claiming that it is most frequent in summer, while others maintain that the greatest number of cases occur in winter.

Exciting Causes.--Bronchial asthma being a neurosis of the pneumogastric nerve, its exciting causes may be divided into those which act upon the nerve directly, and those which are reflected from more remote parts or organs.

In the first class the irritant may act upon the nerve at its origin in the medulla oblongata or upon some part of its continuity. Various poisons, organic or inorganic, when introduced into the system may so change the character and composition of the blood as to interfere with the nutrition of the respiratory centre, and thus cause more or less embarrassment of respiration; but the attacks of dyspnoea due to these causes are more continuous than those of ordinary asthma, and are wanting in many of the symptoms which we have described as characteristic of that disease. These forms of dyspnoea are usually the result either of some constitutional disease or of some poison introduced into the system, both of which act by diminishing the proportion of red corpuscles in the blood. Of this we have examples in the dyspnoea sometimes observed in syphilis and malarial fever and in lead and mercurial poisoning--the so-called a. saturninum and a. mercuriale. It is true that there have been instances in which the paroxysms of asthma have come on at regular intervals and have yielded to quinine, but it is not regarded as proved that such cases were due to malarial poisoning (Sée).

Enlarged bronchial glands pressing upon the pneumogastric nerve may cause asthma, and this explains why it is so frequent in children after attacks of measles and whooping cough (Williams and Biermer). Others have remarked that asthma is often coincident with hypertrophied tonsils (Schaeffer). In the great majority of cases the exciting cause does not act directly upon {192} the pneumogastric nerve, but upon the skin or some other remote organ, whence it is transmitted to the nervous centre and reflected back through the nerves of respiration to the bronchi.

Biermer believes that the irritant in many cases, instead of being directly transmitted to the medulla oblongata, causes a fluxion to the exposed mucous membrane. He thinks that the absence of catarrhal symptoms is more apparent than real, the evidences of congestion being unappreciable during the early stages of the disease. According to Riegel,[12] the action of the irritant may be explained in one of three different ways--viz. 1st, both the spasm and the fluxion may be the common result of the irritant; 2d, the catarrh may cause the spasm; or, 3d, the spasm may secondarily produce catarrh.

[Footnote 12: Op. cit., p. 256.]

Although cold may not be so frequent a cause of asthma as was formerly supposed, low temperature undoubtedly acts as an irritant upon the terminal branches of the respiratory nerves, especially the pneumogastric, and in the manner just described may produce spasmodic contraction of the bronchi. The effect of cold is of course much more deleterious when it is associated with sudden changes and diminished barometric pressure, high winds from the east and north being particularly prejudicial. Aside from its meteorological characteristics, the locality itself exercises a potent influence in the production of asthma; and here, again, we have an example of the capricious character of the disease. A patient who for years has suffered with asthma may change his residence and find immediate relief, but of the special factors which engender the disease in one place and cure it in another we know as yet but little. It is, however, a generally acknowledged fact that removal from the country to a crowded city will often diminish the severity and frequency of the attacks, and English writers mention numbers of cases of asthma which have been permanently cured by a prolonged residence in the foggy atmosphere of London. A very slight change is often sufficient to afford relief, and sometimes removal to another part of the same city is all that is necessary. The town of Aiken in South Carolina is divided by a ravine into two sections: the elevation, soil, and exposure are alike in almost every respect, but persons have been known to suffer severely with asthma on one side and to enjoy perfect exemption from it on the other. A gentleman who resides at Bath in the same neighborhood is perfectly free from asthma at his home, but invariably has an attack as soon as the train begins to cross the Savannah River at Augusta, which is only a few miles distant. More remarkable still is the case mentioned by a French writer of a young man who was unable to sleep in the front rooms of a house without having a paroxysm, but who did not experience the slightest inconvenience when he occupied the back rooms.

Although removal to the city frequently affords relief, there are exceptions to the rule, and many cases are recorded where a change of residence to the country has effected a cure. Ozone, of which but little is as yet known, is supposed by some to be a cause of asthma, and it is not unlikely that the relief afforded by removal to a large city may be partly due to the relatively small proportion of this agent in the atmosphere of crowded localities.

Dust of various kinds, the pollen of plants, certain vapors, gases, smoke, and the emanations from many species of animals, have all been known to excite attacks of asthma. Some persons are so sensitive that the simple act of brushing their clothes is sufficient to bring on a paroxysm. Others are unable to inhale the perfume of roses, lilies, heliotropes, and many other flowers without suffering with an attack. The dust of hay will often cause paroxysms even in those who are not hay-fever subjects. Since Cullen first published the case of an apothecary's wife who had asthma whenever ipecac was powdered in her husband's shop numerous cases of a similar nature have {193} been recorded. Ramadge relates the case of an employé in the East India Company who was compelled to relinquish a lucrative appointment because the smell of tea always provoked a paroxysm of asthma. Many persons are unable to come into close proximity with horses, rabbits, cats, and other animals without suffering, and Austin Flint of New York experienced great inconvenience when absent from home from sleeping upon feather pillows. In his case the asthmatic attack was not brought on by all pillows, but what it was that made one kind more active than another he was unable to determine.

In persons predisposed to bronchial asthma the eating of any indigestible substance may of itself be sufficient to cause an attack, and even an ordinarily full meal, if partaken of late in the day, may have the same effect. Dyspepsia in its various forms and the presence of irritating substances in the intestinal canal are such frequent causes of asthma that they have led to the establishment of several special varieties of the disease--e.g. a. dyspepticum, a. verminosum.

Asthma is frequently due to uterine and ovarian disorders, the so-called a. uterinum.

Voltolini of Breslau has described cases which were evidently due to the presence of naso-pharyngeal polypi, the attacks disappearing with their removal and reappearing with their renewed growth. These statements have been confirmed by subsequent cases observed by Haenisch. Attention has lately been directed to a number of cases in which the asthmatic paroxysm was found to be associated with catarrh of the naso-pharyngeal and laryngo-tracheal mucous membrane. In such cases it is thought that the irritation caused by the pressure of the swollen mucous membrane upon the adjacent nerves is conveyed through them to the pneumogastric, and thus provokes the bronchial spasm. Daly, Roe, Harrison Allen, Hack, and others have traced the paroxysms of hay asthma to an hypertrophied condition of the mucous membrane over the turbinate bones and septum of the nose, which renders it peculiarly susceptible to the action of the irritants which cause that troublesome affection, and have succeeded in curing many cases by simply removing the diseased tissue.

Mental emotion, if sufficiently powerful, may sometimes prevent the occurrence of the asthmatic paroxysm; thus, Steavenson, referring to his own case, states that although subject to frequent attacks he never had one on going up for an examination; and the writer is acquainted with a patient whose attack of hay asthma could frequently be checked by an exciting game of cards.

Asthma, like other neuroses, is much more frequent among the educated and refined than among the coarser and more ignorant classes of society, and those leading luxurious lives are more liable to the disease than those of simple and frugal habits. Of the various professions, those which involve much exertion of the voice furnish the largest contingent; hence it is common among public speakers, clergymen, and lawyers.

In former days the retrocession of cutaneous eruptions was supposed to play an important rôle in the production of asthma, but of late years this theory of causation has found but few advocates among intelligent physicians, the only author of any prominence who still adheres to it being Waldenburg, who has proposed to designate such cases as a. herpeticum.

PATHOLOGY.--We have elsewhere alluded to the various theories with which the older writers endeavored to explain the phenomena of asthma, and need not here refer to them again.

The first step toward a truly scientific theory of the pathology of asthma was the discovery by Reisseisen of the smooth muscular fibres of the bronchial tubes. These fibres are found not only in the large and medium-sized bronchi, but even in those of the smallest calibre, Kölliker having {194} demonstrated them in bronchioles 0.18 millimeter in diameter. It was ascertained by Williams that by irritating the lung he could cause contraction of these fibres, and Longet subsequently proved that the same effect could be produced by galvanizing the pneumogastric nerve. Guided by these important discoveries, most modern pathologists have arrived at the conclusion that bronchial asthma is a spasmodic contraction of the middle and finer bronchi, dependent upon some derangement in the function of the pneumogastric nerve. This, the so-called spasmodic theory, is not entirely new, Willis, as we have before stated, having described as early as 1682 a variety of asthma which he believed to be the result of a "spasmodic action of the muscles and nerves of respiration," and to which he applied the term "asthma convulsivum." Although revived from time to time, it was not until some two hundred years later, and after Romberg had definitely settled the question of the essential character of the disease, that the spasmodic nature of asthma received general recognition. Bergson adopted it in his prize essay in 1840, and ten years later it found a warm supporter in the person of Hyde Salter, whose valuable contributions have added so much to our knowledge of bronchial asthma. The theory that asthma is due to spasm of the bronchial muscles met with but little opposition until 1854, when Wintrich, after a series of experiments, arrived at conclusions directly opposed to those of Williams and Longet in regard to the contractility of the muscular fibres of the bronchi, and refused to accept the spasm theory on the ground that it afforded no rational explanation of the phenomena of asthma. He believed that the various symptoms of that disease were due to tonic spasm either of the diaphragm alone or of the diaphragm and the other muscles of respiration. These experiments of Wintrich were so carefully conducted, and his standing as a specialist in respiratory diseases so high, that his theory found many supporters, and might perhaps have been generally accepted had it not been for the distinguished French physiologist, Paul Bert, who in 1870, with improved methods of scientific research, succeeded in demonstrating that Williams and Longet were after all correct in their statements as to the contractility of the bronchial muscles.

One of the most zealous advocates of the spasm theory of asthma, and at the same time its most learned expositor, is Biermer,[13] whose classical lecture on that disease, which appeared a short time after the publication of Bert's experiments, is perhaps the most satisfactory work ever published on the subject. He defines bronchial asthma as a "neurosis depending upon tonic spasm of the bronchial muscles and caused by faulty innervation of the pneumogastric nerve." He claims that this theory is confirmed by clinical experience--that the suddenness with which the attack comes and disappears, and the long and forced expiration with the sibilant râles and other evidences of stenosis which accompany it, admit of no other explanation. In support of this view he calls attention to the rapidity with which the paroxysm yields to chloral, all of its symptoms disappearing within from five to ten minutes after the administration of a moderate dose of that agent. Wintrich and his supporters, besides denying the contractility of the bronchial muscles, object to the spasm theory that the distension of the thorax and descent of the diaphragm, both constant symptoms, are incompatible with spasmodic closure of the bronchial tubes, and that constriction from such cause by impeding the entrance of air into the alveolæ would be more likely to cause diminution in the size of the thorax than its enlargement, and that the diaphragm, instead of descending, would be drawn upward. Biermer acknowledges that this to a certain extent is true, and concedes that constriction of the tubes would interfere with both acts of respiration, but claims that it does not do so {195} to the same extent in the two movements. The spasmodic constriction acts as a sphincter which is readily overcome during inspiration, but prevents the escape of air during expiration, the latter movement being slower and less complete than the former. Were the expiratory pressure exerted upon the contents of the alveolæ alone, it would readily overcome the spasmodic constriction of the bronchi, but it also compresses at the same time the bronchioles. "When the bronchi are spasmodically contracted, they are subjected during expiration to the general pressure of that movement plus the pressure of the spastic contraction of the bronchial muscles. The walls of the bronchioles being soft and compressible, the expiratory pressure, instead of overcoming the obstruction and opening them, would tend to close them all the more tightly." He calls attention to an analogous condition which obtains in capillary bronchitis, when, owing to swelling of the mucous membrane and to the accumulation of secretion in the tubes, the alveolæ are cut off. Here, too, the expiratory pressure is often sufficiently powerful to overcome the obstruction, but if under these circumstances it is too feeble, collapse of the lung ensues. When, on the other hand, the inspiration is strong enough to overcome this obstacle, air enters the alveolæ, and, being imprisoned there, causes inflation of the air-cells as in asthma. That collapse of the lung does not occur in the latter disease is due to the fact that the inspiratory act is always sufficiently powerful to overcome the spastic contraction of the bronchioles.

[Footnote 13: A. Biermer, "Ueber Bronchial Asthma," Sammlung klinischer Vorträge, No. 12, Leipzig, 1870.]

The air entering the lung during inspiration is pent up by the spastic constriction of the bronchi, which, acting as a valve, admits of its passage in one direction, but impedes its escape during expiration, and thus causes inflation of the air-cells and insufficient aëration. Owing to the distension of the alveolæ the thorax is expanded and the diaphragm forced downward. A tetanic spasm of the diaphragm lasting for hours, such as that which Wintrich describes, and with which he endeavors to explain the descent of that muscle as well as the other symptoms of asthma, is not only improbable, but is contrary to clinical experience. If the diaphragm were thus spasmodically contracted, it would remain fixed in one position, but Biermer has demonstrated that there is more or less rhythmic movement of that muscle even during the paroxysm; but if no movement of the diaphragm were observed, it would still be no proof of tonic spasm of that muscle, as its immobility might be due to other causes. According to Biermer, the inflation of the lungs and their insufficient ventilation afford a satisfactory explanation of the most important symptoms of asthma, as Breuer[14] has shown, in his paper on the automatic regulation of respiration through the pneumogastric nerve, that various embarrassments of respiration must be corrected by some suitable modification of the act itself; hence when, as in asthma, the lung is unable to empty itself, the expiratory act must be strengthened and prolonged to overcome the obstruction occasioned by the spasmodic constriction of the bronchial tubes; whereas incomplete filling of the lung would necessitate increased inspiratory effort. According to Biermer, "expiratory dyspnoea is as characteristic of obstruction of the finer tubes," be it from spasm, as in asthma, or from stoppage with viscid mucus or from swelling of their lining membrane, as in bronchitis, as the same condition during inspiration is of narrowing of the larger air-passages--an important point in differential diagnosis to which we shall again have occasion to refer. He is unable to explain the relationship between bronchial spasm and catarrhal hyperæmia of the air-passages, but believes that it may be accounted for as follows: "Either the bronchial fluxion causes the spasm--that is, that there exists between them a causal connection--or the hyperæmia and the spasm are the {196} joint effect of the exciting (centripetal) nerves; in other words, both are due to reflex action."[15]

[Footnote 14: "Die Selbsterneurung der Athmen durch den N. vagus," Sitzungsbericht der K. K. Akademie der Wissenschaften zu Wien, Bd. lviii. Abtheilung ii., Nov., 1868.]

[Footnote 15: In presenting Biermer's theory the writer has drawn freely upon that author's well-known lecture on "Bronchial Asthma," as published in Volkmann's Sammlung klinischer Vorträge, loc. cit.]

Another explanation of the phenomena of asthma is that proposed by Lebert,[16] who, although he concedes that bronchial spasm is an all-important factor, denies that it of itself is sufficient to account for the sudden and enormous inflation of the lungs observed in that disease. He doubts the possibility of a valvular closure of the bronchi, as claimed by Biermer, but believes that the bronchial spasm, which he regards as primary, causes secondary spasmodic contractions of the diaphragm and of the inspiratory muscles of the neck and chest. The spasm of the diaphragm he believes to be tonic in its character, but not continuous, thus meeting Biermer's objection to the Wintrich theory, that tonic spasm of that muscle lasting longer than a few minutes would inevitably cause fatal asphyxia.

[Footnote 16: Klinik der Brustkrankheiten, 1ster Band, 2te Hälfte, p. 438.]

Theodor Weber,[17] rejecting the above theories on the ground that neither bronchial spasm nor tonic contraction of the diaphragm is capable of explaining why catarrhal secretion should come on at the close of an attack in which at the commencement there was no catarrh, attributes the phenomena of asthma to sudden swelling of the bronchial mucous membrane, the result of dilatation of its blood-vessels produced through the agency of the vaso-motor nerves; thus reviving the fluxionary theory of Traube. In support of this theory he cites the result of Von Loven's[18] experiments, which prove that irritation of the sensory nerves is followed by reflex engorgement of the territory to which they are distributed. Weber considers that this engorgement of the bronchial mucous membrane is somewhat similar to the acute swelling and stoppage of the nostrils to which many persons are subject--a closure which often does not last longer than a few moments, and which is attended with increased redness and swelling of the Schneiderian membrane. The mucous membrane of the nostril and that of the bronchi being both parts of the respiratory tract, and somewhat similar in structure, he concludes that the process in the nostrils is analogous to that which occurs in the bronchi during the asthmatic paroxysm. As additional proof of the correctness of his hypothesis he cites the fact that such occlusion of the nostrils is often the precursor of the asthmatic attack, and in some cases continues throughout the paroxysm. See investigations of Daly, Roe, Allen, and Hack, further on.

[Footnote 17: "Ueber Asthma Nervosum," Tageblatt der 45 Versammlung deutscher Naturforscher u. Aertze in Leipzig, etc., 1872, p. 159.]

[Footnote 18: Naturforscher u. Aertze in Leipzig, etc., 1872, p. 159.]

The idea that asthma is due to swelling and engorgement of the bronchial mucous membrane appears to have been confirmed by the tracheoscopic observations of Stoerk.[19] On examining the air-passages with the laryngoscope, he could see the mucous membrane of the trachea as far as visible (that is, to the bifurcation) grow red with the onset of the paroxysm, and resume its normal appearance after the termination of the attack. He opposes the spasm theory, denies the correctness of Biermer's conclusions, and adopts Weber's explanation of the asthmatic phenomena. He agrees with Wintrich that spasm of the diaphragm occurs, but claims that it results from the tension to which it is subjected by the inflated alveolæ: the diaphragm being forced downward by the distended lung, its fibres are stretched, and the result is a tonic spasm of that muscle. His objections, although well stated, are not sufficiently conclusive to cause us to accept his opinion in preference to that of Biermer and other supporters of the spasm theory.

[Footnote 19: Mittheilungen über Asthma bronchiale, etc., Stuttgart, 1875.]

{197} Max Schaeffer maintains that asthma is due to bronchial fluxion, as advocated by Weber, but claims that the hyperæmia is followed by spasm of the bronchial muscles, the former being primary and the latter secondary. He also, with many other recent writers, believes that asthmatic attacks are often associated with pathological conditions in and about the upper air-passages, such as naso-pharyngeal and laryngo-tracheal catarrh, polypi, hypertrophied tonsils, and enlarged cervical glands; all of which act as irritants, which, being transmitted through the neighboring nerves to the vagus, induce the bronchial spasm.

Among the older and discarded theories is that of Bree, who in a work published at the commencement of the present century expressed the opinion that the dyspnoea of asthma was simply an effort on the part of nature to rid the bronchial tubes of an irritating substance supposed to have accumulated in them previous to the attack. He believed that this materia peccans was thrown out with the expectoration which occurs toward the close of the attack. He regarded the violent efforts made by the respiratory organs to expel this offending substance from the bronchial tubes as similar to the tenesmus of dysentery or the painful contractions of the bladder when irritated by a rough calculus. Bree was unable to define more clearly the nature of this offending substance, but of late years another writer, Leyden,[20] has discovered in the sputa of asthmatics certain peculiar crystals to the irritating effects of which he attributes the various symptoms. These crystals had been observed previously by Charcot in the blood of leukæmic patients, and subsequently by Neumann in the medulla of the bones of patients who had died of that disease. Leyden describes the expectoration in asthma as tough, grayish-white, and very frothy. Imbedded in a transparent hyaline mass are a number of small bodies, some thread-like, others in the form of little plugs or flakes. Under the microscope these little bodies are found to consist of a mass of brownish cellular detritus containing large numbers of crystals. These are colorless, octahedral in form, with sharp points, and vary greatly in size, some of them visible at once, while others are seen only with the highest powers of the microscope. Their composition has not been determined, but is supposed to be a substance resembling mucin. Leyden's idea is that the sharp points of these octahedral crystals irritate the terminal ends of the pneumogastric nerve in the mucous membrane of the bronchi, and that this irritation, being transmitted to the nervous centre, is reflected back, and thus causes spasm of the bronchial muscles. It seems, however, that these crystals are not peculiar to bronchial asthma, having been also found in chronic catarrh and other affections of the bronchi.[21]

[Footnote 20: "Zur Kentniss des Bronchial Asthmas," Virchow's Archiv, Band liv., 1871.]

[Footnote 21: Not being able to obtain the original paper, the writer is indebted for the greater part of what he has written in regard to the Leyden theory to the treatises on asthma by Knauthe in Eulenburg's Encyclopædie der gesammten Heilkunde, and by Riegel in the work already quoted.]

Of the different theories of bronchial asthma which have just been presented, that of Biermer, although unsatisfactory in many respects, offers the best explanation of the pathology and symptoms of that disease.

PATHOLOGICAL ANATOMY.--Bronchial asthma being a purely functional neurosis, the organs involved present no anatomical changes specially characteristic of that affection. It is true that in cases of long standing, in which, owing to oft-repeated attacks, the air-cells have become distended and their walls attenuated, we find the lungs in the condition which will hereafter be described as emphysema, but these, as well as the evidences of chronic catarrh observed in these cases, are due to the secondary affections, and not to the primary disease.

As previously stated, a certain amount of hyperæmia of the mucous {198} membrane of the larynx, trachea, and bronchi may be observed during life with the aid of the laryngoscope; but whether this condition leads to permanent tissue-changes observable after death is exceedingly doubtful.

In the pneumogastric nerve pathologists have as yet been unable to discover, either at its origin or along its course to the lungs, any alteration in structure capable of explaining the phenomena of bronchial asthma.

DIAGNOSIS.--The suddenness of the attacks; the occurrence of the paroxysm usually in the latter half of the night; the slow, labored expiration, with the whistling, wheezing sounds which accompany it; the expectoration of catarrhal sputa toward the close of the attack; the normal respiration and absence of all signs of disease during the interval between the paroxysms,--are the features by which a case of simple uncomplicated asthma may be readily recognized. When these symptoms are present in their integrity in an otherwise healthy subject, there is no difficulty in arriving at the diagnosis; but, unfortunately, the picture is not always complete. The asthma may be complicated with organic disease of the heart or lungs, while primary disease of these organs, as well as certain affections of the nervous system, may produce symptoms closely resembling those of bronchial asthma, and from which it is very essential to distinguish them.

The following are some of the affections which may be mistaken for bronchial asthma:

1. Bronchial catarrh may be accompanied with more or less difficult respiration, but even in its worst forms it never causes the severe attacks of dyspnoea observed in bronchial asthma, and, as Riegel justly remarks, the severity of the symptoms in the latter disease are out of all proportion to the insignificance of the physical changes.

The dyspnoea of bronchitis comes on more gradually, the attacks being dependent upon a variety of accidental circumstances; whereas the asthmatic paroxysm usually occurs quite suddenly in the night without any apparent cause. The cough in bronchitis is severer and the expectoration more abundant than in asthma; the latter is also different in quality, becoming purulent as the disease advances, whereas in asthma it seldom loses its mucous character. These points of difference and the presence of the other symptoms of bronchitis are sufficient to differentiate that disease.

2. Emphysema is frequently associated with asthma, either as a cause, as is believed by many, or as an effect of that disease. It is often exceedingly difficult to determine whether the emphysema when present is the cause of the dyspnoea (symptomatic asthma), or whether the inflation of the air-cells and other symptoms are not the result of the bronchial spasm: a careful inquiry into the history of the case will often decide the question. The points of difference between the two diseases are very similar to those to which we have just called attention as the distinguishing features between the dyspnoea of bronchitis and the true asthmatic paroxysm. The suddenness with which the attack comes and goes, the severity of the symptoms compared with the insignificance of the local lesions, the absence of dyspnoea in the intervals between the attacks (in uncomplicated cases), are all the reverse of what is observed in emphysema. In that disease the attacks develop more gradually; there is always more or less shortness of breath, and the evidences of changes in the structure of the lung are quite marked.

3. Dyspnoea resulting from cardiac disease is often very severe, but may be distinguished from bronchial asthma by the presence of the various murmurs and other physical signs by means of which that class of diseases is recognized. The asthmatic paroxysm, as a rule, comes on when the patient is most quiet, usually during sleep. The attack of cardiac dyspnoea, on the contrary, is always brought on or aggravated by physical exertion, mental excitement, or some other apparent cause. In asthma the respiration during {199} the intervals between the paroxysms is quite natural; in cardiac dyspnoea there is always more or less embarrassment. Pain in the region of the heart, in many cases quite severe and extending down the left arm, may direct attention to that organ as the source of the dyspnoea.

4. Spasm of the glottis, croup, oedema of the glottis, tracheal stenosis, are all attended with more or less violent attacks of dyspnoea. We are indebted to Biermer for having directed attention to an important symptom by means of which all these affections may be distinguished from bronchial asthma. In the latter, and in all other diseases causing narrowing or obstruction of the finer bronchi, the dyspnoea is during the expiration, but if the impediment be in the larger air-passages the dyspnoea will be during the inspiration. "Dyspnoea during expiration is just as characteristic of narrowing of the finer bronchi as the same condition during inspiration is of croup and other forms of laryngeal stenosis." In croup the neck is extended and the head thrown back. Notwithstanding the violent inspiratory efforts of the patient, the lungs are but partially filled; the air in them becomes rarefied, causing a yielding of the less-resisting parts of the thorax--e.g. the supraclavicular space, the lower portion of the sternum, and adjacent costal cartilages--and a sinking in of the abdomen. During expiration, which is accomplished quickly and with comparative ease, the thorax resumes its natural form. In bronchial asthma, on the contrary, the head is thrown forward, and the shoulders fixed in such a position as to enable the muscles of expiration to work to the best advantage. The thorax, instead of sinking in, is expanded and abnormally round, giving on percussion the peculiar pasteboard-box sound (Schachtelton) which Biermer has described as characteristic of inflation of the alveolæ. In croup the sibilant râles are heard during inspiration, while in asthma they are more pronounced during expiration.

5. Spasm of the diaphragm is another affection from which it may be necessary to distinguish bronchial asthma. This rare disease, which is almost always associated with hysteria, is characterized by a short inspiratory movement, during which all the muscles of inspiration are brought into action, and we have the same sinking in of the more yielding portions of the thorax which has just been mentioned as one of the distinguishing features of laryngeal stenosis. After this the thorax remains fixed for a few seconds, the muscles of inspiration remaining in a state of contraction. There then ensues a quick and powerful expiratory effort, accompanied by a sound not unlike that of hiccough; then another inspiration, with a repetition of the above symptom; and so on until the attack is over. It will be seen from this description that this affection resembles singultus more than asthma, and that there is but little likelihood of its being mistaken for the latter disease.

6. Paralysis of the posterior crico-arytenoid muscles, like croup, spasm of the glottis, and all other affections which produce narrowing of the larger air-passages, is distinguished by the dyspnoea being inspiratory, and not expiratory. The function of the posterior crico-arytenoid muscles being to enlarge the glottis, the result of their being paralyzed would be to lessen the opening through which the air passes to reach the lung; and in viewing the cords in such a case with the laryngoscope it will be found that the opening is reduced to a narrow chink. Another distinguishing feature is that the dyspnoea is continuous, and, unlike bronchial asthma, does not come on in paroxysms.

7. An affection which, like asthma, comes on in the night during sleep is the condition known as nightmare, and, like the former disease, is characterized by labored breathing. To distinguish it, it is only necessary to awaken the patient, when the immediate cessation of all symptoms will at once remove all doubt as to the nature of the affection.

8. Through carelessness or ignorance intercostal neuralgia has been {200} sometimes mistaken for asthma. Pain along the course of the nerve and the presence of the points douloureux, which Valleix has described as characteristic of neuralgic affections, are sufficient to establish the diagnosis.

9. Embolism of one of the middle or larger branches of the pulmonary artery is also characterized by great embarrassment of respiration, but is not likely to be mistaken for asthma by any one at all familiar with the two affections. The cachectic appearance of the patient, the intense anxiety depicted on his countenance, the evidence of cardiac disease or of some affection of the vessels, the weakened cardiac impulse, the thready and at times irregular pulse, together with evidences of more or less pulmonary oedema, are sufficient to distinguish this form of dyspnoea from that of asthma.

PROGNOSIS.--As there is no well-authenticated case of death from uncomplicated asthma, the prognosis quoad vitam may be regarded as absolutely favorable. That death never occurs during the severe paroxysms of asthma may be due to the action of the deficiently aërated blood upon the respiratory centres, and bronchial spasm, causing relaxation when the symptoms have become most threatening. The asthmatic, if his case be incurable, may live for a number of years, and even attain to extreme old age, but his life will be one of intense suffering, which becomes more intolerable as he advances in years. Sooner or later, bronchitis, emphysema, or heart disease is developed, which in its turn may lead to renal disease and dropsy.

Such is the almost invariable result in middle-aged and elderly persons; in the young, however, the chances of recovery are much more favorable. Salter[22] states "that in youth the tendency is invariably toward recovery, whereas in one attacked with it after forty-five the tendency is generally toward a progressive severity of the disease and the production and aggravation of those complications by which asthma kills." The favorable result in childhood he attributes to the recuperative power of youth: growth and change, being more rapid than later in life, enable the system to repair during the intervals whatever damage may have been sustained during the paroxysms.

[Footnote 22: On Asthma, Am. ed., p. 168.]

There is another class of cases in which, owing to our being able to recognize and remove the cause, the prognosis is quite favorable: thus, if it has been discovered that the disease is due to some local influence, change will often effect a cure, and the patient will remain well as long as he remains in the locality which agrees with him, but generally relapses if he ventures to return to the place where he first contracted the disease. The same may be said of that form of asthma in which the disease is due to some trade or pursuit necessitating the inhalation of irritating dust or gases: the indications are obvious. Cases in which the paroxysms have been traced to the presence of nasal polypi or to a tumor pressing upon the course of the pneumogastric nerve have been promptly cured by the removal of these growths. In all these cases it is presupposed that there is no organic disease, for the presence of any one of the serious complications we have mentioned would dissipate all hope of cure.

In arriving at a prognosis it is all-important to inquire into the severity and frequency of the attacks, as violent paroxysms at short intervals soon lead to incurable complications. It is also essential to ascertain the condition of the patient during the intervals between the paroxysms: if at that time he feels well and does not suffer with shortness of breath, we may infer that as yet no organic change has occurred; if, however, he complains of more or less dyspnoea during the intervals, we may safely conclude that some organic disease has set in and that the case is incurable. Salter attaches great importance to the persistence of expectoration during the intermissions, regarding it as indicative of bronchitis, and therefore as an unfavorable indication: to use his own words, "Spitting is one of the worst signs in asthma."

{201} Briefly, those cases may be regarded as favorable in which the patient is young and has no inherited tendency to the disease, is free from the many complications of asthma, and in whom the attacks are light and occur at long intervals. On the other hand, all cases may be regarded as unfavorable in which the patient has reached or passed the middle period of life, has inherited a tendency to asthma, if the attacks are severe with short intervals, or if he has some one or more of the secondary affections of the disease.

TREATMENT.--The treatment of bronchial asthma consists of measures to mitigate and relieve the paroxysms and prevent their recurrence.

A. Of the Paroxysm.--A patient suffering with an attack of asthma will generally instinctively assume the position in which he can use the muscles of respiration to the greatest advantage, but if found in the recumbent posture he should be advised to sit up in bed and grasp the knees with his hands, so as to gain a position which admits of the more ready entrance of air into the lungs. In severe cases it is better to have him rise from the bed and support the head with the hands, the elbows resting on a table in front of him. An ingenious suspension-apparatus, intended to promote the comfort of persons suffering with severe dyspnoea, was extensively advertised several years ago, and may possibly still be furnished by the instrument-makers. It consists of a cross-piece suspended from the ceiling, to which straps are attached for supporting the shoulders without in any way pressing upon the chest; it is also provided with a band for the support of the head. In severe and protracted cases, when, notwithstanding the patient's exhaustion, he is unable to rest upon pillows, such an arrangement might afford great relief. If not undressed, the clothing should be so arranged as to interfere as little as possible with the respiratory movements. An abundant supply of fresh air is essential, and to secure this one or more windows should be thrown open.

Asthma being the most capricious of diseases, remedies often acting differently in each individual case, it is well before commencing treatment to follow Salter's advice and inquire of the patient what remedy has usually afforded the most prompt relief in previous attacks, and thus avoid the risk of prolonging suffering by using remedies which, although apparently indicated, may in his case, owing to peculiar idiosyncrasies, prove to be useless or even injurious.

We have seen that the disease is often due to some special cause, such as the inhalation of an atmosphere laden with the perfumes of certain flowers, with ipecac, dust, etc., the removal of which, if practicable, should of course precede all attempts at treatment. The condition of the stomach and bowels should be inquired into, and if found overloaded they should at once be relieved, the one by an emetic and the other by enema.

In the absence of any hint afforded by the previous experience of the patient the choice of the remedial agent will depend upon the severity of the attack. In the majority of cases, when severe, no remedy will afford such prompt relief as the subcutaneous injection of morphia. To be effective, the dose should be a full one, a fourth to a third of a grain, either alone or, if there is likelihood of this occasioning nausea, combined with one one-hundredth to one-eightieth of a grain of sulphate of atropia. The writer is aware that the use of opium and other hypnotics in bronchial asthma is discouraged by one of the most distinguished authorities on that disease, Salter, who claims that they are not only worthless, but often injurious. He believes that sleep tends to promote the paroxysm, reflex action being much more active then than during the waking hours, and that any agent which induces such a condition is necessarily contraindicated--that, in his opinion, in addition to exalting reflex action, it acts prejudicially, as "by lowering sensibility it prevents that acute and prompt perception of respiratory arrears which is the normal stimulus to those extraordinary breathing efforts which are necessary to restore the balance." These objections, although supported by {202} scientific evidence, are insufficient to cause the abandonment of an agent which in the hands of others has proved so prompt and efficacious in relieving the terrible sufferings of asthma, and Salter himself admits that since writing the above he has had cases in which it has been of signal service. A serious objection to its use is that the dose has to be increased as the patient becomes accustomed to its use. In confirmation of its marked beneficent effects, I give the following extract from Steavenson's treatise on asthma. Describing his own experience, he says:[23] "Sedatives and antispasmodics I should consider most serviceable drugs, but above all in value I should place the hypodermic injection of morphia. This has never failed to relieve an attack in myself, and I have never seen it fail in other patients. The objection to it is that if often used the dose must be increased; but it is better to increase the dose of morphia than suffer the agonies of asthma and allow those organic changes in the constitution to take place which I have described when speaking of the pathology of the disease. I have now used morphia for five years, but my attacks are so quickly relieved and so reduced in frequency that I have never yet had to increase the dose I commenced with--namely, one-sixth of a grain."

[Footnote 23: Op. cit., p. 29.]

Having administered the morphia, other measures for the relief of the patient should be resorted to. The feet and hands should be immersed in hot water to which a small quantity of mustard has been added. Dry cups between the shoulder-blades or sinapisms over the chest or epigastrium often afford marked relief.

If, on account of the existence of an idiosyncrasy on the part of the patient or from other causes, opium cannot be employed, we have in chloral hydrate a substitute which is almost as efficacious and perhaps even more prompt. Next to morphia, it is the most valuable remedy, and many esteem it superior to that drug, over which it possesses the advantage of not being followed by the disagreeable effects which so often succeed the administration of opiates. It should be given in doses of thirty or forty grains, and repeated if the paroxysm does not yield.

The inhalation of chloroform has long been esteemed as a potent agent in overcoming the bronchial spasm. One would naturally suppose that the use of such a powerful sedative as chloroform would be a dangerous proceeding in a disease which, like asthma, is attended with so much embarrassment of respiration and circulation; but experience does not justify this fear, and Salter, who has used it with good effect in 12 out of 13 cases, assures us that he has administered it "in the very agony of the worst attacks; that, so far from fearing it under such circumstances, it has been able to relieve the intensest asthma that nothing else would reach; that he has given it, and that he has never seen any bad effects from it." He goes on to state that as chloroform relaxes the bronchial spasm, and thus removes the cause of the "asphyxial stoppage, the intensity of the apnoea, so far from being a reason against the administration of chloroform, is the great reason for its immediate employment." He considers neither muscular weakness of the heart nor valvular disease as any contraindication to its administration, provided the circulation is not materially affected. According to Stokes, the paroxysm is not entirely suppressed by chloroform, but returns as soon as the patient passes from under its influence; hence it must be repeated as occasion may require. It should always, if possible, be given at the commencement of the paroxysm, and should never be allowed to produce complete insensibility, nor should so seductive a remedy be left in the hands of the patient. The danger of the self-administration of chloroform is only too well attested by the frequent accounts in the journals of persons found dead in their beds from the effects of that agent, death in such cases being usually due to the patient's {203} unconsciously leaving the handkerchief over the mouth and continuing to inhale the chloroform after having become insensible. When given sufficiently early, a few whiffs may be all that is necessary to overcome the paroxysm; and this repeated as soon as it threatens to return, will often enable us to control the symptoms without resorting to larger quantities.

An old and still very popular treatment--said to have been introduced by an American, Nicholas Frisi,[24] in 1843--consists of the inhalation of the fumes of burning saltpetre or in smoking cigarettes made of paper which has been soaked in a saturated solution of that substance. Inhaled into the bronchi, it is supposed to act as an anæsthetic, and produces relaxation of the constricted bronchial muscles. In point of efficiency these inhalations rank quite high, and are probably more generally used than any other remedy. Aside from the relief which they undoubtedly afford, this method derives much of its popularity from being within easy reach of the patient himself. The preparation of the papers is exceedingly simple: A sheet of bibulous paper is dipped into a saturated solution of the nitrate of potassa prepared with cold water; after drying it is divided into strips of the size required. These papers are burnt before the patient, the windows and doors of the apartment having been previously closed to prevent the escape of the fumes. Nitrate of potassa has been prepared in a variety of other ways for the use of asthmatic patients, one of the most convenient of which is the Kidder pastilles so extensively used in this country. Another method is to roll the paper prepared as above into cigarettes, the smoke of which is inhaled by the patient. The nitre is best used early in the attack, but is also beneficial when the paroxysm is at its height. The efficacy of this treatment is attributed by Germain Sée to the formation of protoxide of nitrogen and carbonic acid gas, which act as an anæsthetic, and perhaps also to the particles of carbon in the smoke floating in the air, a smoky atmosphere being beneficial to many asthmatics.

[Footnote 24: Germain Sée, op. cit., p. 709.]

The smoking of the Datura metel having been found efficacious in asthma in India, Anderson of Madras in 1802 sent some of the leaves to Gen. Gent, an English officer, by whom they were introduced into England. Simms of Edinburgh, believing that the Datura stramonium might prove equally good, tested it with such good results that it soon came into general use, not only in asthma, but in other forms of dyspnoea. This is the ordinary Jimson or Jamestown weed which is so widely distributed over the Southern, Middle, and Northern States, and, like nitrate of potassa, is much used, not only by the profession, but largely as a household remedy for asthma. The dried leaves are either smoked in a pipe or in the form of a cigarette. The effects, however, are quite uncertain, sometimes acting like a charm, while at others it affords no relief; its physiological action is that of a sedative. Of late years another species of Datura has been introduced--the Datura tatula. Its properties and uses are similar to those of stramonium, but it is supposed to be less narcotic.

Belladonna and its alkaloid, atropia, are often used in the treatment of asthma, but their action is uncertain and often unsatisfactory. The three last-mentioned remedies are also used in combination, as in the well-known Espic cigarettes, the formula for which, according to Trousseau, is as follows, viz.:

Rx. Fol. belladonnæ, gr. vj; Fol. hyoscyami, gr. iij; Fol. stramonii, gr. iij; Fol. phillandrii aquatic. gr. j; Ext. opii, gr. ¼; Aq. lauroceras, q. s.

{204} The leaves, after being cut up, should be thoroughly mixed, after which they are moistened with the cherry-laurel water, in which the opium has been previously dissolved. The wrapper of the cigarette is also soaked in the same solution and dried. One or two of these cigarettes should be smoked during the attack. Abbott has been very successful with belladonna applied as a spray (drachm j of the extract to one ounce of water) when the spasm threatens.

Tobacco is a powerful depressant, and in those who are unaccustomed to its use is an invaluable remedy in asthma. In the uninitiated it excites nausea, vertigo, cold sweats, and other symptoms of relaxation which Salter not inaptly compares to those of sea-sickness. "The moment this condition can be induced the asthma ceases, as if stopped by a charm." It may, however, be asked whether the remedy is not worse than the disease. Those who retain a vivid recollection of the horrible consequences of their first smoke will hesitate before prescribing tobacco for one unaccustomed to its use. There are many who, not wishing to lose the beneficial effect of tobacco in asthma, never smoke unless a paroxysm threatens.

Lobelia, like the above also a depressant in its action, was formerly much employed in asthma. It is still used, but its effects are disagreeable and by no means certain.

The intimate nervous connection which exists between the lungs and stomach would naturally lead us to anticipate good results from emetics. In asthma, as in laryngismus stridulus, an emetic often affords prompt relief and arrests the paroxysm. The nausea which precedes the act of vomiting, acting as a depressant, causes relaxation of the spasm, while the emesis by unloading the stomach removes an important source of irritation. Like tobacco and lobelia, remedies of this class are only beneficial when pushed far enough to produce the symptoms of depression and collapse to which we have alluded; these once established the relief is usually complete. Tartar emetic and ipecacuanha are the representatives of this class most used in asthma. Tartar emetic, owing to the excessive and long-continued depression which it occasions, is now rarely employed, having been almost entirely superseded by ipecacuanha, which is equally efficacious and more prompt. Its effects also disappear more rapidly than those of antimony. Like other remedies intended to cut short the paroxysm, ipecacuanha should be given as early as possible. It should be taken in full doses of at least twenty grains.

Bromide of potassium, as is well known, acts upon the vaso-motor nerves, causing contraction of the arterioles of the brain and spinal cord, and thus inducing a state of partial anæmia which results in a lessening of the irritability of these organs, quieting muscular spasm and inducing sleep. These effects would naturally lead to its employment in spasmodic asthma. Although occasionally used with success in shortening the paroxysm, it is better adapted, as suggested by Riegel, for use during the intervals, when, if given continuously, it sometimes diminishes the severity of the paroxysms and causes them to recur less frequently.

Nitrite of amyl, a most valuable addition to our materia medica, has been extensively used in the treatment of asthma, but the reports of the results attained are too contradictory to admit of our forming any just estimate of its merits. The general opinion is that it relieves the dyspnoea and makes the patient for the time being more comfortable; and this accords with my own experience. The usual method of administration is to drop one or more minims upon a handkerchief and to inhale the vapor. It is also used internally, and, in the single case that has come under my observation, with benefit. The following case, reported by Pick and cited by Riegel,[25] is instructive as showing the favorable effects of nitrite of amyl: "The case was that of a medical student who from his youth onward had suffered with {205} asthmatic troubles, which increased as he grew older and had proved rebellious to all remedies. Nothing except expectorants and narcotics afforded him the slightest amelioration of his symptoms. On inhaling nitrite of amyl he experienced immediate relief, which lasted for some time after the inhalation. He was enabled to breathe deep and with comparative ease. The relief afforded was but transitory, but, on the other hand, was so sure that the patient resorted to it whenever the attack came on." The same writer reports two other cases in which he succeeded by means of nitrite of amyl in relieving the paroxysms and in increasing the interval between them.

[Footnote 25: Op. cit., p. 295.]

More agreeable to the taste and at the same time more effectual than the potassium iodide is hydriodic acid. It is best administered in the form of a syrup, preferably that prepared by Gardener of New York.

Salter, who appears to have had more experience with alcohol than any other writer, narrates the case of an elderly Scotch lady who, having exhausted all the known medicines and other agents used in asthma, was finally relieved by full doses of whiskey. This was invariably successful, but the dose, of course, had to be increased as the disease grew older. He also mentions another case in which nothing except chloroform afforded any relief. This he describes as the severest he has ever witnessed. "I have never seen or heard of spasms so violent or that seemed so nearly to put life in peril. His most intense spasms he calls 'screaming spasms,' from the strangling cries that the want of breath compels him to make. At the time of which I am speaking he lived on the same street with myself, and, although his house was half the length of the street from mine, his nurse has often assured me that if the doors had been open I could have heard his screams at my house at night. All remedies except the chloroform had failed, when one day his nurse advised him to try brandy. It afforded him almost instantaneous relief. He took enormous quantities of it, the first day a quart, and in the course of two months as much as twelve gallons. The spasm invariably stopped as soon as he took it, and for the last five months that he was under observation he had only what he called a 'thickness, a tight, constricted breathing,' several times during the night." Salter is particular in stating that the brandy should be given strong and hot.

Another stimulant highly recommended by Salter is coffee. In stating his objections to the use of opium it will be remembered that one of his reasons for not availing himself of that remedy was that it caused sleep, and that the exaltation of reflex action in that state favored the asthmatic paroxysm. Coffee, being a strong excitant of the nervous and vascular system, has the contrary effect and keeps the patient awake. It should be prepared as a strong infusion without the addition of either sugar or milk and given some time before the expected paroxysm. Administered in this manner, he claims that coffee will relieve two-thirds of all cases of asthma. The relief afforded is, however, very unequal, being in some cases complete, while in others it is only slight and transitory.

Quebracho in the form of an extract has been much used of late years in the treatment of asthma and other affections attended with dyspnoea. It has been found quite useful in mild cases.

The induced electrical current has been recommended by Schaeffer as a means of cutting short the paroxysm. His method is to place one pole on either side of the neck immediately below the angle of the jaw and in front of the sterno-cleido-mastoid, so as to cover the course of the pneumogastric and sympathetic nerves. The current should be sufficiently strong to enable the patient to feel the passage from one side of the throat to the other. It is applied for fifteen minutes twice a day for six days, twelve sittings being usually sufficient to afford relief. When the current is first applied it not {206} infrequently causes dilatation of the pupils, but this is succeeded by contraction when the treatment begins to manifest its beneficent effects.

B. During the Intervals between the Paroxysms.--The diet and daily regimen of the asthmatic should be most carefully regulated, the best and most skilfully directed treatment being of little avail if these important matters are neglected.

The asthmatic patient should be encouraged to pass much of his time in the open air, but the amount of walking he should do will of course depend upon his strength and freedom from secondary affections of the heart and lungs. In a case of simple uncomplicated asthma the more the patient walks the better he will feel; but this is not to be construed to mean that he is to walk until exhausted; on the contrary, his walks should at first be quite short, proportioned to his strength and wind, and then gradually extended, but under no circumstances should he be allowed to overfatigue himself. With a view to keeping the skin in the best possible condition the body should every morning be sponged with water, the temperature of which must be suited to the condition of the patient. If he be feeble and anæmic, the water should be tepid, but whenever admissible cold is to be preferred. After the bath it is essential that the skin be thoroughly rubbed with a coarse towel until it becomes slightly reddened. The cold bath properly used not only invigorates the system generally, but by enabling the body to stand the vicissitudes of temperature diminishes the risk of the patient's taking cold.

The intimate relations existing between the lungs and stomach, and the fact that asthmatics usually suffer at the same time with dyspepsia, make the question of diet an all-important one. Their meals should consist of good, nutritious food, rigidly excluding all heavy, indigestible substances, such as cheese, nuts, dried fruits, etc. The meals should be taken at regular hours, and, as asthma almost always comes on at night, it is important that the principal repast should be in the morning or early part of the afternoon, and that any food taken between that and the hour for retiring should be of the lightest possible description. The more empty the patient's stomach, the better will be the chances of his passing a good night. Alcoholic drinks, coffee, and other stimulants should only be allowed when prescribed as medicines, as they have a tendency to aggravate the hyperæmia of the air-passages, which is one of the prominent features of the disease. Constipation should of course be carefully guarded against.

Aside from the apparently well-established fact that asthmatics do well, and often remain so, in the damp, foggy air of crowded cities, we have no means of determining beforehand what locality will suit a case of asthma. Change of climate in such cases is a mere matter of experiment, but when such change is determined upon the patient should at first try a place which is in every respect the reverse of the one he has previously lived in. If his former residence was in a city, he should remove to the country; if the old place was dry, the new one should be damp; if he has lived in a flat, low country, let him try the mountains; and vice versâ. As already stated, removal from the pure air of the country to the foul, smoky air of a city densely populated often affords complete relief, but so soon as the patient returns to his old home the asthma reappears and is as bad as ever.

As regards its capriciousness as to locality, I quote the following interesting case from Salter's work on asthma: "G. C----, a confirmed asthmatic, a native of a city in Scotland in which he resided, having been a sufferer for many years, came to London in 1838 for the sake of receiving the best medical advice. He took apartments in the centre of the city of London, somewhere near St. Paul's. His intention was to wait for an attack, and as soon as one came on to present himself to his physician, that he might witness it and have a clear idea of the state he was in. He waited six weeks, much to {207} his mortification, not only without experiencing one, but without any difficulty of breathing whatever. His health altogether improved; he slept well and gained flesh. Being tired of waiting, he went back to Scotland without having seen his physician at all, and, to his great disappointment, he had not been in his native city many days when he was attacked in the usual way, and continued to suffer just as before his visit to London. Subsequently, finding it necessary on matters of professional business frequently to visit London, he experienced the same result on all occasions as at his first visit--perfect immunity from his disease. To use his own expression, 'he felt in London like a renewed man.' On his first arrival in town he was in a miserable state: he could not move without feeling his shortness of breath distressingly; he got no rest at night, and was seldom able to lie down in his bed. But in London he could do anything--eat, drink, sleep. The consequence was he gained flesh and strength, and went back to Scotland looking quite a different man. This was the invariable result."

Having once found a place which agrees with him, the asthmatic should remain there, as change of climate when no good is effected often does harm.

Arsenic has long been a favorite remedy in asthma, and is undoubtedly of great value in a number of cases. It was used in the form of a vapor by Dioscorides, and, notwithstanding its poisonous properties, has always occupied a prominent place in the therapeutics of diseases of the air-passages. In Styria and other parts of Lower Austria arsenic is habitually eaten by many of the peasants to enable them to breathe more readily while climbing over their elevated mountains and to endure the fatigue incidental to their long pedestrian journeys. The same habit is said to prevail in China, where, however, it is not taken internally, but is smoked mixed with tobacco. Its physiological effects are thought to be due to the increased oxidation of the blood which it promotes, as is proven by the great increase of urea observed after its administration. The blood thus oxygenized stimulates the vital centre, and thus the nerves and muscles of respiration are incited to increased activity, as a result of which the respirations become freer and more easy. Those who believe in the herpetic diathesis derive an additional indication for its administration from the good effects which it manifests in cutaneous diseases. It is best administered in the form of liquor potassii arsenitis (Fowler's solution), giving at first only three drops in a wine-glassful of water after each meal, and increasing the dose one drop each day until the patient takes thirty drops in twenty-four hours. Should any toxic symptoms supervene--pain in the stomach or diarrhoea, puffiness of the lids or redness of the conjunctiva--the arsenic should be at once suspended, and not resumed until they shall have subsided. Thus given, it is quite safe. Trousseau recommends its use in the form of cigarettes, which are prepared as follows: "Twenty grains of the arsenite of potassium are dissolved in half an ounce of water, and a sheet of bibulous paper soaked in this solution until it is all taken up. The paper is then dried and divided into twenty equal pieces, which therefore contain one grain arsenite of potassium each. Each paper is then rolled in the form of a cigarette. In smoking them the patient should endeavor to inhale the smoke into the bronchi. He should take only four or five whiffs once a day."

Iodide of potassium often affords most satisfactory results in the treatment of asthma, but in many cases it fails entirely. It is a drug which must be given for a long period at a time, occasionally for weeks, before it manifests its effects, and want of perseverance may account for its failure in many cases. It forms one of the chief ingredients in Aubrée's antiasthmatic elixir, the formula for which is somewhat uncertain. According to Trousseau, it is as follows: {208}

Rx. Rad. polygalæ, gr. xl; Coque c. aqua fervida, ounce iv ad ounce ij; Filtrat, adde Potass. iodid. drachm iv; Syrup, opii, ounce iv; Spts. vin. gallic. ounce ij; Tr. coccionellæ, q. s. ad coloraud. Filtra.

Of this Trousseau states three tablespoonfuls are taken "in the morning fasting, at noon, and in the evening, until the asthma disappears." Each dose contains no less than forty-five grains of the iodide of potassium and four-fifths grain of extract of opium. Aubrée himself always insisted that each dose should be followed by a "tablespoonful of chocolate pastille, which neutralizes the irritating action of the iodide of potassium."[26]

[Footnote 26: Trousseau, op. cit., p. 656.]

A remedy resembling in its effects the one just mentioned is nitro-glycerine. It is administered in the form of a one per cent. alcoholic solution, in doses of half a drop, increased to three should the smaller dose prove inefficient. Its effects manifest themselves in from three or four minutes to a quarter of an hour, and disappear within an hour after its administration. The dose should be increased with great caution, as a single drop of the above solution has been known to produce alarming symptoms. The euphorbia pilulifera, much lauded by Australian physicians for its wonderful effects in bronchial asthma, promises to rank as an invaluable remedy in the treatment of that disease. It is best administered in the form of a decoction prepared by steeping one ounce of the fresh, or half that quantity of the dried plant, in two quarts of water, and simmering it down to one quart. The dose of this decoction is three or four wineglassfuls during the day, the last dose preferably in the evening, after supper.[27]

[Footnote 27: Boston Medical and Surgical Journal, 1885, p. 66.]

Leyden, whose theory has been mentioned elsewhere, has proposed a new treatment based upon the solubility of the Charcot crystals in chloride of sodium and carbonate of sodium. A solution of one part of these salts in one hundred parts of water should be inhaled twice daily in the form of a spray.

Oxygen has often been used in asthma, but is now seldom administered except in cases associated with great anæmia.

Sée gives the following statistics of the results of the treatment with compressed air in asthma and its secondary affections. Bertin used it in 15 cases of emphysema, all of which he cured, and in 92 cases of nervous and catarrhal asthma with emphysema, of which 67 were completely and 22 partially cured, while it was only unsuccessful in 3 cases. Of Sandahl's 77 cases of asthma with emphysema and bronchitis, 57 were much relieved, and of 14 uncomplicated cases, all were completely relieved. Compressed air may be applied either by placing the patient in a pneumatic cabinet or by means of the portable apparatus of Waldenburg. It must be remembered, however, that in the cabinet the compressed air acts upon the whole body, while in the portable apparatus only the air-passages and alveolæ are subjected to pressure; hence if the latter is used the amount of pressure must be considerably diminished. Notwithstanding the success claimed for this method of treatment, it should be used with caution, and if the case is complicated with emphysema it should either be regarded as contraindicated, or, if employed, the pneumatic cabinet should be used and not the portable apparatus. In the former, or "air-bath," the exterior pressure of the compressed air acts as an auxiliary to "the elasticity of the thorax and to the abdominal gases in" expiration, and at the same time, by compressing the vessels outside the thorax, aids the venous circulation. The same force exercised on the inner surface of the {209} tubes tends to lessen the hyperæmia of the bronchial mucous membrane (Moeller).[28] When the portable apparatus is used, expiration in rarefied air causes retraction of the thorax, and thus in a measure overcomes any tendency to emphysema. A better plan than to use either singly is to combine the two--to expire into rarefied and inspire compressed air--which may be readily accomplished with several of the improved portable apparatuses.

[Footnote 28: Thérapeutique locale des Maladies de l'Appareil respiratoire, Paris, 1882, p. 283.]

The inhalation of sulphuretted hydrogen as practised at Eaux Bonnes, Cauterets, Aix-la-Chapelle, and other sulphur baths, is said to have cured some cases, while in many others great benefit is claimed to have been derived from its use; but allowance must be made for exaggeration in many of the reports published.

In giving the treatment of asthma no allusion has been made to Grindelia robusta and other recently-introduced remedies, partly because the writer has had no experience with them, and again where he has tried them they have given negative results.

{210}

HAY ASTHMA.

BY W. H. GEDDINGS, M.D.

SYNONYMS.--Hay fever; Hay cold; Summer catarrh; Catarrhus æstivus (Bostock); Freuhsommer katarrh (Phoebus); Autumnal catarrh (Wyman); Rose cold; June cold; Pollen fever; Pollen catarrh (Blackley). Fr. Catarrh de foin; Catarrh d'été; Ger. Roggen Asthma.

DEFINITION.--A form of catarrh caused by some irritant floating in the atmosphere; appearing in the spring, early summer, or autumn; attacking persons predisposed every year at the same time, the patient being at other periods free from the disease; characterized by symptoms resembling those of influenza, the chief of which are sneezing, redness, swelling, and increased secretion of the conjunctivæ and of the mucous membrane of the whole respiratory tract from its commencement in the nostrils down to the finest bronchi; frequently culminating in more or less severe attacks of asthma.

HISTORY.--Bostock, an English physician, is entitled to the credit of having been the first to recognize and describe this peculiar affection, for although, prior to his time, Heberden[1] had alluded to symptoms which are now supposed to be referable to hay asthma, and Cullen had noted the fact that some persons have asthma oftener in summer than in winter, neither of these writers recognized the true nature of the disease.

[Footnote 1: Commentary on the History and Cure of Diseases, 4th ed., London, 1816, chap. "Destillatio," p. 113.]

Bostock's first description of hay asthma appeared in the form of a paper, "Case of a Periodical Affection of the Eyes and Chest," which he read before the Medico-Chirurgical Society in London in 1819.[2] This was a description of his own case. Nine years later he gave the details of 18 additional cases and mentioned 10 others.[3] In the second paper, having noticed that the disease as known to him, the American rose or June cold, prevailed only in the late spring and early summer, he styled it catarrhus æstivus. Rejecting the popular theory, that hay asthma is due to the emanations from hay, flowers, etc., he maintained that heat was the real cause of the disease.

[Footnote 2: Medico-Chirurgical Transactions, London, 1819, pp. 161-165.]

[Footnote 3: Ibid., London, 1828, pp. 437-446.]

It appears singular, in view of its frequency at the present time, that notwithstanding the attention which had been directed to it only 18 cases should have been collected during the nine years which intervened between the publication of the first and second articles by Bostock, and tends to prove that in those days the disease could not have been as common as at present. That this was indeed the case is rendered all the more probable by the indisputable fact that, owing to the more general education of the people and to the requirements of a so-called advanced civilization, other nervous diseases are certainly much more frequent than they were formerly. The great prevalence of hay asthma among the educated is a further proof of the correctness {211} of this conclusion. It must, however, be remembered that diagnosis did not then occupy the position it now does, and it is not unlikely that it was often overlooked or confounded with other diseases.

During the five years which succeeded the publication of Bostock's second paper no less than five treatises on hay asthma appeared in England, some of them by the most prominent medical men of that period. They are remarkable as showing the great diversity of opinion entertained at that early date as to the etiology of the disease. Thus, Macculloch[4] (1828) attributed it to the air of hot-houses and green-houses, while Gordon[5] (1829) attributed it to the flowers of grasses, particularly those of the Anthroxanthum odoratum, and suggested that grass asthma would be a more appropriate name than hay asthma.

[Footnote 4: An Essay on the Remittent and Intermittent Diseases, London, 1828, vol. i. pp. 394-397.]

[Footnote 5: London Medical Gazette, 1829, vol. iv. pp. 266-269.]

Even as late as 1859 the disease appears to have been scarcely known in Germany, for Phoebus, who has since published a most excellent work on the subject, on being consulted by a colleague suffering from hay asthma frankly confessed that he was unacquainted even with the name of the disease. This incident, and the belief that he had before him a comparatively unworked field, stimulated him to investigate the disease. By addressing circulars to the various medical societies and hospitals, not only in his native country, but also in other parts of Europe, as well as by personal interviews with patients and by publishing requests for information in the various medical journals, he collected a large number of cases and gained much valuable information concerning the disease. The results of his assiduous and painstaking labors were published in 1862 in the form of a valuable work,[6] which, although over twenty years old, is still regarded the best authority on the spring variety of hay fever.

[Footnote 6: P. Phoebus, Der Typische Freuhsommer Katarrh, Geissen, 1862.]

Previous to the year 1859, when Phoebus's circulars directed attention to it, hay asthma seems to have been almost unknown in France, as, with the exception of a single case by Cazenave of Bordeaux (1837), who described it as a new disease, we find previous to that date no mention of it in French literature.

The first case of hay asthma published in America, a typical one of the autumnal form of the disease, is recorded by Drake in his work, The Principal Diseases of the Interior Valley of North America, p. 803, published in 1854.

It will be seen by this brief summary of the history of hay asthma that the disease was first recognized in England in 1819, where in 1828 it became generally known, and that at the time of the publication of Phoebus's work (1862), with the exception of one or two isolated cases in France and the United States, England was the only country in which it was generally known and understood. Since the publication of Phoebus's valuable work numerous additions have been made to the literature of the disease, but with the limited space at my disposal I can only refer to a few of the most important that have appeared in the last two decades.

In no country has the subject of hay asthma attracted more attention than in the United States, and in no other has its study been rewarded by the discovery of so many new and interesting facts. To Morrill Wyman of Cambridge, Mass., we are indebted for the first elaborate American work on hay asthma, or rather the autumnal variety of that affection, which Wyman believes to be a distinct disease in no way connected with rose cold, June cold, and other forms which appear in the late spring and early summer.[7] He had previously described the disease in his lectures as early as 1854, and {212} also in a paper read before the Massachusetts Medical Society in 1866. Being himself a sufferer from it, he naturally devoted much time and attention to its study, and his work may be justly considered the most valuable contribution to the literature of the disease which has appeared since that of Phoebus. Another American work on hay asthma is that of the late Beard of New York.[8] He elaborates the nervous theory of the disease, and establishes three varieties--the first appearing in the spring, the second in midsummer, and the third in autumn. In 1877, Elias Marsh of Paterson, N.J.,[9] read an exceedingly valuable paper before the New Jersey State Medical Society, in which he describes a series of experiments which led him to believe that hay asthma is caused by the pollen of plants. In Europe the best treatise on the subject that has been published of late years is undoubtedly that of Blackley of Manchester, who by a series of ingenious and carefully-conducted experiments claims to have found in the pollen of certain plants the true cause of the disease. To all of these works we shall again have occasion to refer in the course of this article.

[Footnote 7: Autumnal Catarrh, Cambridge.]

[Footnote 8: George M. Beard, M.D., Hay Fever and Summer Catarrh, New York, 1876.]

[Footnote 9: "Hay Fever or Pollen-Poisoning," an essay read before the New Jersey State Medical Society by Elias Marsh, M.D., Paterson, N.J., 1877.]

ETIOLOGY.--In scarcely any other disease is there such a diversity of opinion in regard to the cause as in hay asthma. We have seen how Bostock and his contemporaries differed on this point, he attributing it to heat, while of the others one claimed that it was caused by the air of hot-houses and green-houses, and another insisted that it was neither of these, but the flowers of certain grasses. Since that period other theories of causation have been advanced, but the same diversity of opinion as to its origin which marked its early history continues even at the present day.

In treating of the etiology of hay fever the various causes may be divided into two classes--viz.:

Predisposing Causes.--The fact that hay asthma is frequently transmitted from one generation to another, so well established by Wyman, is now very generally admitted, and will become more apparent in the future, as in estimating this feature it must be remembered that we have to deal with an affection which seventy years ago was entirely unknown and which has only recently become generally recognized. That the fact of the hereditary transmission of the predisposition is becoming every year more generally accepted is made apparent by the replies to two sets of circulars addressed to hay-fever patients in different years. Thus, Wyman, whose circular was issued at least eight years ago, received 18 affirmative replies out of 80, a little less than 25 per cent.; while to the writer's circular, issued in 1882, there are 25 affirmative replies out of 66. Numerous instances have been recorded where the disease attacked not only two, but even three, generations of the same family.

Hay asthma appears to be much more prevalent among males than females, the proportion being 3 males to 2 females. There is no apparent reason for this discrepancy other than that males are as a rule more exposed to the vicissitudes of weather, and that the restless energy with which many of them carry on their avocations predisposes to the disease.

The causes which produce hay fever act alike upon many thousands, an infinitesimal percentage of whom are attacked. There must therefore be some individual peculiarity which predisposes certain persons to the affection, but, aside from the facts that those attacked are usually of a nervous temperament, and that the respiratory mucous membrane of many of them is extremely sensitive, and that the vascular erectile tissue over the turbinated bones and lower portion of the septum is often hypertrophied,[10] there are no {213} known peculiarities by which it can be recognized. What races are subject is a question which thus far has received but little attention. To the writer's knowledge, the only well-established fact relative to race susceptibility is that negroes are exempt from the disease, and that in India (Blackley) it does not occur among the natives.

[Footnote 10: Roe, The Pathology and Radical Cure of Hay Fever, 1883, p. 9.]

Statistics show that it is much more common in youth and middle age, and that comparatively few are attacked after forty, as will be seen by referring to the following table:

Age when First Attacked. | Wyman's Cases. | My Own Cases. | Total. -------------------------+----------------+---------------+------- Under 10 | 11 | 10 | 21 10 to 20 | 11 | 17 | 28 20 to 30 | 25 | 13 | 38 30 to 40 | 8 | 11 | 19 40 to 50 | 11 | 5 | 16 After 50 | 2 | 1 | 3 -------------------------+----------------+---------------+-------

Wyman is of the opinion that females are attacked later in life than males.

Without knowing the numerical proportion which the various professions and occupations bear to each other, it is impossible, even with the aid of statistics, to determine which of them is most subject to hay asthma; but the annexed table shows conclusively that those who do brain-work are much more frequently attacked than those who earn their living by manual labor:

| Wyman. | My Own. | Total. --------------------------------+--------+---------+------- Statesmen | 1 | 0 | 1 Clergymen | 6 | 3 | 9 Jurists and lawyers | 6 | 2 | 8 Physicians and medical teachers | 8 | 4 | 12 Dentists | 1 | 0 | 1 Pharmacists | 0 | 1 | 1 School-teachers | 3 | 0 | 3 Students | 6 | 1 | 7 Military officers | 3 | 0 | 3 Authors, editors, etc. | 0 | 1 | 1 Mechanical engineers | 0 | 1 | 1 Bankers | 3 | 1 | 4 Bank officers | 2 | 1 | 3 Merchants | 11 | 7 | 18 Brokers | 0 | 1 | 1 Manufacturers | 12 | 3 | 15 Clerks | 1 | 1 | 2 Artisans | 1 | 1 | 2 Farmers and gardeners | 4 | 2[11]| 6 Butchers | 1 | 0 | 1 Laborers | 0 | 1 | 1 --------------------------------+--------+---------+-------

It will be seen by the above that of 100 cases, only 12 were engaged in outdoor pursuits, and that the remaining 88 followed occupations necessitating confinement within doors and entailing more or less intellectual effort; which proves conclusively that the earlier writers on hay asthma were correct in regarding it as a disease of the more cultured classes of society. The writer agrees with Wyman that the large increase in the number of hay-fever sufferers may in a great measure be attributed to the circumstance that many {214} who were formerly pursuing agricultural and mechanical pursuits are now engaged in occupations which require more or less intellectual effort.

[Footnote 11: One of these was an amateur and highly educated.]

To determine the value of temperament I have followed Beard's example, and in my circular of inquiry propounded two questions: 1st, the temperament of the patient's family; 2d, his own temperament. To the first query I obtained replies which showed that the nervous temperament predominated in 28 out of 37 cases; or, in other words, the family temperament was more or less nervous in two-thirds of the cases. As regards the patients themselves the temperament was as follows:

| My Own. | Beard. | Total. --------------------+---------+--------+------- Sanguine | 8 | 18 | 26 Nervo-bilious | 5 | 23 | 28 Nervous | 23 | 67 | 90 Nervo-sanguine | 9 | 27 | 36 Nervo-lymphatic | 0 | 3 | 3 Lymphatic | 3 | 0 | 3 Sanguino-bilious | 4 | 5 | 9 Bilious | 7 | 29 | 36 Sanguino-lymphatic | 0 | 1 | 1 Bilio-lymphatic | 0 | 1 | 1 --------------------+---------+--------+-------

It thus appears that the nervous element predominates in no less than 157 out of 233 cases.

Other diseases do not appear to predispose to hay asthma, nor, on the other hand, is that affection a cause of any other disease. The question whether naso-pharyngeal catarrh is more common among hay-fever subjects has, after careful investigation, been decided in the negative.

Exciting Causes.--It is generally conceded that the suggestion of a large number of remedies in the treatment of a disease is good evidence that no effective curative agent has as yet been discovered. This observation regarding therapeutics equally applies to etiology, a long array of causes usually developing the fact that great uncertainty exists as to the real causative agent. Hay fever affords a most striking proof of the truth of this remark. The simple enumeration of the various agents which have been accused of causing the attacks would cover several pages. An example of the multiplicity of its supposed causes is afforded by the replies to the question in Beard's circular, "What is the cause of your attacks?" no less than thirty-three agents being accused of causing the disease. Of these I propose to confine myself to a few of the most prominent.

Early in the history of hay asthma heat was considered its chief cause, Bostock, its first describer, having held that view, as have also many of his successors. It is now generally conceded that heat of itself is not a cause, although by promoting vegetable growth and causing dust it may still be regarded as an indirect factor in its etiology. That heat of itself is not a cause is proved by the occurrence of the disease not during the intensely hot weather of midsummer, but in the late spring and early fall. It, however, undoubtedly produces a temporary aggravation of many of the symptoms. This appears to be especially the case in the autumnal variety, as those who have the disease in the spring seldom complain of any ill effects from heat.

"Strong light, sunshine, especially when it falls upon the face, will produce a violent paroxysm of sneezing, and the other symptoms then follow in quick succession; and moving from shade to sunshine, even when not otherwise annoying, will do the same." This is the opinion of Wyman, and coincides with that of Phoebus, Abbott Smith, and others, and is amply confirmed by {215} the experience of the writer. This applies also, though in a less degree, to artificial light, especially gas-light.

Dryness of the atmosphere, by promoting dust, may be regarded as an indirect cause. Hay-fever patients agree almost unanimously that their symptoms are aggravated on clear, bright, dry days, and that they feel most comfortable in damp and cloudy weather.

There is no evidence to show that electricity is in any way connected with the etiology of hay fever.

Ozone is certainly not a cause, as hay-fever patients feel best on the sea-coast and ocean, where ozone is most abundant.

Long before hay fever was recognized by the medical profession hay was supposed by the general public to be the cause of the disease. In England especially, but also in the north of France and in Switzerland, this opinion prevailed very generally. Some suppose that the dust which it contains is the real cause, while others attribute it to its peculiar odor. In those susceptible to its influence it appears to make but little difference how they come in contact with it, whether in an open field where it is mowed, by driving behind a wagon loaded with it, or by entering a stable or loft where it is stowed away. It is not, however, the cause of the autumnal variety, as it is harvested in the temperate regions of North America, where this form of disease is most common, in June or early in July, which is six or eight weeks earlier than the period at which the attacks commence. That hay is a cause of the earlier variety of the disease is evident from the experience of numerous intelligent invalids, who trace it to that agent from the fact that the outbreak coincides with the blooming or harvesting of hay, and that removal from the locality in which they are exposed to its emanations is followed by relief. It must be remembered, however, that hay does not consist of dried grass alone, but that it contains other plants and flowers, as well as a large amount of dust.

The flowers of grass, especially those of the Anthroxanthum odoratum, may be regarded, like hay, as one of the causes of hay fever--a fact that was early recognized by Gordon and others. Blackley[12] cites the case of an Indian medical officer of high rank, whose statement is as follows: "I have suffered from hay fever for about thirty-five years; I have had it both in India and in England. The period at which the attacks come on is not fixed, the date of the attacks depending more on the grass ripening late or early than on any other circumstance. They always begin toward the end of the hay season, when the grass is fully in flower, and cease slowly and gradually--not directly--on gathering in the grass."

[Footnote 12: Hay Fever, its Causes, Treatment, etc., p. 47, London, 1880.]

Rye, oats, and wheat in bloom may also be ranked among the exciting causes of hay fever.

Indian corn in bloom often causes symptoms of hay fever, but that it does so only in certain cases is evident from the fact that the disease does not exist in some places where large quantities of corn are raised (Wyman).

Geraniums, roses, heliotropes, and other sweet-scented flowers often bring on attacks. The bean in bloom and elderflowers are also regarded as causes.

Ragweed, also known as Roman wormwood, Ambrosia artemisiæfolia, a weed which extends almost over the whole of the United States, is a powerful cause of the autumnal variety, but, like all the other agents which have been accused of causing hay fever, is by no means general in its action, many patients being able to inhale the dust shaken from the flowers with perfect impunity even during the critical period. On those susceptible to its influence it will act not only during the hay-fever season, but also at other periods of the year. Wishing to study the plant, I procured during the fall several {216} specimens of it and placed them between the leaves of a large quarto volume. During the winter my wife, who is a sufferer with hay fever, accidentally opened the book, and, seeing the plant, not knowing its nature, picked it up and smelt it. She immediately began to sneeze, the eyes and nose itched intensely, there was profuse lachrymation; in short, all the symptoms of a mild attack of hay fever supervened, the effects of which lasted until the following morning. The case is interesting from the fact that in this instance the experiment was made unconsciously, and the effects could not therefore be attributed to the imagination, the patient being entirely ignorant of the nature of the plant. The prevalence of autumnal hay fever appears to coincide with the blooming of the ragweed, and conforms to the geographical distribution of that plant, which grows wherever the disease prevails, while in exempted localities it is seldom found or never seen. In Bethlehem, N.H., a diligent search was made for it for two days by a botanical friend without his finding a single specimen, although in the neighboring town of Littleton, which is within sight of Bethlehem and is not exempt, the plant is quite abundant. Marsh states that he saw none of it in New Brunswick nor at Moosehead Lake.

Dust of various kinds is more frequently designated by invalids themselves as the cause of their disease than any other agent. Thus, in reply to his question as to the cause of hay fever, Beard received 104 replies assigning dust as the cause, while 540 attributed it to thirty other agents. All kinds of dust, both in and out of doors, are accused, but that of railway-cars is supposed to be the most potent.

There is but one case on record in which animal parasites were the cause of an attack--that of Bastian, who while engaged in the spring investigating the anatomy of the Ascaris megalocephala, one of the parasites of the horse, noted that its emanations not only in the fresh state, but after having been kept in spirits for two years, invariably caused itching about the eyelids, irritation of the conjunctivæ, with continuous sneezing and other symptoms resembling hay fever. These symptoms ceased after two months, and did not return until the following spring. He finally became so sensitive that the wearing of the coat in which he had worked during the examinations was sufficient to bring on the symptoms.[13]

[Footnote 13: Salisbury in Infusorial Catarrh and Asthma attributes hay asthma to an animalcular organism, the asthmatos, but his assertions have not as yet been confirmed by other investigators.]

Helmholtz, himself a sufferer from hay fever, discovered that the secretion of his nasal mucous membrane contained during the attack a number of vibriones, and, never being able to find them there at other times of the year, concluded that they were the cause of the disease. Binz of Bonn having discovered that quinine was inimical to the vibriones, Helmholtz supposed that that agent would be the proper one to employ in the treatment. He used it with success, injecting a saturated solution into the nostrils, the injection each time affording marked relief.

THE POLLEN THEORY.--Believing from his own experience and that of others that hay fever was due to the pollen of certain plants, Blackley of Manchester instituted a series of ingenious and instructive experiments to prove the correctness of his conclusions. In his first set of experiments a very small quantity of the pollen of various plants was applied to the lining membrane of the nostril. That of the Lolium italicum produced at first a slight feeling of anæsthesia at the point to which the pollen had been applied, followed "by a feeling of heat which gradually diffused itself over the whole cavity of the nostril and was accompanied by a slight itching of the part. After some three or four minutes a discharge of serum came on and continued at intervals for a couple of hours." The mucous membrane became so swollen {217} as to partially occlude the nostrils and impede the entrance of air. When rye was used the symptoms were much more violent, and were attended by violent and long-continued fits of sneezing. With wheat and oats the effect was equally decided. The same experiment was tried with other orders of plants with varied success, some of them being very active, while others were found to be quite inert. One grain of the pollen of Alopecarus pratensis was applied to the fauces, causing itching and diffused redness. That of the Lolium italicum rubbed into the abraded skin of the forearm, as in vaccination, produced itching and swelling.

Marsh,[14] who has repeated Blackley's experiments in America, gives some very interesting facts in regard to the pollen of the Ambrosia artemisiæfolia. On the 5th of August, 1874, he placed a few sprigs of the ambrosia in full bud, but without open flowers, in a glass of water in his office. The next day the flowers were open, and on handling the plant for the purpose of preparing some microscopic specimens from it, the pollen was freely scattered around. This caused in him severe coryza of twenty-four hours' duration, with occlusion of the nostrils and serous discharge. On August 13th he repeated the experiment, this time intentionally applying some of the pollen to the nostrils. This produced such severe symptoms that he had to have recourse to a hypodermic injection of morphia for their relief. These, however, continued into his regular attack, which should have been due a few days later.

[Footnote 14: Op. cit., p. 14.]

Having proved that the pollen of certain plants was capable of producing hay asthma, Blackley next turned his attention to the determination of the amount of that substance floating in the atmosphere of different places and at various periods of the year. The plan which he found best adapted to his purpose was to expose slips of glass to the open air for a given length of time, so as to allow any solid matter the air might contain to deposit upon the glass. On each of these slips a space of one centimeter square was made sticky by covering it with a mixture of water, proof spirit, and glycerin. These were exposed to the atmosphere for twenty-four hours, and then placed under the microscope and the number of pollen-grains adhering to the moistened square counted. These slides were exposed at the height of four feet nine inches above the ground, "the average breathing-level," and were placed in a grass meadow four miles south-west of Manchester. The experiment was begun early in April, 1866, and continued until the 1st of August. Only a small quantity of pollen was found during the first month. On May 30th it appeared in much larger quantities, and continued to appear on most of the days until August 1st. Barometric pressure did not influence the deposit of pollen, but whenever the air was drier the quantity was increased. A fall of rain, especially if attended with lowering of temperature, had the effect of materially lessening the number of grains. The largest quantity of pollen was obtained on June 28th, the day after the highest temperature of the season, showing that a large deposit of pollen coincides with, or follows, a marked rise in temperature. Fully 95 per cent. of the pollen collected belonged to the Graminaceæ, but this would not apply to other localities and countries, in which that of other plants would naturally predominate. These experiments were quite successful in demonstrating that the rise and progress of the disease corresponded with the amount of pollen present in the atmosphere. A third set of experiments was made by attaching the glass slides to kites, to determine the amount of pollen present in the air at different altitudes. These experiments revealed the fact that grass pollen was much more abundant at elevations of 500 to 1500 feet than near the surface of the ground. Marsh also investigated this portion of the subject, only, instead of attaching the slides to kites, they were placed in the attic windows: he arrived {218} at conclusions in regard to the pollen of ambrosia similar to those which Blackley had reached with reference to the Graminaceæ.

The experiments of Blackley justify the belief that the cause of the early form of hay fever, which prevails in England, is to be found in the pollen of a number of plants, especially grasses and grains, which bloom in the late spring and early summer, while those of Marsh prove conclusively that the Ambrosia artemisiæfolia, or Roman wormwood, is certainly one, and probably the chief, cause of the American or autumnal variety of the disease.

GEOGRAPHICAL DISTRIBUTION.--Both varieties of hay fever prevail in the United States, but the late variety is much more frequent, and may be regarded as peculiar to this country. The distribution of the early form of the disease is much more extensive. It is quite frequent in Great Britain, and, according to our present knowledge, it extends over France, Belgium, Holland, Switzerland, Italy, Russia, and in the plains of India (but only among foreign residents). Further investigations will probably show that it also extends over the other temperate regions of Europe. As before stated, the autumnal form is confined to the United States, where it prevails much more extensively than was formerly supposed. Commencing in Florida, where it is quite rare, it extends northward up to Eastport, Maine. Its northern border is defined by Wyman[15] as follows: "From the St. Croix, south of Houlton in Maine, or about the line of 600 feet elevation above the sea-level, the line of exclusion turns eastward, following approximately the border of the elevation just mentioned, excluding the interior lakes of Maine, which are about 1000 feet above the sea, and, descending toward the south, strikes the White Mountain region at its northern portion. Thence, turning toward the St. Lawrence River and running along the height of land which divides the waters falling into the Atlantic from those falling into the St. Lawrence, parallel to the St. Lawrence, it strikes that river north of Lake Champlain." Thence along the southern border of the Great Lakes to the south of the island of Mackinaw, between Lakes Huron and Michigan. "It then crosses the lake and runs north of Lake Winnebago to St. Paul, Minn., leaving the Lake Superior copper-regions beyond its influence." From this point the line is undetermined, but there is evidence to show that the disease occurs in Colorado. The statement of previous authors, that the disease does not prevail in California, is confirmed by a statement recently made to the writer by Hatch, secretary of the Board of Health of that State, who adds that several parties have removed there to avoid the disease. Southward, the line runs along the Mississippi River to New Orleans, where the disease prevails. The southern and eastern borders are the Gulf of Mexico and the Atlantic Ocean.

[Footnote 15: Op. cit., p. 63.]

SYMPTOMS AND COURSE.--No better description of an attack of the autumnal form of hay fever has ever been written than that of Wyman, who, being himself a sufferer from the disease, has had exceptional opportunities for studying it in all its details. I therefore extract the following from his work:[16]

"All the cases agree in the time of annual return, about the 20th of August, varying but a few days from this date in different years. By some individuals it is believed to be remarkably punctual, being first noticed on precisely the same day of the month, and, it is even asserted, at the same hour of the day. It is first perceived as a slight itching in the palate and in all parts about the roof of the mouth, soon followed by similar sensations, apparently in the Eustachian tube, extending from the throat into the ears, and inducing the sufferer to attempt relief by swallowing and by rubbing his tongue against the back part of the hard palate, and by pressing and rubbing the external orifice of the ear to give motion to the parts within. There is often a sense of tension about the forehead, especially over the eyes in the region of the {219} frontal sinuses. In a day or two the nostrils are affected; there is irritation of the lining membrane, sneezing, and a stuffing and obstruction of the nostrils. This obstruction is peculiar; it occurs in paroxysms of short duration, one or both nostrils becoming suddenly obstructed, and in two or three minutes as suddenly relieved; at other times the obstruction is more prolonged. But, however complete, it is in many individuals almost immediately relieved by active exercise, rapid walking, leaping, or any movement indeed which gives warmth to the extremities.

"At first these attacks occur only in the morning or on first rising; as the disease advances they occur later in the day, but still in short paroxysms. At this stage the discharge from the nostrils is limpid and almost free from mucus; it is often very copious, especially during or immediately following attacks of sneezing. Holding down the head is often accompanied by a rapid dropping of the same fluid without sneezing. With this trouble in the nostrils come watering of the eyes and itching along the edge of the lids and in the conjunctivæ generally, but most at the inner corners. This irritation occurs also in paroxysms of a few minutes' duration. It is so intense that it is difficult for the sufferer to refrain from rubbing the eyeballs violently, which soon relieves them, notwithstanding that such treatment increases the turgidity of the vessels until the whole conjunctival surface is of a nearly uniform red. The eyelids are swollen, their edges red and inflamed; the small glands are also inflamed, and in some cases pustules or styes form and break, leaving an excoriated surface which heals slowly. The whole face is often red and swollen, especially in the morning. The senses of taste and smell are much impaired, in some cases almost abolished; and at times there is partial deafness, with a sense of obstruction of the internal ear. The lining membrane of the external tube is sometimes much irritated, even to the extent of producing a thin discharge, without evidence of the irritation extending to the tissue beneath. Swallowing is interfered with, especially when the nostrils are so obstructed as to prevent the perfect motion of the parts necessary to this act. The lining membrane of the mouth, tonsils, and pharynx partakes of the general irritation, and becomes red; and sometimes there is soreness of the throat. The lips become dry, cracked, and swollen. The skin is easily irritated and excoriated, and the excoriations are not so readily healed as in health. Many also suffer from itching of the skin, especially of the scalp, back, and chest, at times accompanied by a slight papular eruption. During some portion of this period there is chilliness, or rather sensitiveness to cold; more or less pain or sense of oppression in the head; the appetite diminishes; there is lassitude and weakness, the skin hot and dry, with other signs of a febrile movement.

"Toward the end of the second week to these symptoms are added irritation of the membrane lining the air-tubes; a frequent and dry cough, commencing with a sense of tickling in the upper part of the windpipe, but little relieved by the cough or only after long coughing; and the expectoration of a small quantity of transparent, glairy mucus. The severity of these bronchial symptoms depends much upon the condition of the atmosphere: if dry and dusty, the cough is much worse; dampness and a rainstorm give relief.

"During the third week the affection of the lungs gradually increases; the cough, still with very little expectoration, is more troublesome, especially in the night, sometimes compelling the patient to spend an hour or two sitting up, and not infrequently is spasmodic in its character, producing convulsive retching or even vomiting.

"The disease may now be assumed to be at its height. It is in this stage also that in some cases asthmatic symptoms appear, and, although they are sometimes severe, are not long continued. At the end of the third week the catarrhal symptoms diminish, the tickling of the fauces ceases, the eyes and {220} nose improve; but the cough is apt to continue longer, and the heart's action is easily accelerated by exercise, and the pulse is sometimes intermitting. The skin is dry and warmer than natural.

"During the fourth week in September these symptoms gradually diminish, and by the end of September or the first frost are nearly gone, leaving weakness and a more or less altered state of the mucous membrane of the air-tubes, the effect of the prolonged irritation, from which the patient, if otherwise in good health generally soon recovers."

[Footnote 16: Op. cit., p. 9.]

The spring form of the disease, known as June cold in the United States and as hay fever in England, differs from the late variety in the time of its occurrence, the attack coming on, as its name implies, in the late spring, usually between the 15th of May and the 15th of June, sometimes much earlier; one of my patients reporting that she commences to sneeze as early as the middle of April. The attacks in this variety usually cease during the first or second week in July, although a few continue on into August--a fact which induced Beard to establish a third or middle form of the disease. The symptoms are essentially the same in both varieties, but are much less severe in the early form, which is also of shorter duration. They differ as to cause, the spring variety being usually due to newly-mown hay. It occasionally happens that one person has both forms of the disease, or that a person who has hitherto had the early form fails to have it in the spring and is attacked in autumn.

INDIVIDUAL SYMPTOMS.--There is occasionally a stage of incubation, lasting about a week, during which there is slight feverishness and undue susceptibility to nervous impressions. The patient often experiences a feeling of lassitude and weakness; the digestion is disturbed, as indicated by a coated tongue, want of appetite, and constipation; he is disposed to be wakeful, and when he does sleep his rest is often disturbed by unpleasant dreams.

The first effect of exposure to the irritant is itching of the nose, slight in the beginning, but increasing in severity as the disease advances, until it at last becomes unbearable. The mucous membrane is red and swollen, the swelling being often so great that it interferes with the passage of air; a watery discharge sets in, which, although slight in the early stages, soon becomes copious, and in severe cases is so abundant that it actually streams from the nostrils. Sometimes, when both nostrils are stopped, if the patient changes his position and lies on the side the uppermost nostril will become free. These symptoms are attended with sneezing--not the sneezing of an ordinary coryza, but powerful sternutatory efforts repeated in quick succession and utterly uncontrollable. In one case which has come under my observation the sneezing invariably brought on menstruation in advance of the regular period, and on some occasions caused abortion.

These symptoms just mentioned often appear and disappear with great rapidity, especially in the early stages of the disease, and are usually worse in the morning on awakening.

Itching of the eyes begins at the inner canthus and generally extends over the greater portion of the conjunctiva, slight at first, but becoming more troublesome as the disease progresses. There is also redness of the conjunctiva, sometimes of the lids alone, at others extending over the whole mucous membrane, and giving to the eyes a bright-red appearance. The lids in severe cases are not infrequently oedematous, lachrymation is greatly increased, and the tears, trickling down the face, are liable to cause excoriation of the skin. Pustules and styes often form on the lids. There is more or less photophobia, according to the severity of the attack.

Owing to the occlusion of the nostrils the patient is often compelled to breathe through the mouth, thus causing an uncomfortable drying of the mucous membrane. There is a peculiar itching of the hard palate, which {221} the patient attempts to relieve by rubbing the roof of the mouth with the point of the tongue. This itching sensation extends over the pharynx, posterior nares, and upward through the Eustachian tubes to the ears, causing a disagreeable irritation, which the patient tries to alleviate by thrusting the tip of the finger into the external meatus. The mucous membrane of the pharynx is red and swollen. The dryness observed early in the attack gives place later to increased secretion, which is sometimes quite abundant. On the anterior surface of the velum of one of my female patients I observed a hard papule about the size of a lentil, which she assured me was always coincident with the attack, and never appeared at any other time.

In addition to headache, which is quite common, patients frequently complain of a heaviness and fulness, also of a peculiar sensation as though the head were constricted by a band. This latter symptom I have found present in about one-half of the cases investigated.

Itching of the skin is quite common, especially of the face, between the shoulder-blades, and over the sternum, and is frequently accompanied by a slight vesicular eruption and occasionally by urticaria.

The whole respiratory tract is in a state of catarrh, but there is very rarely any cough during the first week. This usually commences in the second week, and at that time is short and dry, and becomes every day more frequent until the third week, when it changes its type and becomes paroxysmal. During the first three weeks there is little or no expectoration, and what there is consists of small transparent glutinous masses. About the fourth week the irritation reaches the finer bronchi, and in many cases there is more or less asthma, which, like ordinary bronchial asthma, usually comes on at night. The asthma is sometimes quite severe and long-continued. Wyman states that very few escape cough. This does not accord with the writer's experience, as in 65 of his cases 15 had no cough.

Hay-fever patients suffer greatly from mental depression, complain of lassitude, and their capacity for intellectual labor is diminished. They are often troubled with insomnia, and when such patients do sleep it is in a fitful way, and their rest is often broken by unpleasant dreams.

NOMENCLATURE AND CLASSIFICATION.--The various terms used to designate this disease are all misnomers, and up to the present time none has been devised which conveys any idea of the true character of the disease. Hay fever is incorrect, because hay is only a cause in a limited number of cases, and fever is by no means a prominent symptom. Hay asthma should be discarded, for asthma is far from being a constant accompaniment of the affection. Autumnal catarrh or early spring catarrh only serves to designate the time at which the two forms usually appear, but conveys no idea of the disease in its entirety; while the term pollen catarrh or pollen fever is objectionable on the ground that, although the disease is most frequently produced by that agent, there are causes other than pollen which may excite it.

Hay fever is variously classified by different authors, some, like Thorowgood and Beard, regarding it as a neurosis, while others (Bostock, Phoebus, and Wyman) appear to regard catarrh as its distinguishing feature. Zuelzer has recently classed it among the acute infectious diseases, but assigns no reason for placing it in that group.

DIAGNOSIS.--To any one at all familiar with the symptoms of the disease the diagnosis of hay fever is quite easy. Its distinctive features are: It appears at the same time every year (the early form about the 1st of June and the later about the 20th of August); the severity of the local symptoms which usher in the disease--sneezing, stoppage of the nostrils, the inflamed condition of the eyes, and above all the itching of the nose, eyes, skin, and mucous membrane of the root of the mouth. A detailed differential diagnosis {222} is not as important now as it was formerly, when, as in the days of one of its early describers, Phoebus, "Man sah sie nicht, wo sie war, und sie sah, wo sie nicht war."

PROGNOSIS.--The number of elderly persons with hay fever, many of whom have passed the allotted threescore years and ten, and the fact that no one has ever been known to die from the disease, affords conclusive evidence that it does not shorten life. On the other hand, when once affected, except in those cases relieved by operative procedure, the patient remains subject to it during the remainder of his life. A few isolated cases are said to have recovered, but such a result is extremely rare. It is thought by some that a prolonged residence in the South may mitigate the disease, and eventually cure it, but this assertion lacks confirmation. It does not, like bronchial asthma, lead to secondary affections, the interval between the attacks giving the organs time to recuperate, nor does it predispose to other diseases.

TREATMENT.--Aside from its surgical treatment, to which I shall refer farther on, the only effectual remedy for hay fever consists in removal to a region which is exempt from the disease. By going to such a locality before the attack occurs, and remaining there throughout the critical period, complete immunity from the disease may be secured. The time of departure and return must be determined by the previous experience of the invalid in regard to the date upon which his former attacks have commenced. As the disease seldom comes on exactly on the same day every year, but often varies three or four days, he should be in his place of refuge at least a week before the usual time for the attack, and should remain until he can return with perfect safety. This is usually about the middle of July in the early variety, and after the first frost severe enough to kill vegetation in the autumnal form.

In the milder form which occurs in the spring the seashore affords considerable relief, except when the wind is from the land. It is therefore uncertain, and is only indicated when the circumstances of the patient prevent his visiting one of the exempt localities. On the eastern coast of the United States there are several places of this character, such as the Isles of Shoals, a group of rocky islands with little or no vegetation off the coast of New Hampshire, the climate of which is very like that of the ocean; and Fire Island, near New York. Similar to the above, but much more exposed to land influences, are Mount Desert and Nantucket.

The ocean itself affords complete exemption, and a sea-voyage is the surest means of avoiding the disease. It is true that persons have been known to be affected with hay fever even in mid-ocean, but in such cases it is more than probable that the cause of the attack could have been traced to the cargo. A case of this character came under the writer's observation during a voyage from New York to Charleston during the month of September, and was evidently caused by hay, a number of bales of which were stowed on the forward deck of the vessel. It makes comparatively little difference what particular voyage is undertaken, provided the vessel's course does not bring her too near land; but for most hay-fever patients a trip to Europe is to be preferred, especially for those suffering with the autumnal form, as by going to that country, where this variety does not exist, they avoid the necessity of remaining nearly two months on the water. A voyage to California is almost as good, and for the same reasons.

Whether this applies to the so-called June or rose cold, which is quite common in Great Britain and prevails to some extent on the Continent, has not as yet been definitely determined, but it is more than probable. Whether patients who have contracted the disease in Europe would escape in America is exceedingly doubtful. Two of the cases reported to the writer, who were first attacked (with the early form) in Europe--the one in Switzerland and the other at Florence--continued to have the disease after their return to {223} this country; while, on the other hand, an English lady who was subject to the disease at home escaped entirely during her residence of three years in the Southern States. Of the exempt regions in the United States, the one most frequently resorted to, and which at the same time affords the surest relief, is that of the White Mountains of New Hampshire--not the whole of it, but a certain portion, which is bounded on the west by a line drawn from Littleton to Lancaster (but not including the former place, which is only partially exempt), on the north by Canada, on the south by Franconia, Crawford House, and Jackson, while to the east it extends as far as Bethel in Maine. Of the various places contained within this territory, Bethlehem and Jefferson, Whitefield, White Mountain House, Fabian's, Twin Mountain House, Crawford House, Glen, Gorham, and Mount Washington, may be regarded as entirely exempt; Franconia Notch almost equally so; while Dalton, Lancaster, and Bethel must be ranked as uncertain. Another exempt region extends to the north and east of the one just described, and comprises the lake region of Maine. Petoskey in Northern Michigan, at the head of Little Traverse Bay, is said to afford almost entire relief, and is resorted to by a large number of patients from the Western and South-western States. There are also several places in Vermont which offer more or less immunity, such as Mounts Mansfield and Stow, both of which, however, are inferior to those first mentioned. Canada, with the exception of a few cases reported at Toronto, St. Catherine's, and at a few places near its southern border, appears to be exempt. The same may be said of the Adirondack Mountains and Pottersville on Schroon Lake and Marquette. The Catskill Mountains and several places high up on the Alleghanies, such as Cresson, Pa., Oakland and Deer Park in Maryland, afford relief in many cases. Colorado is said to be exempt, but several patients who have gone there failed to obtain relief. California is free from the disease, and many hay-fever patients have escaped their attacks by removal to that State. I know of no place in the Southern States which affords relief except Florida, where the disease is rare; several cases have been entirely relieved during their residence there. In others, however, the experiment was unsuccessful.[17]

[Footnote 17: Two patients in their replies to the writer's circular claimed to have been entirely exempt--the one (early form) at Beaufort, and the other (autumnal) at Mount Airy, Habersham county, Ga. Wyman mentions four cases that were relieved at or near Beaufort.]

The relief obtained by resorting to an exempt locality after the attack has begun is very prompt, all symptoms of the disease disappearing within a few days after the arrival of the patient. While residing at Bethlehem, N.H., I was called one evening to see a German who had just arrived on the train from Fall River. His condition was most pitiable: his eyes were fiery red, the nose and face were terribly swollen, while the water streamed from both eyes and nose. The asthma was at its height, and his struggles for breath were fearful in the extreme. A quarter of a grain of morphia was injected into the arm, and after providing other means for his comfort I left him for the night. The next morning, while preparing to pay him an early visit, the patient himself appeared at my office, bright and cheerful, and so much changed that I at first failed to recognize him. A single night had served to dissipate all traces of his hay fever.

Unfortunately, a journey to the mountains, and a residence there of six or eight weeks, are not within the reach of every one afflicted with the disease; and for these unfortunates something must be done to relieve, or at least mitigate, their sufferings. If unable to visit any of the exempt localities, a sufferer may secure a certain degree of comfort by exposing himself as little as possible to the exciting causes of hay fever. As it is well known that heat and dust aggravate the symptoms, the windows of the apartment occupied {224} by the patient should be so arranged as to exclude the sunlight and every precaution taken to avoid the presence of dust. He should eat good, nutritious food, avoiding the use of all stimulants, except perhaps a little light wine at dinner. Anything which induces dyspepsia must be carefully guarded against, and care taken to keep the bowels regular.

Blackley[18] advises as a surer method of excluding the irritant (pollen) the hanging of a curtain of thin calico before the door and fitting into the lower portion of one of the windows a screen made of two layers of thin black muslin enclosed in a square frame. When in use both curtain and screen should be moistened with a solution of carbolic acid, ten grains of the acid to one pint of water. For those who are compelled to go out he has devised a very ingenious respirator. Having taken an exact cast of the nasal passages from the margins of the alæ and septum to the inferior turbinated bones, he constructed with the aid of these, by means of the galvano-plastic process, cases of silver fitting exactly all the folds and depressions of the cavity. Several layers of platinum wire, 0.001" to 0.007", were arranged in the cases. The sieve thus formed was moistened before using with a 1/10 per cent. solution of carbolic acid. To prevent the pollen from coming in contact with the eyes, they were protected with spectacles provided with accurately-fitting gauze guards. The result of wearing this apparatus was an almost perfect freedom from unpleasant symptoms.

[Footnote 18: Op. cit., p. 267.]

In the absence of any specific, the medicinal treatment of hay fever is necessarily confined to palliative measures. Debility being one of the prominent symptoms, tonics are indicated, and in this way quinine, at times regarded almost as a specific, may be of use. It should be given in doses of one or two grains three times a day before and during the attack. Thus administered, it is undoubtedly of great utility in many cases. Arsenic, whether in the form of Fowler's solution or the iodide of arsenic, as suggested by Blackley, may also be used with advantage. Galvanism, which was used successfully by Hutchinson of Rhode Island, is strongly recommended by the late Beard. He advises that the negative pole be placed at the epigastrium "and the positive applied a moment over the forehead and on top of the moistened head, then over the front and back of the neck, and down the upper and middle of the spine." The current used should be mild and the sittings short. The writer has had no personal experience with this method of treatment, nor has it been generally adopted.

The injection into the nostrils of a saturated solution of quinine by Helmholtz, although apparently useful in his case, has not met with like success in the hands of others.

The troublesome itching and burning of the eyes and face are most readily relieved by bathing the parts at first in tepid and then in cold water, repeated several times a day, and with mild astringent collyria, such as a strong infusion of tea or of one or two grains of sulphate of zinc to an ounce of rosewater. If the lids be much inflamed and the skin excoriated, the following ointment may be applied:

Rx. Bismuth. subnit. drachm ss; Ungt. simpl. ounce j. M. Ft. ungt.

The pharyngeal symptoms are best controlled by chlorate of potassium as a gargle, or, better still, in the form of the compressed tablets now prepared by many of our druggists. The treatment of the asthmatic symptoms differs in no way from that which we have recommended for the paroxysms of BRONCHIAL ASTHMA, the details of which were fully described in the preceding article.

In 1880, Harrison Allen of Philadelphia published an article[19] directing {225} the attention of the profession to the fact that many cases of chronic nasal catarrh which had resisted the ordinary methods of treatment could be readily cured by restoring the permeability of the nasal passages.

[Footnote 19: Am. Journal of Med. Sciences, January, 1880, Philadelphia.]

In April, 1882, William H. Daly of Pittsburgh, Pa., in a paper[20] read before the American Laryngological Association, gave the histories of three cases of hay fever which he had succeeded in curing by means of operative procedure. In each of these cases the tissue over the inferior and middle turbinated bones was hypertrophied, and in one case it was so extremely sensitive that the slightest touch with the probe was sufficient to excite a violent paroxysm of sneezing. In these the diseased tissue was removed with the galvano-cautery or by the application of glacial acetic acid.

[Footnote 20: "On the Relation of Hay Asthma and Chronic Naso-pharyngeal Catarrh," Archives of Laryngology, vol. iii. No. 2.]

The following year (1883) a much more elaborate article[21] on the same subject was published by John O. Roe of Rochester, N.Y. After describing the highly vascular and somewhat erectile tissue covering the inferior turbinated bones and lower portion of the septum, the turbinated corpora cavernosa of Bigelow, he calls attention to its great susceptibility to the action of irritants, whether applied locally or to some remote portion of the body, citing as an example of the latter the swelling, and sometimes almost complete closure, of the nostrils supervening after exposure of the body to the action of a current of cold air. In this situation the tissue is liable to become hypertrophied, and in that state its susceptibility is greatly increased. If, when in this condition, it is exposed to the action of pollen, dust, or any other irritant, the substance produces a local irritation which is reflected through the sympathetic nerves to other parts of the respiratory tract; and it is to this reflected irritation that Roe attributes most of the phenomena of hay fever. He regards it as analogous to certain forms of laryngeal catarrh which, according to the recent testimony of many distinguished laryngologists, are clearly traceable to disease of the nasal cavity. Applying this theory to the treatment of hay fever, he removed the hypertrophied tissue in five cases, and in every instance succeeded in preventing a recurrence of all symptoms of the disease. His operation consists in the removal of the diseased tissue by means of Jarvis's wire écraseur and the galvano-cautery, caustics having proved less effective. The wire snare is best adapted for the removal of the tissue over the posterior portion of the turbinated bone, where, owing to its being pedunculated, it is readily caught in the wire loop. Over the anterior portion of the turbinated bone, as well as over the septum, the growth is more sessile, and is best destroyed by means of the galvano-cautery. To avoid inflammatory reaction and to guard against other unpleasant symptoms it is advisable to remove only a small portion of the growth at a time. After each operation the part should be sprayed with warmed vaseline to allay the irritation occasioned by the burning, and this should be continued until the surface is sufficiently healed over to admit of a repetition of the operation. The cauterization should be repeated until every trace of the diseased tissue is removed.

[Footnote 21: The Pathology and Radical Cure of Hay Fever, New York, 1883.]

Prior to the publication of Roe's article Harrison Allen had operated successfully on two cases, the histories of which he has not as yet published, but has kindly communicated by letter to the writer, together with a description of his method of operating. This latter differs but little from that of Roe, except as regards the time at which the operation should be performed, Roe maintaining that the operation should never be performed when the patient is suffering from an attack of hay fever, while Allen considers this immaterial, and does not hesitate to operate even when the symptoms are at their height. If symptoms of hay fever recur after the operation, the nares should be {226} carefully examined, and if, as is usual in such cases, any remnants of hypertrophied tissue be discovered, these should be at once removed. The operation is not regarded as a very painful one, and a patient of Allen's upon whom he had operated during an attack assures me that he left the doctor's office feeling much better than when he entered it. This is mentioned because hay-fever patients are excessively nervous, and timidity on their part has hitherto prevented many of them from availing themselves of this form of treatment.

It will be seen that, thus far, the operation has been performed in but ten cases, but the results have been so uniformly successful as to justify the belief that it is capable of relieving many cases of this hitherto intractable disease. Whether this hypertrophied condition is present in every case, as claimed by many, or in even the majority of cases of hay fever, has not as yet been determined; and until further observation shall have decided this question it will be impossible to form an opinion in regard to the general application of this method of treatment.

{227}

DILATATION OF THE BRONCHIAL TUBES, CIRCUMSCRIBED AND DIFFUSED.

BY SAMUEL C. CHEW, M.D.

DEFINITION.--Enlargement of the calibre of a bronchial tube or tubes, whether confined to a limited portion of one tube, or reaching throughout a great part of its extent, or involving several or many tubes.

SYNONYM.--Bronchiectasis, from [Greek: bronchos], a bronchial tube, and [Greek: echtasis], an expansion.

HISTORY.--The change in the physical condition and size of a bronchial tube, designated as bronchial dilatation, never occurs as a primary affection, but is always the result of some preceding disease, especially of chronic bronchitis or fibroid phthisis. The full consideration of its pathological origin belongs, therefore, to the natural history of those causative affections.

Later writers have in general followed Laennec's description of the different varieties of bronchial dilatation; which, indeed, can hardly be improved upon, for such was the accuracy of that great clinician and pathologist as an observer that nothing was likely to escape him as regards physical conditions, though he may sometimes have been in error as to the theoretical explanation of what he saw. Previously to Laennec's observations dilatation of the bronchial tubes was, as he remarked himself, almost entirely overlooked both by pathologists and practitioners. The reason of this is evident from the considerations that a smaller tube when dilated would, except to the most careful examination, closely resemble a larger tube of normal size, and that a large dilatation might be mistaken by the ear at the bedside and by the eye at the necropsy for a pulmonary vomica.

Two principal forms of bronchial dilatation are met with. In the first, or diffused bronchial dilatation, known also as the cylindrical form, the tube is uniformly enlarged in calibre, so that, whereas in the normal state it would have admitted only a fine probe, in its enlarged condition it may be of the size of a goosequill. In this state it may be readily mistaken, when seen by itself, for a larger tube; but the alteration is conspicuous when the tube is seen to be larger than the branch from which it is given off. In the second or circumscribed form, which is also termed sacculated dilatation, a pouch-like or fusiform distension occurs in the continuity of a tube. In a third form, which is far less common, several successive enlargements are met with in the course of one tube, which thus presents a beaded appearance. It happens at times that all of these different varieties of dilatation may be encountered in the bronchial tubes of the same lung. The second, or sacculated, form is the most common, especially in young persons.

ETIOLOGY.--In both of the more common forms of bronchial dilatation the previous existence of bronchitis is to be regarded as the chief causative agency, though other conditions may serve to increase the dilatation when it has once been established. Laennec's observations led him to connect the {228} occurrence of bronchitis with the production of dilatation of the bronchial tubes, though his explanation of the mechanism of this production was erroneous, inasmuch as he considered the accumulation of secretion in the affected tubes, and the forcible inspiratory efforts made in coughing to dislodge this accumulation, to be the direct causes of the enlargement. The part played by bronchitis in producing dilatation is, however, less immediate and mechanical than Laennec held it to be. It may, in a general way, be considered the direct cause of the cylindrical and the indirect cause of the saccular form of dilatation.

The long continuance of chronic bronchitis gives rise to weakness and atony of the bronchial walls, so that they yield to the pressure brought to bear upon them in the violent or protracted and repeated respiratory efforts that are made in coughing. In such cases the tubes which are themselves affected by the inflammatory process may yield throughout a greater or less extent of their continuity, and thus the cylindrical form of dilatation may be established. The same mechanism may be supposed to give rise to the beaded variety of the disease if the inflammatory action should be greater at several points along the course of a tube, with intervals of tissue in a healthier or less atonic state.

In the saccular form, on the other hand, the dilatation does not occur in the portion of the tube which is chiefly affected with the inflammatory process, but is the consequence of a local capillary bronchitis involving the ultimate ramifications of the affected tube and occasioning collapse of a portion of the lung. This collapse operates in two ways in causing a pouch-like dilatation of an adjacent bronchus--partly through the atmospheric pressure within the affected tube, tending to fill the space created by the collapsed portion, and partly by the traction of this collapsed lung-tissue outside of the tube.

In addition to the part played by bronchitis and atelectasis of the lung in occasioning bronchial dilatation, another important factor in its production is to be found in the condition described by Corrigan in 1838 as cirrhosis of the lung, and since recognized as interstitial pneumonia or fibroid phthisis. In this affection there is formed around the blood-vessels and terminal bronchi, as well as around the air-vesicles, a hyperplasia of the connective tissue, which, as is the case with connective-tissue formations in other situations, ultimately contracts, obliterating the air-cells, smaller bronchi, and blood-vessels, and thus converts the lung-tissue into a tough, fibrous mass. By the contraction thus produced the bronchial tubes of a larger size, which have been previously weakened by bronchitis and have lost their elasticity, are subjected to traction on all sides, and thus become dilated. Dilatations of all forms may thus be produced, cylindrical, sacculated, or beaded, according to the amount of lung involved in the contracting process and to the degree and situation of the bronchitis which favors the dilating action.

The determining causes, then, of bronchial dilatation are--1st, chronic bronchitis; 2d, atelectasis; and, 3d, fibroid phthisis or cirrhosis of the lung.

SYMPTOMATOLOGY.--The general symptoms of bronchial dilatation, as well as the course and duration of the affection, are such as belong to the pulmonary diseases favoring its production, especially chronic bronchitis and fibroid phthisis. The cough and dyspnoea of these diseases are aggravated by bronchial dilatation; but these symptoms, together with the impairment of nutrition, are due rather to the underlying affections than to the mere fact of dilatation. Increased and fetid expectoration, which often occurs in bronchial dilatation from retained and altered secretion, is by no means characteristic of this condition, since it may occur where no sign of dilatation exists.

There is generally some degree of dulness on percussion over a dilated {229} bronchial tube, due to the condensation of the lung-tissue surrounding it, and varying in extent and degree with the amount of that condensation, and also with the amount of secretion retained within the tube. Sometimes, however, increased resonance of a tympanitic character is observed, especially if the dilatation be of the saccular form and near the surface of the lung. Such differences in the percussion sound are analogous to what occurs over a pulmonary vomica, which will generally give a dull sound, though, if the cavity be superficial and thin-walled, it may yield a tympanitic resonance. On auscultation bronchial respiration may be heard along the course of tubes affected with cylindrical dilatation when they are free from secretion; and this is more intense in proportion as the tube is more dilated and the lung-tissue around it more condensed. Bronchophony and increased vocal resonance also occur, and if mucus be present in the dilated tubes coarse moist râles will be heard. In a saccular dilatation there may be true amphoric breathing, with the gurgling sounds heard in a vomica. In some cases there is an alteration in the appearance of the chest-wall, which is retracted by the shrinking of the condensed lung beneath.

Now, of the auscultatory signs that have been mentioned, the bronchophony and increased vocal resonance, together with the percussion dulness, belong also to pneumonia, which, however, at least in its acute form, can be distinguished from bronchial dilatation by the previous history, the febrile movement, and the general phenomena of the case, and by the fact that the tubal breathing of pneumonia, besides being less persistent, is most frequently met with in the lower part of the lung, and that of bronchial dilatation in the upper part.

But the diagnosis between a dilated bronchus and pulmonary phthisis is in some cases a very difficult problem, the signs of the cylindrical form closely simulating those of the stage of deposit in phthisis, because involving the same physical condition, and those of the saccular variety corresponding often with the auscultatory signs of a cavity. In the former case there may be the same localized dulness on percussion, the same bronchial or broncho-vesicular breathing, and the same sinking or contraction of the chest-wall apparent on inspection. In the latter case there may be equally in saccular dilatation and in a vomica amphoric breathing, gurgling, and pectoriloquy. In the establishment of the diagnosis between these two conditions Austin Flint, Sr.,[1] justly attaches importance to the circumstance that there is in general a greater degree of percussion dulness over a cavity than over a dilated bronchus, so that a relatively greater prominence of the auscultatory signs as compared with the degree of dulness makes the diagnosis of dilatation more probable. But the most important evidence on the point is to be gotten from the history of the case. If in a case where the auscultatory signs would leave the examiner in doubt there were found loss of flesh, fever, night-sweats, quickened pulse, and the other general phenomena belonging to phthisis, the existence of this affection would be rendered probable in the highest degree, and the auscultatory signs should be taken as corroborating an opinion founded on the general symptoms.

[Footnote 1: Dis. of Resp. Organs, p. 353.]

Positive evidence, again, may be furnished by a microscopic examination of the sputa; the discovery of particles of lung-tissue or the so-called bacillus tuberculosis pointing clearly to phthisis. Conversely, the absence of the general symptoms of phthisis would, in a case presenting the above auscultatory signs, render it probable that they are due to bronchial dilatation. Long-continued cough and abundant expectoration are the chief symptoms common in both forms of disease. There are, however, some cases in which even with the most careful examination and weighing of evidence the physician will be left in doubt, inasmuch as in some cases of otherwise {230} well-marked phthisis the usual constitutional symptoms are absent or imperfectly declared. In such exceptional cases the estimate of probabilities is to be based on the fact that while bronchial dilatation is comparatively rare, pulmonary phthisis is extremely common.

PATHOLOGY AND MORBID ANATOMY.--Enlargement of the bronchi may be met with throughout almost the entire extent of a lung; when limited to a part of the organ the change most frequently occurs, according to Laennec, Rokitansky, and other observers, in the superior lobe and toward the anterior border. The tubes of the third or fourth order in respect to size are most frequently affected, the primary bronchi being never involved except in association with tracheal dilatation.

In the different forms of dilatation the bronchial walls are found in various states. In the cylindrical variety they are for the most part thickened and hypertrophied, both as to the mucous and the fibrous coats; the mucous membrane being in a catarrhal state, covered often with muco-purulent discharge, and easily broken down and detached, while underneath the white fibrous coat is sensibly thickened.

In the sacculated form, on the other hand, the bronchial wall generally presents a thin and atrophied appearance, the mucous membrane undergoing but little change, except that the stretching to which it has been subjected gives it a smooth and shining look. This difference in the degree of thickening of the bronchial walls in the two forms of dilatation is in part due to the fact that in the saccular variety the enlargement in calibre is far greater than it is in the cylindrical form for a corresponding extent of a tube, so that its wall is much more stretched and attenuated, and thus the tendency to hypertrophy which has play in the cylindrical form is more than overcome in the saccular. But the chief reason of the difference in the state of the walls in the two forms of dilatation is found in the different modes in which they are respectively brought about, as already described.

DIAGNOSIS.--It has been shown that the determination of the existence of bronchial dilatation is at times one of the most difficult problems in diagnosis, from the fact that the auscultatory signs belonging to it may be equally met with in other affections, especially in pulmonary phthisis. The diagnosis is to be established, when this is possible, only by a careful consideration of the physical signs in connection with the general symptoms, so that the sources of doubt arising from the one set of phenomena may be as far as possible corrected by the other. These signs and symptoms, and the various affections to be discriminated by them, have been sufficiently set forth under the head of Symptomatology. While in this way a clear conclusion may be reached in many cases, yet there are others in which, notwithstanding the utmost care, there may still be a doubt as to whether the symptoms and signs indicate a dilated tube or a pulmonary cavity.

PROGNOSIS.--The prognosis of bronchial dilatation is directly connected with that of the affections which chiefly give rise to it--viz. chronic bronchitis and fibroid phthisis. When chronic bronchitis has lasted long enough to cause dilatation, it is seldom if ever cured, and, though improvement may take place from time to time in its symptoms, yet the dilated bronchi can hardly undergo diminution in their size. And in fibroid phthisis, while the progress of the disease is often very slow, yet it is on a downward grade, and the connective-tissue contraction giving rise to the dilatation increases with the advance of the malady.

TREATMENT.--The treatment of cases of bronchial dilatation resolves itself in great degree into that of the underlying and causal diseases on which it depends. As regards methods specially directed to the areas of dilatation, they consist of alterative, astringent, stimulant, and antiseptic remedies, either administered by the stomach or used by the process of inhalation. Cough {231} may be allayed with the syrup of lettuce containing in each dose from one-eighth to one-fourth of a grain of sulphate of codeia or 10 or 12 drops of the spirit of chloroform. If expectoration is very profuse, sulphate of atropia, in the dose of one-hundredth to one-eightieth of a grain, or the extract or tincture of belladonna, may be used. Turpentine and eucalyptol have a controlling influence over this symptom, and are specially beneficial if the bronchial secretion is fetid. They may be given by the mouth in the dose of minim v-xx in emulsion, and applied also by inhalation of their vapor or by spray. Inhalations of solutions of carbolic acid, minim j-x to an ounce of water, are more effective than anything else in checking fetor of the expectoration and the breath. This agent may also be administered by the mouth in the dose of fluidrachm j-iv of a 1 per cent. solution.

{232}

EMPHYSEMA.

BY SAMUEL C. CHEW, M.D.

DEFINITION.--The term emphysema is derived from [Greek: emphysaô], to inflate, and signifies an increased amount of air in a part or the whole of one or both lungs. Accordingly as the situation of this excess of air is (a) in the air-vesicles or (b) in the connective tissue between the lobules, emphysema is divided into Vesicular emphysema and Interlobular or extra-vesicular emphysema.

HISTORY.--These two affections are different pathologically and anatomically, vesicular emphysema being a much more common and important affection than the interlobular form. The distinction between the two forms was first drawn by Laennec. Previously to his time the essential difference between them was unknown; and, as the accurate diagnosis of the disease can be made only by auscultation, its existence was no doubt very often entirely overlooked. It has been remarked by Rokitansky[1] that "had Laennec done nothing else for medical science, his discovery of this diseased condition, and of the causes giving rise to it, would have sufficed to render his name immortal."

[Footnote 1: Path. Anat., vol. iv. p. 53, Am. ed.]

VESICULAR EMPHYSEMA.

Vesicular emphysema may be defined as an absolute or relative increase in the amount of air contained in the vesicles of a part or the whole of one or both lungs. As a substantive disease it occurs in two principal forms--hypertrophic and atrophic; but besides these it is met with as a secondary affection due to other diseases and limited to certain areas of the lungs, sometimes acute and sometimes chronic in its production and duration. It will therefore be best to consider the disease under the following different forms:

1st. Acute lobular emphysema; 2d. Chronic lobular emphysema; 3d. Hypertrophic lobar emphysema; 4th. Atrophic lobar emphysema.

1. Acute Lobular Emphysema.

This form of the disease is the result of the rapid distension beyond their natural size of air-vesicles which had previously been healthy. It is most frequently met with in children and as the consequence of bronchitis or {233} whooping cough. The paroxysms of cough occurring in these affections, especially in the latter, are attended by deep inspirations, by which the vesicles are directly distended, and by violent expiratory efforts, with closure of the glottis, so that the air is forced into those portions of the lungs where there is least resistance, particularly at the apex and along the margins. In a large proportion of cases of acute lobular emphysema, when the distending cause is removed by the cessation of the cough, the vesicles return to their normal size through their natural elasticity, which has not been destroyed. But in some cases, when the cough has been of unusual violence or of very long duration, the change may be permanent through loss of this elasticity, and thus a form of chronic lobular emphysema is produced.

SYMPTOMS AND SIGNS.--Unless emphysema of this form is extensive and extreme in degree, it is not attended with symptoms additional to those of the affections giving rise to it. When very great it may occasion increased percussion resonance.

TREATMENT.--The treatment is only what is required by the causal affections.

2. Chronic Lobular Emphysema.

In many cases emphysema is confined to a limited number of lobules, especially at the apices, the anterior borders, or about the base of the lung; and being gradual in development and permanent in duration, it is then termed chronic lobular emphysema. This is the form frequently met with in the different varieties of pulmonary phthisis, in which its development seems supplementary to the incapacitation of other portions of the lung. The lobules nearest to the surface of the lung or immediately beneath the pleura are found to be most distended, so that they often project beyond the adjacent surface.

Chronic lobular emphysema is chiefly of interest in connection with the other pulmonary diseases which give rise to it. The mechanism of its production is like that of acute lobular emphysema, but the diseases occasioning it being chronic the emphysema to which they give rise is equally permanent. At the apex of the lung, its most common situation, it is very often associated with tubercle in a calcareous state. The changes accompanying this deposit of tubercle favor the loss of elasticity in the vesicles of the apex, and the violent expiratory efforts, with closure of the glottis, occurring in the attacks of cough to which phthisical patients are subject, force the air into this part especially, and also into other regions of less resistance, and thus occasion permanent distension of the vesicles.

SYMPTOMS AND SIGNS.--The signs of this form of emphysema are so often masked by those proper to phthisis that the detection of the former is difficult or impossible. This, however, is of no practical importance in respect to treatment. At times the distension of the vesicles at the apex is so great as to produce bulging in the supra-clavicular region and to overcome the dulness due to deposit by the resonance it occasions.

TREATMENT.--No special treatment beyond that of the causative affections is required.

3. Hypertrophic Lobar Emphysema.

This is a substantive affection, and is much the most important form of the disease, both in its origin and development and in the consequences to which it leads. Though sometimes limited to one lung, or even to a single lobe of {234} one lung, yet it more commonly involves the greater part of both lungs, which are increased in size, as shown by the alteration of the contour of the chest during life and by the appearance of the organs after death. This enlargement of a lobe or of a whole lung is of course the aggregate of the increase in size of the individual vesicles, the changes in which form the pathological units of the disease.

ETIOLOGY.--In no disease is the study of etiology as throwing light on treatment, both medicinal and hygienic, of more value than in emphysema, the important question being as to whether it takes its origin from some immediate mechanical cause acting upon the healthy cell-walls, and thus distending them, or whether they suffer such distension only when they have been previously weakened by some degenerative process in their tissue. The importance of determining this point correctly with reference to treatment is obvious.

In partial and lobular emphysema the change may have been wrought by causes mechanical in their nature and directed specially to the affected parts, such as have been already referred to; but in the general diffused or lobar form of the disease, in which by degrees the greater part or the whole of a lung is involved, we are almost compelled to assume the existence of some degenerative process or tendency coextensive with the malady and determining its existence. That any one form of degeneration is present in all cases has never been proved; indeed, it may be said to have been disproved. Rainey's view, that the change in the air-cells is essentially dependent on fatty degeneration of their walls, was based mainly on observations made upon a single case, and, although favored by the eminent authority of C. J. B. Williams, it has not been substantiated. The same thing must be said of Sir William Jenner's teaching, that fibroid degeneration is the essential lesion. Though both fibroid and fatty changes are found in not a few cases, yet in others a careful examination has failed to detect either the one or the other of them, so that neither can be regarded as the essential condition explaining all cases. Nevertheless, it is probable in the highest degree that a degenerative change of some kind, due to imperfect or perverted nutrition of the cell-walls, always exists in general lobar emphysema, though its nature may sometimes elude observation.

In cases of well-marked emphysema there may be no discoverable morphological changes in the walls of the alveoli, though, as remarked by Hertz,[2] "a tissue-relaxation may be present in the lung without our being able to recognize any corresponding microscopic abnormality."

[Footnote 2: Ziemssen's Cyclop., vol. v. p. 373.]

It may be said, then, that while in partial or local emphysema the alteration in the air-vesicles may be effected by extraordinary efforts brought to bear upon healthy cell-walls, in general or lobar emphysema, on the other hand, it may be produced by ordinary efforts acting upon weakened and diseased cell-walls. The morbid change is probably not in all cases alike, being sometimes fatty, sometimes fibroid, degeneration, and in other cases of a kind not ascertained.

In addition to other considerations, the markedly hereditary nature of emphysema in not a few instances would of itself render the existence of some constitutional predisposing cause highly probable. On this point A. T. H. Waters[3] quotes the observations of Greenhow and Jackson. Out of 42 cases collected by Greenhow, 23 showed an hereditary tendency, and in 28 reported by Jackson, 18 were of emphysematous parentage. In stating his belief that substantive or general emphysema is the result of some degenerative process, Waters bases it on the following considerations: 1st. The high degree of development which the disease often reaches, without any {235} previous history of violent or long-standing cough, in connection with either bronchitis, whooping cough, or any similar affection. 2d. The frequency with which the disease attacks the whole of both lungs, and the uniform character of the morbid changes often observed throughout all parts of the lungs. 3d. The hereditary nature of the disease, as shown by observations. 4th. The manner in which the disease is influenced by certain remedial measures which are known to act beneficially on other diseases attended with degeneration of tissue.

[Footnote 3: Diseases of the Chest, pp. 122, 123.]

As to the nature of the immediate exciting cause of emphysema, whether in the general or local form, different views have been maintained. The most important of these are the inspiratory and expiratory theories.

The former of these theories, that in accordance with which the disease is referred to inspiratory action, was maintained by Laennec, and under the influence of his authority was at one time generally accepted. In accordance with this view, the existence of bronchitis is an important factor in the production of emphysema, as undoubtedly it often is in the lobular form. The dilatation of the air-vesicles was attributed to their over-distension by inspiratory efforts allowing the free entrance of air, the escape of which was impeded by bronchial mucus. Inspiration was thus regarded as a more powerful act than expiration, which was considered too feeble to drive the air beyond the accumulated mucus. In this way the air was supposed to accumulate in gradually increasing amount within the cells, which thus became distended.

But in opposition to this view it has been shown by Hutchinson's researches that Laennec was wrong in supposing inspiratory power to be greater than that of expiration; and it is further opposed by the researches of Mendelssohn and Traube, and those of Gairdner, which have shown conclusively that the presence of a pledget of mucus in a bronchial tube, so far from causing distension of the air-vesicles to which it leads, must ultimately ensure their collapse. The collapse thus occasioned, which is most common in the lower parts of the lungs, may lead, partly perhaps through inspiratory pressure, to vicarious emphysema in the upper portions, which receive a relatively larger quantity of air, in accordance with Williams' theory of negative inspiratory pressure.

It is true, then, as maintained by Laennec, that bronchitis may occasion emphysema, but the emphysema does not occur in the vesicles to which the affected tubes directly lead, nor from the force of inspiration applied to these vesicles, as Laennec taught, but in other portions of the lungs.

The expiratory theory affords a more satisfactory explanation of emphysema than does the inspiratory theory, and one more completely in accordance with the physiology of respiration and the anatomy of the thorax.

In ordinary expiration, in which the lungs are uniformly and equably compressed by the chest-walls, there is nothing tending to force air into one part of these organs more than into another, and thus produce emphysematous dilatation. But in forced expiration, such as occurs in the act of coughing, it may be plainly seen, if the chest be uncovered, that the air is driven upward to the top of the lungs, so as to produce a perceptible bulging in the supra-clavicular region. This bulging is notably increased in the coughing-spells of emphysematous subjects; and this fact is urged by Sir William Jenner both as throwing light upon the expiratory act as a principal factor in the disease, and as accounting for the special frequency of emphysema in the upper parts of the lungs. The explanation of this phenomenon is found in the circumstance that in the strong expiratory efforts of coughing the abdominal muscles force the diaphragm upward, and thus compress the lungs from below; at the same time the strong lateral anterior and posterior thoracic walls resist pressure, while the superior part of the thorax, covered over {236} with fascia, but not completely protected by a bony structure, offers least resistance. To this unprotected part of the lungs and to the free margins and borders, which contain normally the smallest amount of air, will the strong currents produced by violent expiratory efforts be driven, so as to cause distension of their vesicles. Thus, the frequent coughing-spells of bronchial catarrh, so commonly associated with emphysema, give rise to the expiratory efforts which are the immediate cause of the emphysema.

While, therefore, it is probable that in some cases and to a certain degree inspiration may have a share in occasioning emphysema, yet expiration is to be regarded as a more important and more frequent factor in its production. This, at least, is probably the case in partial and lobular emphysema, and in some instances of the lobar form where the disease gradually spreads throughout a lobe. But in rapidly-diffused and extensive lobar emphysema such an explanation cannot always be admitted, because sometimes the disease advances steadily, so as to involve the greater part of one or both lungs without the occurrence of any paroxysms of cough which could distend the air-cells by their violent expiratory efforts. In such cases the only distending force would seem to be that of ordinary inspiration, which, while it might have no effect upon healthy lung-tissue, may easily be supposed to exercise sufficient dilating power upon air-cells, the walls of which are in a state of degeneration, and, thus being unnaturally weak, yield to pressure.

SYMPTOMS AND SIGNS.--One of the earliest symptoms of emphysema is shortness of breath; and, though at first it may not be very marked, yet as the disease advances it becomes more and more urgent, especially on going up stairs or walking up hill. Distension of the stomach by a full meal is likely to induce it, and even a slight degree of bronchial catarrh may render it extremely distressing. This symptom is due chiefly to two causes: First, the obliteration of numerous capillaries in the pulmonary system, occasioned by the thinning and destruction of the cell-wells in which they ramify, interferes with oxygenation, so that an increased number of inspiratory acts is required to supply the deficiency, and thus respiration is hurried; and, secondly, the impairment of the natural elasticity of the air-vesicles prevents the expulsion of their contents; the residual air remains, therefore, unchanged, and cannot supply oxygen to the blood; and thus increased expiratory efforts are made in order to expel the stagnant air and obtain a fresh supply. Notwithstanding this increase of both inspiratory and expiratory action, the movements of the chest are but slight. As far as bronchial catarrh is a cause of dyspnoea in emphysematous patients, improvement may take place in the warm dry weather of summer, when this symptom is often much mitigated.

Cough is a very constant symptom, varying in degree with the extent of bronchial catarrh. The act of coughing is feeble and expectoration is effected with difficulty--so much so that sometimes the retained secretion threatens suffocation.

Asthma occurs in paroxysms, and as a distinct phenomenon from the dyspnoea which is more or less constant. The asthmatic seizures often come on in the night after the patient has been asleep; they are characterized by orthopnoea and constriction in the chest, and generally subside with free expectoration.

The physical signs of emphysema are highly characteristic and of great importance. On inspection a peculiar conformation of the chest is observed when the emphysema has lasted for some time, the departure from the normal form gradually increasing in the progress of the disease until, in advanced cases, a degree of deformity is produced which is strikingly characteristic. In the earlier stages, or if the emphysema is local and partial, the alteration in the chest-wall consists only of a prominence corresponding with the dilated {237} portion of the lung. But when the disease is general and occupies a considerable portion of both lungs, a rounded, convex, or barrel-like form of the thorax is produced, most noticeable in the upper part, and due to increased prominence of the ribs. The thoracic portion of the spine becomes more curved, and thus throws the shoulders forward, producing a stooping attitude. The intercostal spaces at the upper part of the chest are frequently effaced by the pressure of the enlarged lung, while at the lower part the depression of these spaces may be increased, especially during inspiration, by the action of the diaphragm. The enlargement of the thorax as a whole is chiefly due to the changes in its upper part, the lower part appearing sometimes by contrast to have lessened in volume. This, however, is in most cases apparent rather than real; but in some instances the dimensions in the lower part of the chest are actually lessened.

The respiratory movements in well-marked emphysema are characteristic and peculiar. The dilatation of the chest which is sought to be accomplished by muscular action is small and disproportioned to the amount of effort put forth, notwithstanding that the need for air keeps the sterno-mastoid and scaleni muscles in constant action. The reason of this is that, the lungs being distended nearly to their utmost capacity, there is but little room for further expansion. As there is only slight enlargement on inspiration, so with expiration the walls of the thorax contract but little at their upper part.

The result, therefore, of their muscular efforts is that the ribs are lifted and the sternum carried forward, so that the whole chest rises and falls in respiration as if its walls formed a solid case. But the character of respiration is by no means the same in all cases of emphysema. More than forty years ago Stokes[4] called attention to the different modes of breathing in different cases accordingly as there is or is not displacement of the diaphragm; and his observations have more recently been reaffirmed by Waters[5] and others. In the one class of cases the diaphragm retains its normal position and the upper part of the chest is very prominent, probably because the disease is chiefly in the upper portion of the lungs. Here there is but little descending movement of the diaphragm in inspiration and the abdomen remains flat. In the other class the diaphragm has been displaced and pushed downward by the enlarged lungs, which have probably been involved in the disease throughout their whole extent. In these cases the abdomen is protruded more or less with every inspiration. The difference between the two types of breathing is important, as in the latter class of cases there is more advanced and extensive disease than in the former, the symptoms being more urgent, and especially the dyspnoea greater. Inspection of the chest shows that the movement of inspiration is more quickly accomplished than that of expiration, which is prolonged, labored, and often wheezing in character.

[Footnote 4: Diseases of Chest, 2d ed., p. 173.]

[Footnote 5: Diseases of Chest, p. 140.]

Percussion and auscultation furnish signs of the utmost importance for determining the existence of emphysema which are in direct accordance with the physical conditions giving rise to them.

Increased resonance on percussion is observable over all portions of the lungs when the disease is general, but it is most marked at the upper part and along the anterior borders. When the disease is partial, the increased resonance is limited to the portions of the chest-wall over the affected areas. This sign is of course due to the greater amount of air in the distended vesicles. In very marked cases the resonance sometimes loses the vesicular and approaches the tympanitic character. There is very little, if any, further increase of the resonance on full inspiration. This is unlike what occurs in health, and is due to the fact that the capacity of the distended lungs is not relatively increased in emphysema, as it is in health, by the act of inspiration.

{238} Over the cardiac region the normal dulness on percussion is lessened or entirely superseded by resonance from the overlapping of the heart by the distended lung. In partial emphysema the heart may escape this encroachment and its area of dulness may not be lessened; and even in some rare cases where the disease is general and far advanced the same thing may be observed, from the lung being bound by pleuritic adhesions, so that it cannot expand in the direction over the heart. But, as a very general rule, it will be found in hypertrophic emphysema that the normal præcordial dulness is lessened or absent. When this is observed the heart is in some cases forced downward, its beat being felt most distinctly in the epigastrium; and in other cases it is carried directly backward, so that its impulse can hardly be detected at all.

Over the posterior wall of the chest percussion gives a clear note at a lower level than in health, because the dilated lung extends farther down toward the bottom of the thorax.

The signs afforded by auscultation are highly characteristic of emphysema, and, like those of percussion, in direct relation with the physical condition of the lungs. The respiratory sounds are notably feebler, because the amount of air entering and leaving the lungs at each act of respiration is less than in health. The distended lungs can admit only a small amount of air at each inspiration, and from their diminished elasticity they can expel but a small amount at each expiration. This feebleness is directly proportioned to the degree of the disease, or, in other words, to the amount of distension; for the greater the distension, the less movement of the lungs and the less play of air. If the disease be unequally advanced on the two sides of the chest, the respiratory murmur will correspondingly vary, being feebler on the side where the disease is most advanced.

Besides this change in intensity, there is also an alteration in the rhythm of the respiratory acts corresponding to what has been referred to above as observable on inspecting the chest. The ratio of inspiration and expiration is always changed in well-marked emphysema--so much so as to be in many instances reversed, the expiratory occupying more than double the time of the inspiratory act. Inspiration is short and quick, because the air enters freely and the limit of the possible expansion of the lungs is speedily reached. Expiration is prolonged, because there is a loss of their normal elasticity, and an effort is made by voluntary action of the expiratory muscles to expel the stagnant residual air. This alteration in rhythm is eminently characteristic of emphysema when the disease is far advanced and occupies a considerable portion of the lungs. Feebleness of respiratory murmur is an earlier sign than alteration in rhythm, and may be observed before any marked prolongation of the expiratory act occurs and before there is any very positive increase of resonance on percussion. Hence it is of great importance if not otherwise explicable, as it sometimes is by unusual thickness of the chest-walls, because it indicates, taken by itself, an early stage of emphysema in which treatment may be most likely to be beneficial. It is sometimes found in very advanced stages of emphysema that the respiratory sounds are almost totally inaudible; but in general, while both murmurs are feeble, expiration is more appreciable than inspiration. If, however, the disease is associated with bronchitis, either constantly or intermittingly, the proper auscultatory signs of the accompanying affection may be observed, though modified by the emphysema. Thus, moist and dry râles according to the stage of the bronchitis, sibilant or sonorous, subcrepitant or mucous râles according to the size of the bronchial tube involved, may be heard, the abnormal sounds being notably prolonged during expiration.

It can hardly be doubted that the sign referred to by Laennec as "perfectly pathognomonic of emphysema," and described by him as "the dry {239} crepitant râle with large bubbles" (râle crépitant sec à grosses bulles), is in most cases, if not always, dependent upon coexistent bronchitis. Certainly, many cases of emphysema are met with in which, in the absence of bronchitis, no such sound is heard. The signs or combination of signs which are indeed "perfectly pathognomonic of emphysema" are increased resonance upon percussion, associated with marked feebleness of respiration and prolonged expiration. This association of signs is always indicative of emphysema, because it can be explained only by the physical conditions involved in this disease.

Auscultation of the cardiac region gives results corresponding with those afforded by percussion and palpation. When the lung is distended sufficiently to overlap the heart, the sounds belonging to the latter organ will be more or less indistinct and distant, and sometimes scarcely audible. If the heart be pushed to the right or downward instead of being driven backward, the sounds may still be distinct, but they are out of place and have their greatest intensity under the sternum or at the epigastrium. The proper signs of hypertrophy or dilatation of the heart, which may be revealed on post-mortem examination, and the mechanism of which will be referred to farther on, are to a great degree masked during life; for the overlapping lung prevents the detection of increased cardiac dulness by percussion or increased impulse by auscultation.

Palpation of the chest serves to confirm the evidence supplied by inspection. The effacement of the intercostal spaces, the lessened mobility of the ribs, and the situation of the apex-beat of the heart are signs of importance of which the sense of touch takes cognizance.

COMPLICATIONS AND SEQUELÆ.--Bronchitis is one of the most frequent of the affections complicating emphysema. In the partial form of the malady it often sustains, as has been already seen, a direct causal relation to the emphysema. When the disease is diffused and general, bronchitis is sooner or later almost always encountered, and is then of a congestive rather than an inflammatory type, being often unaccompanied by fever, and in part due to interference with the circulation through the smaller bronchial arteries. For, as some branches of these vessels are distributed in the interlobular areolar tissue, and others ramify upon the walls of the smallest bronchial tubes, a constant pressure may be made upon them by the dilated air-vesicles, and this obstruction of the circulation through them may occasion passive congestion. The bronchitis accompanying advanced emphysema is generally attended with free secretion, amounting in some cases to a bronchorrhoea so profuse as seriously to imperil life by suffocation, the danger being increased by the difficulty in expectorating that exists. The discharge from the bronchi is often in such cases of a muco-purulent character. So urgent is the danger sometimes arising from this complication that unless it be relieved death may quickly ensue. The face and other portions of the surface become livid or leaden, the whole body more or less cool, the pulse weak and hurried, and copious râles are audible even without applying the ear to the chest. Life is threatened both by the accumulation in the respiratory passages obstructing the entrance of air, and by the tendency to the formation of heart-clots from the embarrassment to the pulmonary circulation and the consequent malaëration of the blood.

Another very common complication of emphysema is asthma, which, indeed, is sure to occur in greater or less degree of violence and at longer or shorter intervals in all cases where the disease has become extensive. The attacks often come on in the night, arousing the patient from sleep. The tendency to a nocturnal occurrence of asthma may be due to the recumbent position favoring passive congestion of the lungs, and to the diminished activity of the respiratory process during sleep when it is not aided by {240} voluntary effort. From both these causes an irritation may be set up determining reflex spasm of the bronchi. Moreover, the paroxysmal occurrence of asthmatic attacks is an illustration of the general law in accordance with which morbid neurotic conditions frequently occur intermittingly, though the eccentric cause of them is constantly existing, as witnessed in the subjects of epilepsy or angina pectoris. The frequent recurrence of these attacks of spasmodic asthma is in all probability the cause of the hypertrophic state of the muscular tissue in the bronchial tubes which is often met with as a part of the morbid anatomy of emphysema.

The structural alterations of the heart that occur in emphysema are the results, more or less directly, of the mechanical conditions involved in the disease. Earliest in the sequence of changes affecting this organ are non-compensative hypertrophy and dilatation of its right chambers; and by some writers it has been maintained that the alterations due to emphysema are found only on this side of the organ. This, however, has been completely disproved by extended observations, and it has been shown that left hypertrophy and dilatation, while not such direct consequences of emphysema as the corresponding changes on the right side, are yet frequently encountered, and are plainly due to the disease in the lungs.

The hypertrophy and dilatation of the right chambers of the heart are easily understood when it is considered that the constant pressure of the enlarged air-vesicles of the emphysematous lungs interferes more and more with the circulation through the pulmonary capillaries, and that there is thus a constant impediment to the onward course of the blood from the pulmonary artery, and a continuous backward pressure within the right ventricle and auricle. The effort to overcome this pressure leads to hypertrophy, and ultimately, as this effort is less and less effective, to dilatation of the right chambers.

It would appear as though the readiness with which the alterations on the right side of the heart may be explained has led, if not to their being more frequently observed, yet at any rate to their being more emphasized, than are the corresponding changes on the left side. Some writers have referred only to those on the right side, giving the correct explanation of them, but making no mention of the similar condition on the other side. Thus, Rokitansky[6] refers to the obstruction to the circulation occasioned by the expansion of the air-cells in pulmonary emphysema as one of the causes of dilatation of the right ventricle and auricle, but says nothing of similar changes on the left side. Other pathologists, however, as Lebert and Gairdner, have shown that at least in long-standing emphysema the left side is also not infrequently involved in disease.

[Footnote 6: Path. Anat., vol. iv. p. 130.]

What explanation, then, is to be given of those changes in the left chambers which, if less frequent than hypertrophy and dilatation on the right side, are yet certainly not uncommon? Evidently, they cannot be referred to obstruction in the pulmonary circulation; for this, while producing backward pressure into the right compartments, must, on the contrary, lessen the amount of blood received by the left chambers, which therefore have no excessive labor thrown upon them from this cause, and so cannot become hypertrophied in such a manner.

The explanation is probably to be found partly, as suggested by Waters,[7] in the altered position of the heart occasioned by the emphysema, and partly in the remora of the venous circulation.

[Footnote 7: Diseases of the Chest, p. 152.]

There are thus two factors to be considered, the first of which applies to the right heart as well as to the left. As to this first, the more extensive the emphysema the greater is the degree of displacement that the heart {241} undergoes; and as the normal position of the ventricles with reference to the arteries emanating from them offers the easiest course to the blood-currents, any departure from this position causes an embarrassment, and consequently increased labor, in the left chambers as well as the right; hence one explanation of the hypertrophy on both sides. As to the second factor, the obstruction to the general capillary circulation necessitates an increased effort of the left ventricle to overcome it; and so, as far as it is concerned, another cause of hypertrophy is in operation.

It is frequently observed in advanced emphysema that there is a marked disproportion between the forcible heart-beat and the feeble radial pulse, the former being due to the hypertrophy, and the latter to the small amount of blood received and propelled by the heart.

Besides these changes in the size of the heart and the thickness of its walls, constituting hypertrophy or dilatation as the case may be, a displacement of the entire organ is a not uncommon consequence of emphysema. The direction of this displacement may vary, so that it may be either directly backward, the heart being overlapped by the distended lung, or it may be downward or to the right of the sternum. A much greater degree of displacement of the heart may result from the pressure of pleural effusion than from emphysema of the lung; but when due to pleurisy it is generally of shorter duration and admits of perfect restoration, whereas when caused by emphysema it is usually permanent. The writer has at present under his care a case of extreme displacement of the heart to the right, the apex-beat being felt and seen to the right of the sternum; but in this patient, while extensive supplementary emphysema of the left lung, due to the almost complete incapacitation of the right lung, has probably had a share in causing the displacement, yet a more important cause of it has been contraction of the right side of the chest, the result of absorption of an old pleural effusion which has left the lung bound back and adherent. This case closely resembles one reported by Stokes as presenting "the singular phenomenon of the displacement of the heart to the right side, consequent on the removal of an effusion of the right side."[8]

[Footnote 8: Diseases of the Chest, p. 467.]

Dropsy is to be regarded as one of the most notable complications and consequences of emphysema; for when the disease is of long standing the loss of balance between the arterial and venous circulation occasioned by the obstruction to the passage of blood through the lungs gives rise ultimately to effusion of the serum, which is first seen in the lower extremities, and may subsequently become general.

In consequence of the disturbances in the circulation and respiration which have been considered, it is not surprising that the nutritive function should be impaired, as is found often to be the case in the subjects of old emphysema, who present a cachectic and anæmic appearance, partly due to malaëration of the blood, and partly to imperfect performance of the assimilative functions occasioned by passive congestion of the alimentary tract. Still another cause may be found, as suggested by Hertz,[9] in the insufficient supply of the elements received from the lymph through the imperfect emptying of the thoracic duct into the distended left subclavian vein.

[Footnote 9: Ziemssen's Cyclop., vol. v. p. 382.]

There has been much discussion as to the connection between emphysema and pulmonary phthisis, some pathologists having held that the two affections are incompatible with each other, and that emphysema may thus exercise a prophylactic influence against phthisis. Careful and extensive observations furnish no valid grounds for such a belief. So far as supplementary emphysema is concerned, it is a common thing to find emphysematous patches at the bases and along the margins of lungs the apices of which are tuberculous. In such cases the increased inspiratory labor thrown upon some portions of the {242} lungs in consequence of impaired function of other parts accounts for the emphysema. But, besides this common condition, cases are met with in which the emphysematous portions are themselves beset with tubercle. Such a case is reported by Waters,[10] in which an emphysematous lung was found studded with tuberculous matter, which on microscopic examination was seen in the air-sacs and ultimate bronchial tubes.

[Footnote 10: Diseases of the Chest, p. 156.]

While emphysema ensures no absolute immunity from tuberculous diseases of the lungs, yet the physical condition involved in it does lessen the liability to tuberculous deposit, which is favored by active hyperæmia, and active hyperæmia is not apt to occur in an emphysematous part of a lung. It likewise lessens the liability to such pulmonary affections as hæmoptysis, oedema, and perhaps pneumonia. The diminished pulmonary circulation occasioned by the shrinking and obliteration of the capillaries explains the infrequency of hæmoptysis. The same cause, together with the smaller amount of interlobular areolar tissue that the emphysematous lung contains, lessens the liability to oedema, because there are both less blood from which the serum can be effused and less of the tissue in which it can be collected and held. And the infrequency of pneumonia in an emphysematous lung is owing to the absence of conditions favoring hyperæmic changes.

DURATION AND TERMINATIONS.--No definite limit can be assigned to the duration of emphysema, as the progress of the disease varies very much in different persons according to the underlying cause, and according also to the care taken in avoiding those influences which promote its development, such as physical exertion or exposure to cold and damp. Many persons with extensive emphysema, if they can secure favorable climatic conditions, and thus escape attacks of bronchial catarrh, will live on for years in comparative comfort, whereas in others the disease may advance with rapidity to a fatal issue if their situation in life necessitates hard work or exposure to causes that induce frequent attacks of bronchitis. The immediate cause of a fatal termination is generally either apnoea resulting from extensive bronchitis, or asthenia from impaired action of the heart, or both of these conditions together.

PATHOLOGY AND MORBID ANATOMY.--From examinations made at various stages of the disease in those who have died of emphysema it is seen that the earliest change is a dilatation of the air-sacs, which become gradually more distended, their walls growing thinner, until they may yield at some points and perforations occur. As the disease advances the perforations become larger and more numerous, until the walls are so far destroyed that several sacs or even lobules are blended together, forming only one cavity. The alveoli may be dilated to the size of a mustard-seed, or even a pea, without undergoing rupture, and may thus become visible by the unaided eye; but when the emphysematous spaces are as large as a hazelnut or small walnut they consist of numerous air-sacs, or even of several lobules, fused together by the atrophy and breaking down of the interalveolar and interlobular tissues. When the cavities thus produced by the fusion of several sacs or lobules are in the subpleural portion of the lung, they will sometimes project beyond the adjacent surface, so as to form appendages of the size of a small walnut which appear to be connected with the lung by a pedicle. It is remarked by Waters that perforation of the cell-walls is much more common in lobar than in lobular emphysema, even though the dilatation of the sacs may be as great or greater in the latter than in the former affection; which is due, no doubt, to the fact that the extensive and diffused changes in the lobar form are dependent upon a degenerative process, in consequence of which the walls are specially prone to give way.

All the changes just referred to, from the earliest and slightest degree of distension to extreme attenuation and perforation of the walls, with final {243} coalescence of several sacs and the formation of appendages, may be met with at the same time in different parts of the same lung. The most advanced changes are found most commonly at the apices and free margins of the lungs, while in the deeper parts an earlier stage only may have been reached.

The blood-vessels in the cell-walls are diminished in calibre by the atrophy of these walls and by the constantly-increasing air-pressure, so as to admit only the watery part of the blood; and thus is explained the pigmentary change in the surrounding tissues where the blood-corpuscles collect. Ultimately, many of the vessels are obliterated, and the backward pressure thus induced extends to the pulmonary artery, and thus gives rise to hypertrophy and dilatation of the right side of the heart, as already explained. It is this pressure on the vessels in the alveolar walls that causes also passive hyperæmia of the bronchial mucous membrane, and thus produces a tendency to bronchitis, which so often occurs as a consequence of emphysema, while, again, primary bronchitis is frequently a factor in the production of the disease. The principal change in the bronchial tubes, in addition to the hyperæmia and softening of their mucous membrane due to coexisting bronchitis, is a hypertrophic thickening of their muscular coat, the result probably of repeated spasmodic action in the asthmatic attacks.

DIAGNOSIS.--The chief points by which the diagnosis of emphysema is determined have already been referred to under the head of Symptoms and Signs. The most important of these are the auscultatory signs; for, although the general symptoms and history of the case may point with probability to the nature of the malady, yet if these alone be regarded other affections may easily be confounded with it.

The auscultatory signs proper to emphysema are increased resonance upon percussion, feeble respiratory murmur, and prolonged expiration. Any one of these physical signs may be met with in other affections than emphysema, but when they occur conjointly they point only to this disease. In addition to them the alteration in the form of the chest-wall, so that it becomes rotund or barrel-shaped, and the asthmatic character of the breathing, are important indications. The diseases most likely to be mistaken for emphysema are phthisis, bronchitis, pneumothorax, and pleural effusion.

In the early stage of phthisis feebleness of respiratory murmur with prolonged expiration might suggest the existence of emphysema; but, apart from the fact that these signs at any time when a doubt might be felt are generally confined to the top of the lung in phthisis, the diminished percussion resonance, the bronchial or broncho-vesicular breathing, the bronchophony or bronchial whisper, and increased vocal resonance and fremitus--all of them proper signs of phthisis and all wanting in emphysema--would by their presence or absence clearly establish the differential diagnosis between the two affections. In more advanced phthisis, when softening has taken place and a cavity exists, difficulty in discriminating between the two diseases could hardly arise.

Emphysema is so frequently associated with chronic bronchitis and with intercurrent attacks of acute bronchitis that it is often important to determine whether these latter affections exist independently or are complications of the emphysema. The question is in general settled by the history of the case and by the conformation of the chest, showing whether previous dilatation of the air-cells has taken place or not; as also by the presence or absence of the special signs of emphysema when those of the bronchial affection are encountered.

Capillary bronchitis, from the urgent dyspnoea attending it and the vesiculo-tympanitic resonance which it sometimes presents, especially in the upper and anterior parts of the chest, may possibly be mistaken for emphysema, from {244} which, however, it may be distinguished by the quickened pulse and high temperature that belong to this form of bronchitis, as also by the rapid diffusion of the subcrepitant râle over both sides of the chest in capillary bronchitis; whereas this sign is absent or less marked in emphysema. Moreover, capillary bronchitis is most common in childhood, when diffused emphysema is less frequently met with.

Pneumothorax is characterized by distension of the chest and increased percussion resonance--signs which belong also to emphysema; but the possibility of error is avoided by the consideration that whereas in emphysema the respiratory sound is feebler than natural, in pneumothorax it is strongly exaggerated and amphoric in character; and there are also the additional signs of metallic tinkling and the plashing noise or "Hippocratic succussion sound" made by moving the body backward and forward. Moreover, even as regards the sign in which the affections would appear to resemble each other, a difference may be observed on careful examination; for the percussion note of pneumothorax is purely tympanitic, while in emphysema the increased resonance has still a vesicular character to some degree. Pneumothorax, again, is always a unilateral affection, and emphysema is almost as constant in its occurrence on both sides of the chest.

It might appear that there would be little liability to confuse emphysema with pleural effusion, in view of the very general presence of dulness on percussion in the latter affection and of resonance in the former. But in some cases of fluid effusion in the chest a degree of tympanitic resonance is met with, more especially in children. J. Lewis Smith remarks that "as a rule in the pleuritis of children, at a certain stage of the effusion, percussion produces a sound which is either decidedly tympanitic or which partakes of the tympanitic character."[11] In both affections, moreover, there may be enlargement of the chest. The doubt, if it arise, may be settled by the consideration that in emphysema the altered resonance and the enlargement are on both sides; whereas in pleurisy these signs are in general on one side only; and, further, the enlargement is more marked at the top of the chest in emphysema and at its base in pleural effusion.

[Footnote 11: Diseases of Children, 5th ed., p. 607.]

In concluding the account of the diagnosis it may be said that when the history of a case, the frequent or constant occurrence of dyspnoea, and the more or less rounded conformation of the chest make the existence of emphysema probable, this probability may be converted into a certainty by the discovery of resonance on percussion, feeble respiratory murmur, and prolonged expiration.

PROGNOSIS.--The circumstances, apart from treatment, which especially affect the prognosis of emphysema are the form in which the disease occurs and the ability of the patient to secure immunity from influences which may increase the malady itself or the attendant bronchitis, such as hard work, great exertion of the respiratory organs, and exposure to cold and damp.

Acute supplementary emphysema, even when it affects considerable portions of both lungs, may entirely disappear and the vesicles be restored to their integrity on the removal of the underlying cause. Thus, the vicarious dilatation of air-cells following acute bronchitis or whooping cough in children may leave no sign of its previous existence after recovery from these diseases. In general, the shorter the duration of the causal diseases, the more likely is the emphysema to disappear; for if it be maintained for a considerable time, the elasticity of the cells may be so damaged that they may never return to their natural size.

In hypertrophic lobar emphysema the prognosis in most cases is unfavorable as regards perfect recovery; while yet the disease may not materially shorten life, and with proper care may be compatible with a fair degree of {245} comfortable existence. And, indeed, even in this form of the disease, provided it do not affect a great extent of lung and have not been of very long duration, there is in some cases ground for hope of ultimate recovery, with restoration of the air-cells to their normal condition. Modern methods of treatment have rendered the prognosis in such cases somewhat less unfavorable than it was once held to be.

TREATMENT.--The treatment of emphysema comprises several distinct objects: 1st, the arrest of the degenerative changes which may be going on in the walls of the air-vesicles, and which favor their dilatation; 2d, the restoration, as far as is possible, of the integrity of the lungs, so that they may resume their natural size; 3d, the relief of bronchitis, asthma, and dropsy, which are associated as secondary affections with the primary disease.

To meet the first of these indications, the arrest of degenerative change, iron is among medicinal agents the one most to be relied upon; for, though neither it nor any other means has power to restore loss of tissue or to reproduce integrity of structure when several alveoli are fused into one cavity by the breaking down of their partition-walls, yet by enriching the blood it may improve the nutrition of these cell-walls so that the tendency to dilatation and rupture may be checked. Iron steadily administered in small doses is the best means for effecting this end, and if the patient object to one form of the metal after using it for some time, it may be changed for another. The best preparation of the drug is probably the tincture of the chloride, and one of the best forms for administering this medicine is the mixture of acetate of iron and ammonium (Basham's mixture) introduced into the U. S. Pharmacopoeia of 1880. This is especially valuable, when any dropsical effusion exists, on account of its gentle diuretic action. In addition to iron, other agents promotive of nutrition, such as cod-liver oil and the hypophosphites, may be used with the same view. Stomachic tonics, such as the simple bitters and pepsin, may be useful by aiding digestion and nutrition; and at the same time, by preventing the formation of flatus, they may relieve the dyspnoea caused by upward pressure on the diaphragm. That real benefit may be derived from such measures is beyond doubt; and it is to be feared that some practitioners, in their conviction that no cure can be wrought in those parts of the lung which have actually undergone wasting and rupture, have to too great an extent neglected the use of means which may at least prevent the advance of similar changes in other parts, and thus tend to stay the progress of the disease.

Deep and hurried respiration will increase the air-pressure within the yielding vesicles; for this reason active exercise is objectionable, especially walking up hill, and the use of wind instruments is to be strictly prohibited. Indeed, as regards this last cause of respiratory pressure the patient's inability to practise is in general warning enough, but in the early stages of the affection a caution against it may be necessary.

The suggestion of the use of strychnia against emphysema is not founded on a correct knowledge of the mode of action of this drug; for, although it may stimulate muscular contractility, it has no influence upon the elasticity of the air-cells and no power to restore them to their natural size. Whatever benefit may result from it is due solely to its action on digestion and the improvement in nutrition to which it may thus contribute.

The second indication of treatment, the restoration of the dilated air-cells to their natural size, is possible, if at all, only at an early period of the disease or in portions of the lung which have not gone beyond a moderate degree of cell-dilatation. An enlarged space formed by the fusion of several cells cannot be lessened in size by any means, medical or mechanical, and the loss of respiratory power from the destruction of the cell-walls in which oxygenation is effected does not admit of permanent relief. Where, however, such {246} destruction has not yet taken place and distension is not extreme, there is reason to believe that a return of the cells to their natural size may in some cases be accomplished. The inhalation of condensed air has been recommended with this view; and no doubt good may result from it, due chiefly to the retardation of the breathing and of the heart's action which it occasions, while dyspnoea is relieved by the larger supply of oxygen taken in at each inspiration. This improvement in respiration causes more complete tissue-metamorphosis, and thus aids nutrition and all the functions.

Still greater benefit is to be derived from the exhalation into rarefied air--a measure which acts upon mechanical principles, and has been found to give relief not only to the symptoms of emphysema, but to the organic disease itself; for the retention and stasis of the residual air, which is far larger in amount in emphysema than it is in health, serve at once to keep up the dilatation of the cells and to increase the dyspnoea; and therefore any means which will effect the withdrawal of this air will favor the return of the cells to their normal size, and at the same time relieve the dyspnoea. This benefit is accomplished by the method of expiration into rarefied air, which acts by suction--or pneumatic aspiration, as it may be termed--drawing out the air from the distended vesicles, and relieving them of the continual presence and pressure of this air. Better results would appear to be gotten from the conjoint use of the two methods--the inspiration of compressed air and expiration into rarefied air--than from either one alone.

By the persistent use of these means in cases which have not advanced so far as to defy all treatment not only may the symptoms of dyspnoea, cough, asthma, and impaired nutrition be improved, but the size of the chest may be diminished, as shown by measurement; and this can result only from the return of the distended air-cells, in some degree at least, to their normal capacity.

The apparatus best fitted to effect this double purpose is that of Waldenburg, as modified by Tobold.[12] The method of using it is simple, and can readily be understood by examining the instrument. It must be said that the most valuable action of this apparatus consists in the withdrawal of the air from the cells which it effects, for this tends to produce an organic change for the better--viz. the diminution of the enlarged cells by a sort of suction; while its other action, the supply of condensed air, gives relief to symptoms mainly. In emphysema the expiratory act is relatively more impaired than the inspiratory, and the apparatus is best adapted to the relief of this greater deficiency. Henry Saltzer, formerly of Germany and now of Baltimore, has recently obtained very favorable results from its use in emphysema, not only as regards the dyspnoea and other symptoms, but also in the way of lessening the size of the chest as determined by measurements.[13]

[Footnote 12: This instrument is made by Messrs. J. Reynders & Co. of New York.]

[Footnote 13: A reference to Saltzer's observations and measurements may be found in Weil's Handbook of Topographical Percussion, pp. 107, 108, Leipzig, 1880.]

The third indication of treatment has reference to the complications of emphysema. Of these the most common, and one of the most important, is bronchitis, which is to be treated in the same way as when it occurs as an independent affection. Expectorants to promote and remove secretion and agents to allay cough are very important means, because the retention of secretion and the effort of cough to expel it cause a strain upon the air-cells, and thus increase the emphysema. The local use, by inhalation or spray, of opiates, belladonna, hyoscyamus, and other agents of this class, is often most serviceable by giving relief to the cough without disturbing digestion. As bronchitis is in many emphysematous patients a very chronic affection, and is attended with submucous thickening in the bronchial tubes and consequent diminution of their calibre, the iodide of potassium is an agent of special {247} value for its relief. Whether the influence of this remedy is due to a sorbefacient power or to some other unexplained mode of action, there is no doubt of its great value in chronic bronchitis, so that for this complication of emphysema it claims a very high rank among medicines. The rapidity with which relief is afforded to the cough and dyspnoea of bronchitis, and to the asthmatic paroxysms attending it, by full doses of 10 or 15 grains of iodide of potassium at intervals of four hours, makes it probable that its action is partly neurotic in character. It is remarked by Austin Flint, Sr., that when the iodide has effected a marked improvement in the chronic bronchitis he has known the characteristic deformity caused by the emphysema to be notably diminished.[14]

[Footnote 14: Clinical Medicine, p. 131.]

A dangerous symptom which sometimes arises in the course of the chronic bronchitis accompanying emphysema is profuse bronchial catarrh, which may destroy life by producing apnoea, the surface becoming cold and the pulse feeble and vanishing as the patient seems to be drowning in his own secretion. In this condition the writer has in several instances found prompt and unmistakable benefit from the hypodermic injection of hydrobromate of quinia, and he would strongly advise the use of this agent. The solution he has employed is of the strength of 4 grains of the salt to 20 minims, and of this 15 to 20 minims has been the dose given. Under the action of this remedy the pulmonary capillaries would appear to be so toned that further effusion is checked, and the gasping and cyanotic condition has been speedily succeeded by comfortable breathing. For the same symptom Waters advises the use of moderately large doses of turpentine (drachm doses in aromatic water every two hours) on a plan suggested by Sir D. Corrigan of Dublin.[15]

[Footnote 15: Diseases of the Chest, p. 172.]

As bronchitis has so much power to produce emphysema when the conditions favorable to its occurrence exist, and to increase it when already established, everything tending to prevent it is of great importance. With this view the avoidance of cold and wet, and, when practicable, recourse to a mild climate in winter, are advisable.

The attacks of asthma to which emphysematous patients are subject are to be treated in the same way as the purely spasmodic form occurring independently of discoverable organic disease. If the difficult breathing has come on suddenly and the patient is not laboring under advanced dilatation of the heart, prompt relief may be given by a hypodermic injection of morphia; but if the heart is much dilated, this might endanger too great depression. Chloral is generally unsafe for the same reason. The bromides in full doses may be serviceable in the less severe attacks, and the tincture of lobelia in doses of 10-20 drops every fifteen minutes until slight nausea is felt is often of great benefit, as is also the smoking of stramonium-leaves.

The dropsy met with in advanced stages of emphysema may be so prominent a symptom as to require special treatment. Its cause is found in dilatation and weakness of the right chambers of the heart, which result from obstruction to the circulation through the lungs when compensative hypertrophy is no longer efficient, for then these give rise to passive congestion of the liver and kidneys and remora of the general venous system, with dropsical leakage, seen first and chiefly in the lower extremities. Treatment is therefore to be directed chiefly to increasing the tone of the heart; and for this purpose digitalis is most useful, as it is in other forms of cardiac dropsy. The chief indication of its beneficial action is seen in the better action of the kidneys consequent upon the increased impulsive force given to the heart. When acting favorably, marked relief both of the dropsy and the dyspnoea may be obtained from the use of this agent in the dose of 2 to 4 drachms of the infusion or 10 or 15 drops of the tincture every three or four hours. If {248} the stomach should not bear the digitalis, as is sometimes the case, or if it fail to act or lose its power, the fluid extract of convallaria, recently introduced as synergistic with foxglove, may be employed as a substitute for it.

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

4. Atrophic Lobar Emphysema.

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

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

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

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

In some cases of hypertrophic emphysema there may be, it is true, an appearance of partial contraction of the chest-wall, since where the {249} emphysema has produced a marked bulging of the upper portion of the thorax the part below may seem by contrast to be contracted. But in the atrophic form of the disease no distension is seen at any part of the chest-wall, the whole surface being more or less sunken and contracted. Even in hypertrophic emphysema with distension of the thorax, when the disease has lasted a long time there may be some degree of wasting of the lung-tissue; but this condition does not constitute true atrophic emphysema, which is such from the beginning without any preceding stage of hypertrophy.

DIAGNOSIS.--The diagnosis of atrophic emphysema is to be made by the physical signs studied in connection with the conformation of the chest.

PROGNOSIS.--The prognosis of this affection is hopeless as regards a cure, since the organic change is due to the degeneration of age; yet the disease may continue for years without materially or at all affecting the duration of life.

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

II. INTERLOBULAR OR EXTRA-VESICULAR EMPHYSEMA.

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

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

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

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

{250}

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 {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.

SYNONYMS.--If we go back far in the history of medicine, we find many synonyms, such as Hæmoptoe, Emptoe, Emptoica passio, Pneumorrhagia, Hæmorrhagia pulmonis, Crachement de sang, etc., etc.

DEFINITION.--Bronchial hæmoptysis is the spitting or expectoration of blood which has been effused into the bronchi or bronchioles from the bronchial vessels. Pulmonary hæmoptysis is the spitting or expectoration of blood which has been effused into the air-cells, the inter-alveolar and interlobular tissues. This distinction is not always practicable in diagnosis or practice. It may, however, serve for a grouping of some well-known clinical forms of hæmoptysis.

It is not possible to give indications by which the origin of blood in the lungs may be positively determined except by a reference to other symptoms than the hæmoptysis. In general, bronchial hemorrhage is characterized by a bright-red, fresh color, is aërated, unmixed, and uncoagulated. In pulmonary or parenchymatous hæmoptysis the blood is dark, non-aërated, and coagulated to some degree, and often alternates with a mixed blood and mucus sputum. These distinctions are not reliable, and must be supplemented by all of our clinical resources in the case before us. The author maintains that in the hæmoptysis of phthisis the hemorrhage in the large majority of cases is both bronchial and pulmonary. The typical parenchymatous hemorrhage is found in hemorrhagic infarction and pulmonary apoplexy, which, compared with phthisis, are rare occasions for hæmoptysis. This general statement will form the basis of what follows in this exposition.

HISTORY.--Historically, there are not many phases in the doctrine of hæmoptysis. Controversy has been chiefly confined to its relations to phthisis as cause or effect.

The simplicity and directness of observation of the ancients give a special interest to their views of hæmoptysis. They believed that it was oftener cause than effect. They found a warranty of that opinion in what they thought was a direct conversion of blood into pus, and in the irritating qualities of the latter. Hippocrates'[1] fundamental statements are, "Ex sanguinis sputo, puris sputum malum;" "Ex sanguinis vomitione tabes et puris purgatio per superiora purgatio;" "Ex sanguinis sputo puris sputum et fluor, ubi autem sputum retinetur moriuntur." Another statement of his is given in translation by Peter:[2] "When some of the veins of the lung are ruptured the hemorrhage is in proportion to the size of the vessel; a part, on the contrary, unless the vein be very small, diffuses itself in the lung, putrefies {267} there, and after having putrefied forms pus. As a result, it is at one time true pus, at another pus mixed with blood, and another time it is pure blood, which is rejected; and if the vein was very full it is from it that the mass of the blood comes, and thick pus, mixed with putrefied pituitous secretion, is expectorated."

[Footnote 1: Edition 1696, book 7, p. 1141, Aphorisms 15 and 16, 80 and 81.]

[Footnote 2: Clinique médicale, tome 112, p. 243. The precise locality of this quotation is not given by Peter, but it is from Hippocrates' Opera, ed. Kuhn, Leipsic, 1825, vol. ii. p. 178.]

Thomas Young[3] gives the following sentences from Hippocrates' Predictions and Aphorisms: "The most dangerous consumptives are cured by a rupture of the great vessel which corrodes the lungs;" "Purulent expectoration after hæmoptysis is dangerous;" "In some cases consumption originates from an effusion of blood into the lungs without hæmoptysis, especially after a strain or accidental injury; a collection of phlegmatic humors form around it by causing pain and cough, with purulent and bloody expectoration." All of these quotations show the Hippocratic doctrine distinctly, that the hæmoptysis where it appeared in a case was mostly the cause of the subsequent phthisis, and that phthisis ab hæmoptoe was not only one of the most common, but one of the most dangerous forms.

[Footnote 3: A Practical Historical Treatise on Consumption Diseases, London, 1815, p. 111.]

The doctrine that blood effused into the lungs became pus, and produced corroding and ulcerating effects, appears in many other prominent authors between the Hippocratic writings and the nineteenth century. Celsus[4] (30-40 A.C.) says: "Hæmoptysis is one of the causes of purulent expectoration." Galen[5] (131-201 A.C.) says: "Phthisis is lung ulceration;" and he thinks "that in the greatest number of cases it originates in a mechanical way, through tearing of the tissue by means of an outpouring of blood in consequence of a catarrh or strain." This extract would imply that he thought the hæmoptysis in many cases secondary, but that when it did occur it had the effect which Hippocrates attributed to it, that of producing "purulence of the lungs." Sylvius[6] (1614-1672) says: "Hæmoptysis is one of the causes of purulent expectoration."

[Footnote 4: Young, op. cit., p. 128.]

[Footnote 5: Waldenburg, Die Tuberculose, p. 19.]

[Footnote 6: Waldenburg, op. cit., p. 28.]

Morton's[7] (1689) language partly is: "Decantatum istud medicorum adagium, quod pus sequitur sanguinem;" and then, translated, he says: "It (the adage) appears to have originated in the fact that 'purulence' of the lungs, or phthisis pulmonalis, usually follows hæmoptysis more quickly and oftener than any other disease." In the sentence immediately following he suggests this result may be due to a putrefaction of clots that the hæmoptysis has left behind in the lungs, or to a copious effusion of humors from the whole body to the tender lungs, or to an erosion of some vessel.

[Footnote 7: Phthisiological Ed., 1727, lib. 111, chap. v. p. 95.]

Another theory appears in Hoffmann's language,[8] and was probably suggested, directly or indirectly, by Sylvius's description of tubercles: "The blood is easily extravasated into the pulmonary vesicles, stagnates there and putrefies, corrodes the neighboring parts, and finally destroys the air-passages or they are converted into nodes or tubercles." The blood becomes tubercularized, and the phthisis ab hæmoptoe is established. This idea is found at different periods, and we find a recent French author arguing against this hypothesis.

[Footnote 8: Peter, loc. cit., p. 244; Young, p. 211, Opera; Hoffmann, Physico-medica, Geneva, 1740.]

The reversal of these ideas is generally acknowledged as the results of Laennec's energy and genius, yet similar opinions to his had been expressed by French and English physicians. Bayle does not place phthisis ab hæmoptoe in his classification. Desault,[9] one of Laennec's countrymen, near a hundred years before him, "insists that tubercles constitute the essence of consumption, being generally anterior to hæmoptysis." Mudge[10] says that hæmoptysis is often the consequence of the obstruction produced by tubercles. A {268} preparation for the positive opinions of Laennec is discernible in these and other authors. His views on this particular topic were opposed by Andral. The latter modified his earliest expressions to some extent.

[Footnote 9: Young, p. 220, Desault sur les Maladies venériennes, la Rage et la Phthisic, Bordeaux, 1733.]

[Footnote 10: Young, loc. cit., Radical Cure for a Recent Catarrhic Cough, London, 1779, 2d ed.]

The next important historical epoch in the causative relations of hæmoptysis and phthisis is in the energetic protests of Niemeyer. They were in some respects a return to the Hippocratic doctrine, in that he asserted the predominance of hæmoptysis as cause; but he gave the doctrine a basis better adjusted to a better pathology, in that he made the important element of inflammatory lesions the medium between the effusion of blood and the final purulence or ulceration (ulcus pulmonum) of the ancients. He energetically advocated the doctrine of the positive effect of effusion of blood in the bronchi or pulmonary substance in producing disorganization of the lungs, without reference to any hereditary or predisposing element or existence of tubercles.

Jaccoud[11] calls attention to the fact that Graves had anticipated Niemeyer in the partial revival of the Hippocratic doctrine and the teachings of Morton and Hoffmann on phthisis ab hæmoptoe.

[Footnote 11: Clinique médicale, vol. ii. p. 302, Graves.]

In a recent work[12] there is a general adhesion to the modern modifications of the Hippocratic doctrine in regard to the pathogenetic relations of hæmoptysis and phthisis. There is a decided rejection of the causative influence of tubercle in producing hæmoptysis.[13] "The connection between pulmonary hemorrhage and tubercle stands on no pathological proof;" "From all the evidence I have been able to obtain on this point, tubercle seems to have been very unjustly credited with hemorrhage."[14] He differs from others in attributing much more to the hæmophilic constitution in the production of hæmoptysis. Other phases of the history of hæmoptysis might be given. We shall allude to two only: one is the classification of the varieties. Alexander of Tralles treats of hæmoptysis under three heads: 1, Hæmoptysis by rupture; 2, by erosion; 3, by dilatation. Bricheteau[15] makes four divisions: 1, constitutional; 2, accidental; 3, succedaneous; 4, critical and symptomatic. These two classifications show in themselves their origin, in that the one is representative of a local, and the other of a constitutional, pathogenesis.

[Footnote 12: On Pulmonary Hemorrhage, Reginald E. Thompson, London, 1879.]

[Footnote 13: Page 32, op. cit.]

[Footnote 14: Page 33, op. cit.]

[Footnote 15: Maladies chroniques de l'Appareil respiratoire, Paris, 1851, p. 523.]

The last historical phase is the therapeutic one. We find in the practice of the present day survivals from the ancient authors. Morton recommended ligatures around the limbs to arrest hemorrhage, and bark to prevent hæmoptysis from becoming phthisis.[16] Venesection, which to some extent is a modern remedy, was frequently practised by the older physicians. Erasistratus[17] recommended ligatures, applied to the limbs in several places, to prevent the return of the blood to the lungs; Asclepiades thought this practice founded on an erroneous theory, but experience is in its favor. The head should be kept high, the face wetted with water, the room cool, and the patient perfectly at rest. Lietaud (1765) is cautious of employing astringents or purgatives, but recommended ligatures to the limbs and cold to the scrotum. A drachm of rhubarb was given by Fernelius in hæmoptysis. Bryan Robinson[18] (1752) relates a case in which an emetic of ipecacuanha, taken three times a week, kept off hæmoptysis for eight years, while tar-water constantly brought it on. Marryat (1758, London) "advises two grains of tartarized antimony, and as much of the sulphate of copper, in half a spoonful of water." Ipecacuanha was frequently employed in hæmoptysis by the practitioners of the centuries preceding the nineteenth.

[Footnote 16: Young, pp. 201, 202.]

[Footnote 17: Op. cit., p. 128.]

[Footnote 18: Op. cit., p. 156, ed. 1660.]

As an important preface to the subjects considered in this article we introduce an account of the vascular supply of the lungs.

{269} Before entering into a statement of the distribution of the minute vessels to the lungs it is desirable, in view of the possible diseased connections between the larger bronchial and vascular trunks, to recall some points of the topographical anatomy of the latter. "The root of the left lung passes below the arch of the aorta and in front of the descending aorta. The bronchus, together with the bronchial arteries and veins, the lymphatics and lymphatic glands, is placed on a plane posterior to the great blood-vessels. The pulmonary artery lies more forward than the bronchus, and to a great extent conceals it, while the pulmonary veins are placed still farther in advance." The left bronchus "in passing obliquely beneath the arch of the aorta is depressed below the level of the pulmonary artery, which is the highest vessel."[19] Practically, the chances of abnormal communications lie in the relations of the aorta, more especially the different parts of the arch, to the left bronchus and pulmonary artery, and to the trachea, of the innominate artery to the trachea, and of the glandular structures at the root of lung to the pulmonary artery.

[Footnote 19: Quain's Anatomy, vol. ii. pp. 897, 898.]

The encroachment of aneurism of the subclavian artery on the lung, and consequent communication between it and the bronchus, is another form of accidental or extraneous hæmoptysis.

A recognized classification of the vascular systems of the lungs is into--1st, functional; 2d, nutritive. To the first belong the pulmonary arteries and veins, and to the second the bronchial arteries and veins. Both physiological and pathological experience justifies this division.

Notwithstanding the great attention and labor bestowed upon the circulation of the lungs, there are still unsettled some important points. We adopt from Küttner[20] some of the anatomical data applicable to our subject. The branches of the pulmonary artery follow uninterruptedly the bronchial ramifications. The mutual relations of the artery and bronchus are such that the larger vessel lying in any preparation of the lung directly next to the bronchus, and running in the same direction, can be pronounced to be a branch of the pulmonary artery. In the lungs of the embryo both lie in the same connective-tissue sheath that originates at the root of the lung, enters with them into the root of each lobule, and there spreads out. In the lobules both run not only closely alongside of each other; there appear also branches of the pulmonary artery on the bronchus itself, and press on to the mucosa of the same.

[Footnote 20: "Beiträge zur Kentniss der Kreislaups-verhältnisse der Saugethierlunge," Virchow's Archiv, vol. lxxiii. p. 476, etc.]

With the appearance of the terminal bronchiole this relation is changed. The bronchial artery, as such, ceases; the pulmonary artery--or rather its lateral branches--exclusively surround the alveolar diverticulæ on their external surfaces. At the point where the terminal bronchiole is developed into the infundibula the corresponding trunk of the pulmonary artery divides into a number of branches--"pinselförmig;" each infundibulum receives its stem, which spreads itself after the manner of a feather on its external surface. The terminal branches of the pulmonary artery cover the terminal alveoli. On every lung in which the infundibula and lobules are well distributed the terminal branches of the pulmonary artery extend beyond the borders of the infundibula and lobules into the interlobular and subpleural connective tissue, and here either lose themselves in a capillary distribution or extend to the periphery of an adjoining acinus, being lost in its capillaries.

One peculiarity of the pulmonary artery is that from a large trunk relatively fine lateral branches come. From a vessel of 0.136 mm. come branches of 0.033, 0.016, 0.011, 0.010 mm. The finest disappear immediately as vasa vasorum; the larger pass to the perivascular or peribronchial connective tissue {270} and become capillary, or they appear on the surface of the immediately adjoining lobules and disappear in the capillary paths of the alveoli.

The terminal branches of one and the same principal artery behave differently according as they are distributed to the connective tissue or to the alveoli. In the first case they form wide meshes and narrow tubes, and are not different from the capillary terminations of the body in general. In the other case the meshes are narrow; the vessels in all of the pulmonary capillaries are wide. If these vessels are followed from their origin to their final termination, it will be seen that a considerable part of the pulmonary artery is spread in the interlobular connective tissue; that it is not exclusively a secretory vessel; that the capillary network of all the lobuli are in anastomotic connection.

An anatomical investigation shows that between the branches of the pulmonary artery no anastomoses exist. It is, however, proved that under certain conditions connections between the larger branches of the artery may occur. This artificial connection is favored through peculiarities of terminal branching: wherever two parallel branches of the pulmonary artery are followed, it will be seen that the terminal branches lie alongside of each other without anastomosis. One can be convinced of that, and, further, that the capillaries of only one or two alveoli separate them. These unusually short capillaries between two arteries are those in which differences of pressure in one or the other artery produce wide connections. Küttner agrees so far with those observers who think that between the larger branches of the pulmonary artery no wide anastomoses exist already formed. In this sense the pulmonary artery can be designated a terminal artery; on the other side, however, it must not be forgotten that such connections can arise at any time, and the artery there loses the type of a so-called terminal artery.

He further remarks that the vascular-district supply of the pulmonary artery is not so limited as Cohnheim and Litten believe; that, more than that, some branches of it pass from one lobule to the adjoining one; that others are distributed in the subpleural and interlobular connective tissue and in the bronchial wall.

If the lung of an animal be injected from the pulmonary artery, there is produced a complete filling of the vessels of the bronchial wall and into the subepithelial layer--a fact the more interesting that a similar event can scarcely be produced by a filling of the bronchial artery.

Pulmonary Vein.--Only at the root of the lung do the bronchus, pulmonary artery, and pulmonary vein lie close to each other. In the continuance of the same the artery and the bronchus remain close by each other, but the vein pursues its own course. The branches of the same are, from the hilus to their capillary termination, situated in the interlobular connective-tissue paths. They form on the external margins of the lobules wide blutbuchten, in which the veins of the infundibula enter with short stems. The artery lies intralobular--the vein interlobular. The bronchial veins connect not only with branches of the azygos and superior cava, but also with those of the pulmonary vein.

Bronchial Vessels.--The variety of origin of the bronchial arteries is notable. Whatever their origin, they follow with their chief trunk the bronchus into the parenchyma of the lung, and give off insignificant lateral branches to the connective-tissue layers. There is still another kind of artery, which divides independently in the connective tissue of the lungs, without resting on the bronchial walls; they come from the oesophageal, mediastinal, and pericardial arteries, branch in the mediastinal pleura, appear with these at the hilus of the lung, and form partly an independent mesh of pleural arteries, and partly spread themselves in the interlobular connective tissue.

All the vessels of the serous membranes of the diaphragm can contribute {271} in many ways blood to the hilus of the lung: the unusually fine-branched arteries appear in this way to be in condition to compensate for obstructions (or lesser). The bronchial arteries in comparison with the other vessels of the lungs give off sparingly lateral branches; among the most interesting are the branches which spring directly from the trunks of the bronchial artery, pass through the peribronchial connective tissue, appear at the adjoining infundibula, and lose themselves in capillary terminations.

The capillary districts of the bronchial arteries pass immediately into those of the pulmonary. It is a fact that besides the pulmonary artery the bronchial artery provides the infundibula and alveoli with blood. If the bronchial artery springing from the intercostal and internal mammary arteries be ligated or cut, leaving open the vessels of the mediastinal pleura, and the lung be injected from the abdominal aorta, a mere inspection will show a filling of the parenchyma of the lung; anastomoses between the pleural arteries and the intra-acinous trunks of the pulmonary arteries can be recognized. There is an anastomotic connection between the pleural branches of the pulmonary and bronchial arteries.

The bronchial, as also the pulmonary, artery can be filled by means of the fine arterial branches from the mediastinal pleura.

The principal branches of the bronchial arteries go to the bronchi; at the alveolar passage they here stop as such; their capillaries become continuous with those of the pulmonary artery. The greater part of the few collateral branches nourish the submucous peribronchial and perivascular connective tissue, the nerves, the lymphatic vessels; the smaller part enter the alveoli of other bronchial systems and become capillary.

The branches going to the lung with the mediastinal pleura spread themselves in the pleura and interlobular connective tissue, nourish the large subpleural and interlobular lymphatic vessels, but lose themselves in capillary distribution on the alveoli and infundibula.

The pleural and bronchial arteries anastomose partly with each other and partly with branches of the pulmonary artery.

With reference to the branches of the pulmonary artery going to the bronchi, it may be said that they, without giving special branches to the external layer of the bronchi, press on to the basal membrane and form a compact capillary network in common with the proportionately few branches of the bronchial artery.

Amidst differences of opinion, as between Küttner, Lalesque, and Cohnheim and Litten, there is a concurrence as to the chances of supplementary function by anastomoses between channels that are ordinarily separate. Küttner admits a modified form of terminal arrangement in the pulmonary artery, but at the same time claims an amount of potential connection that is liable to come into actual operation and suspend, if not destroy, the terminal type.

The correlation of both functional and nutrient vessels is so intimate that we believe there is no conclusive argument against the actual transfer of office from one to the other in certain strained conditions of disease; Virchow's experiment proves it.

The wonderful delicacy and distensibility of the enormous network of pulmonary vessels (relation of uncovered space in the alveoli to that covered by the vessels being 50 out of 200, Kuss); their capacity of response to great variations of supply and tension; the prompt supplementary function proven by Litten[21] to belong to the tracheo-oesophageal, pericardial, phrenic, and pleuro-mediastinal arteries, and their equilibrium under the sensitive changes of the aortic system; the slower submission of the lesser circulation to the peripheral impressions, which markedly affect the aortic system; the facts {272} verified by Lichtheim[22] that on closure of any portion of the pulmonary artery the same quantity of blood will pass through the portion remaining open as before; that this is brought about through increase of pressure in the sections still open, and through the simultaneous increased rapidity of circulation and distension of the vessel walls; and that this mechanism is able to compensate for obstruction of three-fourths of the pulmonary artery,--are important factors in the anatomical and physiological relations of hæmoptysis.

[Footnote 21: "Ueber den Hämorrhagischen Infarct," Zeitschrift für klinische Medicin.]

[Footnote 22: Die Störungen des Lungenkreislaufs, by L. Lichtheim, Berlin, 1876, p. 65.]

ETIOLOGY.--The natural history of hæmoptysis is practically that of phthisis: exceptions to this will be noted hereafter. As heredity is largely a determining influence in the latter, it may be assumed that it qualifies its principal symptoms. More or less uniformity prevails in the transmission of normal or abnormal conditions, and we seem to find an illustration of the latter in the correspondence between the percentages of hereditary phthisis and those of hæmoptysis in such cases. Reginald Thompson[23] says that "out of 1064 cases of well-marked inherited phthisis, 426 suffered from hæmoptysis." In his calculation he omitted all those in which the disease began with hæmoptysis. Had these then been included, they would have raised the percentage over that shown by the figures, which is slightly above 40. The rate would not then be much below that given as an average of cases of hereditary phthisis. This percentage of cases of hæmoptysis in hereditary phthisis is a sufficiently uniform transmission to prove the influence of heredity. Its influence is shown not only in the number of transmissions, but in the transmission of types; so that, as we have a family type of phthisis, we may have a family type of hæmoptysis, such as the cases where all the phthisical members of a family are subject to hæmoptysis of uniform characteristics, instances where the same uniformity in type is transmitted, and instances where the phthisical heredity appears to have its survival in moderate and transient attacks of hemorrhage.

[Footnote 23: The Causes and Results of Pulmonary Hemorrhage, p. 110.]

Atavism is also seen in some family histories. We have in view such an instance, where the marked hæmoptysical tendencies of one generation skipped the next to reappear in the third.

A special study of the relation of cases of copious hæmoptysis to different forms of heredity has been made by Reginald Thompson. His table is as follows:

COPIOUS HÆMOPTYSIS. +-------------------+----------------------------------+ | | Cases. | +-------------------+--------+--------+----------------+ | Age at which | Mother | Father | Non-hereditary | | attack commenced. | 123 | 102 | 105 | +-------------------+--------+--------+----------------+ | 5 | ... | 1 | ... | +-------------------+--------+--------+----------------+ | 10 | ... | 4 | 2 | +-------------------+--------+--------+----------------+ | 15 | 27 | 16 | 14 | +-------------------+--------+--------+----------------+ | 20 | 30 | 22 | 20 | +-------------------+--------+--------+----------------+ | 25 | 34 | 24 | 24 | +-------------------+--------+--------+----------------+ | 30 | 18 | 19 | 16 | +-------------------+--------+--------+----------------+ | 35 | 8 | 9 | 12 | +-------------------+--------+--------+----------------+ | 40 | 2 | 4 | 8 | +-------------------+--------+--------+----------------+ | 45 | 3 | 1 | 5 | +-------------------+--------+--------+----------------+ | 50 | 1 | ... | 2 | +-------------------+--------+--------+----------------+ | 55 | | 1 | | +-------------------+--------+--------+----------------+ | 60 | | 1 | | +-------------------+--------+--------+----------------+ | 65 | | | | +-------------------+--------+--------+----------------+

He claims that this table shows that of the cases of direct heredity, cross-heredity, and non-heredity, those who were the subjects of cross-heredity--that is, those from the mother--were more liable to copious hæmoptysis than either the cases of direct heredity or of non-heredity; and the numbers of the two latter so closely correspond as to show that heredity from the father has little influence as regards hemorrhage. The conclusion he draws from the table is that "an heredity is drawn from the mother which differs from that derived from the father, and to this must be attributed the excess of cases of copious hæmoptysis."

{273} This difference will be seen in the following table, which shows the number of cases occurring before and after thirty:

+-----------------+-----+-------------------+------------------+ | Cases. | | Before age of 30. | After age of 30. | +-----------------+-----+-------------------+------------------+ | Mother | 123 | 91 | 32 | +-----------------+-----+-------------------+------------------+ | Father | 102 | 65 | 37 | +-----------------+-----+-------------------+------------------+ | Non-hereditary | 105 | 60 | 45 | +-----------------+-----+-------------------+------------------+

He thinks the explanation is to be obtained from the statistics of hæmophilia, which show a large proportion of transmissions from mothers to sons, and that we have here a strong argument connecting copious hæmoptysis, not with tubercle, but with hæmophilia.

His next table is one of 125 cases of double heredity, calculated upon the same basis as the others, that of 400:

+----------+-------------------------+ | | Cases. | +----------+------------+------------+ | | Double | Calculated | | | heredity | to | +----------+------------+------------+ | | 125 | 400 | +----------+------------+------------+ | 5 | ... | ... | +----------+------------+------------+ | 10 | 3 | 10 | +----------+------------+------------+ | 15 | 20 | 74 | +----------+------------+------------+ | 20 | 40 | 128 | +----------+------------+------------+ | 25 | 23 | 75 | +----------+------------+------------+ | 30 | 15 | 48 | +----------+------------+------------+ | 35 | 12 | 37 | +----------+------------+------------+ | 40 | 9 | 29 | +----------+------------+------------+ | 45 | 1 | 3 | +----------+------------+------------+ | 55 | 1 | 3 | +----------+------------+------------+ | 60 | 1 | 3 | +----------+------------+------------+ | 65 | | | +----------+------------+------------+

which shows a close approximation to the table of cases of cross-heredity from the mother, and that the calculated number for 400 cases of double heredity are almost identical with that of the actual number of 400 cases of cross-heredity between the ages of fifteen and twenty-five--in the first case being 202, in the second 203--and the calculated number of cases before thirty amount to 287, not quite equal to actual number for cases of cross-heredity, which is 294. He concludes that these cases do not show a greater tendency to hemorrhage than is shown in cases of direct and non-heredity. We may accept these figures and calculations as important without endorsing the conclusion which they are intended to sustain--viz. that such hæmoptyses are essentially of hæmophilic origin. It may be stated as a general opinion that hæmophilia does not especially manifest itself in pulmonary hemorrhages, and that hæmophilic families are not specially liable to phthisis.

The hemorrhagic diathesis, as distinguished from the specific bleeders' heredity, does not often manifest its activity through the lungs, and, as correlative, phthisis does not often show hemorrhages in other organs than the lungs.[24] Leudet has met in 244 cases of phthisis 9 times hemorrhages in other organs than the lungs; oftenest by the intestine, the skin, the nasal mucous membrane; more rarely by the brain and urinary organs; 10 times between the muscles of the abdominal walls. These considerations suggest that the phthisical hæmoptysis is distinct from that of hæmophilia or the hemorrhagic diathesis, and has an independent origin.

[Footnote 24: "Rémarques sur la Diathese hémorrhagique," Mém. Soc. de la Biologie, 1859, p. 179.]

Some facts in regard to the previous diseases of patients admitted into the Brompton Hospital with phthisis are given in the second medical report of that institution, which may have a bearing on the special features, such as hæmoptysis. Among 1973 patients admitted, 275 were found to have suffered with well-marked attacks of rheumatism, and 16 had acute symptoms of it while in the hospital, making a larger number than of any other disease, fevers coming next with 238. The connection of forms of hemorrhage with {274} so-called rheumatism suggests a possible influence of that kind in favoring hæmoptyses during the evolution of phthisis. We know of no facts collected with the view of studying this relation. If such a conclusion were sustained, it would tend to confirm the view connecting hæmoptysis with hæmophilia or the hemorrhagic diathesis.

Williams[25] gives a statement qualifying the assumption that the hemorrhagic variety of consumption specially originates in family predisposition, for in 72 cases out of 1000 tabulated cases of phthisis family predisposition was present in only 25 instances. This percentage is scarcely small enough to exclude a predisposition.

[Footnote 25: Pulmonary Consumption, p. 157.]

Considering hæmoptysis in this aspect, as a result of heredity, does not account for all the cases with which we meet. We are surprised occasionally by the appearance of pulmonary hemorrhage where heredity of phthisis cannot be traced. Such persons present the aspect of a vulnerable state; they yield readily to a phthisical invasion. Some of the so-called cases of phthisis ab hæmoptoe are found in this class, yet they may have inherited a phthisical predisposition, brought about by various degenerating influences acting on their ancestors, such as antihygienic surroundings, bad air, insufficient food, frequent childbearing, and excessive nursing. The heredity is not in special symptoms, but in a predisposition which needs only some exciting cause for a specific symptomatology that may be carried forward to the next generation.

One individual may himself yield to the same degenerating influences, and live with more or less of an acquired predisposition until similar exciting causes reveal his specific weakness. Another may find that he has a phthisis directly acquired from a single attack of severe illness without the aid of any element of heredity or of the acquired predisposition. The gradation would then be inherited predisposition, acquired predisposition, and acquired phthisis. Hæmoptysis may find its origin in these several relations of heredity. Combined, they represent the law of uniformity and the law of variation in hereditary transmissions. If these general observations be correct, they show that the ordinarily stated percentage of transmission of hæmoptysis in inherited phthisis does not express the totality of influence operating in the production of hæmoptysis. Something must be subtracted from the so-called non-inherited phthisis and added to the inherited form.

When we attempt to express the relation of acquired or non-inherited phthisis to hæmoptysis, we find no sufficient data. Thompson's table above given is assumed by him as showing that the influences superinducing hæmoptysis in the non-hereditary class are equivalent to the heredity operating through the father, which is quite subordinate.

R. Thompson[26] states that out of 1064 of his cases of well-marked inherited phthisis, 426 had hæmoptysis; of 1016 when phthisis was not known to be inherited, 558 had hæmoptysis.

[Footnote 26: Loc. cit., p. 110. In a later work Thompson (Family Phthisis, London, 1884) states that the general effect of the paternal inheritance is to reduce the number of cases of copious bleeding for the total period of life, but an excess is observed for the special period between twenty and twenty-five; that in the inheritance of the females from the father the number of cases of bleeding is large, the number of the copious cases being twice as many as the moderate. The effect of double heredity upon males was to make the cases of copious bleeding numerous, and that nearly half the total number of cases were disposed to bleed. In females there was an increase in the number of cases of moderate amount. As regards acquired phthisis among males, that hæmoptysis is a well-marked feature, and nearly three-fourths are cases of copious bleeding; as to acquired phthisis among females, that the number of cases is considerably smaller, the reduction being marked in the cases of copious bleeding.]

{275} In a collection of cases of phthisis taken from the Cincinnati Hospital records, amounting to 1266, there were of

Cases of hæmoptysis 475, or 37.51 per cent. " phthisis, with family history of same 332 " hæmoptysis in same 127, or 38.25 " " acquired or non-inherited phthisis 934 " hæmoptysis in same 348, or 37.25 "

In 10 cases there was a family history of hæmoptysis; that is, of a general family peculiarity in that direction. These percentages show no great difference between the relations of inherited and non-inherited phthisis to hæmoptysis, the inherited exceeding by 1 per cent. that of the non-inherited form.

Without here attempting a comprehensive statement of what the predisposition, transmitted or acquired, is, we may mention two influences of important force--a tendency to fragility of vessels and to the catarrhal disposition. It is sufficient to speak of the fact that in no other disease of the lungs than phthisis have we as a common feature this vascular fragility. It differentiates the disease and the symptoms. If it appear in any of them, it should at once excite a suspicion of the phthisical constitution. That it does appear in some such cases without ulterior effects does not invalidate the general statement. It may be put down as a part of the phthisical habit directly concerned in the liability to hæmoptysis. The proof of this proposition is more clinical than anatomical.

The attempt to prove that it is hæmophilic rests upon the application of a few histological examinations of hæmophilic vessels to the phenomena of phthisical hæmoptysis. The assumption of identity has only the doubtful force of analogy. Histological examinations of the vessels in the earliest stages of phthisis and hæmoptysis are too rare to afford sufficient data. In the latter stages the condition is too complex, because of positive inflammatory and ulcerative processes.

Although alterations in the vessels in the early stage of simple inflammation cannot be histologically demonstrated, yet they must exist in order to allow diapedesis. So with early phthisis: in the pre-hæmoptoic stage the alterations are not demonstrated, yet that such disorder of function must have accompanying structural change underlying the phenomena of the initial hæmoptysis is in accordance with physiological and pathological doctrines, and has much consistent clinical force. When we presuppose a delicacy of, or injury to, the blood-vessels of a part, there is the imminence of not only a rupture, and consequent hemorrhage, but of those changes which, leading through stasis and congestion, come to be inflammatory, and which affect still further the vascular structures and adjoining parenchyma.

Besides these changes initiated in the blood-vessels, there are others of close relation to the phthisical constitution, which begin in the vulnerable epithelial elements of the bronchial mucous membrane and of the air-cells. They are the evidences of the dispositio catarrhalis, which received its name from the old observers, and the validity of which has been confirmed by modern pathological and clinical researches.

It is responsible for the great susceptibility to catarrhal affections of the bronchi and air-cells which lays the foundation for chronic catarrhal pneumonia.

These two elements, of fragility of vessels and of the catarrhal tendency, are the tangible instruments of heredity. They are also the factors of the acquired predisposition.

The Vienna Hospital reports, running through more than fifteen years, and embracing more than 20,000 cases, give as the ages most liable to hæmoptysis those between eighteen and twenty-nine years. No statistics as to sex are given.

{276} Of 1266 cases of phthisis[27] taken without selection from the records of the Cincinnati Hospital, there were

Between 10 and 20 years, 81; in this class, hæmoptysis 20 " 20 " 30 " 459; " " " 208 " 30 " 40 " 363; " " " 143 " 40 " 50 " 191; " " " 62 " 50 " 60 " 110; " " " 28 " 60 " 70 " 45; " " " 9 Over 70 " 7; " " " 1 Age not stated 10; " " " 4 ---- --- 1266 475

[Footnote 27: We desire to acknowledge the services of Walter A. Dun, then a resident physician at the Cincinnati Hospital, in collecting these cases from the hospital books.]

Ware in Mass. Med. Soc. Proc. gives ages in 317 cases:

43 up to 20 139 between 20 and 30 77 " 30 " 40

Of Pollock's[28] 351 cases of profuse hæmoptysis,

43 were under 20 years of age. 168 between 20 and 30 " " 100 " 30 " 40 " " 40 over 40 " "

These figures from widely-different sources testify to the fact that the greatest number of cases of hæmoptysis occurs between twenty and thirty years of age, or at least with a variation of only about a year from those extremes. The possibility of hæmoptysis, if we may judge by cases reported, lies anywhere between sixteen days of age and the limit of life. A case of hæmoptysis in a child sixteen days old is alluded to in Nouv. Dict. de Méd. et de Chirurg.[29] The oldest on the list of the Vienna Hospital reports is seventy-two. In our Cincinnati Hospital list we have 7 over seventy years. Others have reported cases beyond these figures.

[Footnote 28: Prognosis in Consumption, p. 311.]

[Footnote 29: Vol. xxix. p. 391.]

A case of death from pulmonary aneurism and hæmoptysis in a child aged two and a half years is reported in London Path. Soc. Trans.;[30] also one by Powell[31] of a child seven months old from a similar rupture--illustrations of the remark that children are subject not so much to initial as to terminal hæmoptysis.

[Footnote 30: Vol. ii. p. 35.]

[Footnote 31: Med. Times and Gaz., June, 1874.]

As to the relations of sex to the amount of hæmoptysis, we have the Table XI. from the second medical report of the Brompton Hospital:

+------------------+-------------------+--------+----------+--------+ | | Males. | Females. | Males. | Females. | Total. | +------------------+--------+----------+--------+----------+--------+ | Below drachm j | | | | | | | in quantity | 843 | 700 | 55 | 83 | 1681 | | From drachm j | | | | | | | to drachm iv | 616 | 482 | 34 | 69 | 1201 | | From ½ oz. | | | | | | | to 4 oz. | 429 | 268 | 13 | 21 | 731 | | Above 4 oz. | 343 | 153 | 9 | 7 | 512 | | Entirely absent | 588 | 193 | 74 | 65 | 920 | | | ---- | --- | --- | --- | ---- | | | 2819 | 1796 | 185 | 245 | 5045 | +------------------+--------+----------+--------+----------+--------+

These results correspond with the general one stated by Williams,[32] that large hemorrhages occurred in 34.76 per cent. of males, and in only 17.67 per {277} cent. of females. In the above table, where quantities of blood above four ounces were noted, the male figure is more than double that of the female. As regards exemption, it is stated that of the cases of decided phthisis which had been free from hæmoptysis, about five-sevenths were males, and under two-sevenths females. In general it may be said that females are more liable to small and males to the larger hemorrhages.

[Footnote 32: Treatise on Consumption, p. 156.]

Of 268 females in our Cincinnati Hospital list, 44 had hæmoptysis--about 13 per cent. Of 998 males, 431 had hæmoptysis, or about 43 per cent.

In the second Brompton Hospital report[33] it is stated that "many of the most violent attacks of this nature (sudden fatal terminations) have depended on a sudden rise in the temperature." The peculiar prevalence of hæmoptysis on the coasts of some warm countries has long since been noted. Archibald Smith,[34] in giving his practical observations on the diseases of Peru, says: "There appears to be a general predisposition to this disease, hæmoptysis." An intelligent individual, himself a sufferer while then a resident on the lower portion of the North American south-western coast, has given me the same statement. Pasley[35] says at least 10 per cent. of the cases of phthisis in Trinidad which die in the hospital terminate in a profuse hæmoptysis; the quantity of blood varies from 15 to 70 or 80 ounces, and the duration of life from the beginning of the hæmoptysis till the end five to fifteen minutes. Of Ware's cases,[36] 83 were in winter, 101 in spring, 69 in summer, 102 in autumn, or 185 in autumn and winter, 170 in spring and summer. In four months of warm weather, June, July, August, and September, 97 cases; in October, November, December, and January, 134; in February, March, April, and May, 124--an average of 129 for the eight cold months, an excess of 32 cases, or about 33 per cent.; in the transition seasons, spring and autumn, 101 and 102. The highest numbers were in March and November, 38 and 39; lowest number in June, 18. These are the only figures obtainable as to our climate, and they do not agree with those given by R. E. Thompson's table,[37] showing the prevalence of hæmoptysis as to months in 1000 well-marked cases:

Jan., Feb., Mar., Apr., May, June, July, Aug., Sept., Oct., Nov., Dec. 67 61 90 95 112 130 128 64 64 55 81 63

The summer months of June and July show the largest numbers, and the months of December, January, and February lesser numbers. The decrease in August is explained in great measure by the diminution in attendance. It is possible that other elements of climate besides temperature may account for this difference between American and English figures.

[Footnote 33: Page 17.]

[Footnote 34: Edinburgh Med. and Surg. Journ., vol. liv., 1840.]

[Footnote 35: Brit. Med. Journ., Jan. 10, 1880, p. 53.]

[Footnote 36: Mass. Med. Soc., 1860.]

[Footnote 37: On Pulmonary Hemorrhages, p. 114.]

A more correct opinion as to the effect of altitude is developing. Archibald Smith[38] more than forty years ago testified to the good effects of removal from the coast to the high sierras of Peru in cases of phthisis with hæmoptysis. His own instances of great improvement following removal to high levels, 5000 to 8000 feet, are conclusive. He also gives instances where renewals of hemorrhagic attacks followed the return to the coast. It was the custom for physicians to send their consumptive patients to the sierras without reference to their hemorrhagic attacks.

[Footnote 38: Loc. cit.]

Similar testimony is accumulating in this country. The Colorado regions are supplying, through their physicians, much material bearing upon the effect of altitudes on hæmoptysis. H. K. Steele of Denver, Col., writes, June, 1883, that "it is the opinion in the profession generally, and I endorse it, that this country acts beneficially in the hæmoptysis of phthisical patients." Jacob {278} Reed, Jr., says[39] that not only does the ascent to this altitude (6000 feet) not predispose to pneumorrhagia in consumptives, but that "hemorrhagic cases do well here; in most cases the bleedings becoming less frequent, in many cases ceasing altogether." By letter May, 1883, he says these cases number between 500 and 600, and he feels justified in the positive statement that not only does altitude not precipitate hæmoptysis, but that "those suffering from this symptom are benefited here, their bleeding becoming less frequent and less in quantity." He makes an exception of florid cases in active progress or old cavities waking up to new action.

[Footnote 39: "Altitude in Reference to Pneumorrhagia," an analysis of 70 cases, read at the eighth annual convention of the Colorado Med. Soc., 1878, p. 66.]

Denison,[40] after an analysis of 90 cases of hæmoptysis out of 202 of phthisis, says: "The advantages of high altitudes are pre-eminently for hemorrhagic cases in the first stage, while hemorrhagic cases with excavations, especially if the bleeding has been recent and softening is in progress, should be interdicted from going to great elevations."

[Footnote 40: Rocky Mountain Health Reports, p. 140.]

He also quotes Herman Weber[41] as recommending "alpine climates, not only as a prophylactic measure against hæmoptysis, but also as a means to promote the cure of the effects of the inflammatory processes resulting from pulmonary hemorrhage."

[Footnote 41: Hæmoptysis as a Cure of Inflammatory Processes and Phthisis, with Remarks on Treatment.]

These statements are sufficient to show that the view formerly prevalent, and still more or less so, that high altitudes have the effect of prolonging or favoring hæmoptysis, is not altogether correct. It should be understood as applying to the extreme heights of 10,000 or 15,000 feet, and that rapidity of transfer and unusual exertion are necessary and qualifying considerations. Jourdanet[42] places the region of safety in phthisis about the mid-point between the level of the sea and the snow-line. The preservative level is lower in Alpine than in American regions. The line of perpetual snow in Mexico being about 4500 meters, the preservative zone would be 2250 meters. In Switzerland, where the line of snow marks 2700 meters, the same zone would be 1350 meters. No such definite limitations are attainable as regards hæmoptysis, but a correspondence of zones might be conjectured.

[Footnote 42: Influence de la Pression de l'Air, vol. ii. pp. 183, 184, 213.]

The belief that pregnancy in some way favors hæmoptysis is a very old one. It has been more or less accepted by modern writers. Trousseau[43] gives his observations to the effect that there are women who during pregnancy, and others who during nursing, spit blood. His belief was that such hæmoptyses were not symptomatic of pulmonary tubercle nor of cardiac disease, but he classifies them as cases of hemorrhagic deviation. Peter[44] speaks of a gravid pulmonary hyperæmia, proven in part by his determination of increased local temperatures in the lower intercostal spaces. Some of his cases do not sustain his theories, and can properly be referred to puerperal accidents, such as emboli in phlegmasia alba dolens. Such cases as we have met with in connection with pregnancy or lactation have had hereditary or acquired tendencies to phthisis. We have under view a case where hæmoptysis always recurs during pregnancy and where there is a family history of phthisis. A brother has pulmonary hemorrhages preceded by inflammatory attacks, which stand in a relation to him corresponding to the pregnant hyperæmia of the sister. The well-known effects of pregnancy or prolonged lactation in developing phthisis are a sufficient explanation of this class of cases.

[Footnote 43: Clinique Medic. Trans., vol. i. p. 531.]

[Footnote 44: Leçons de Clinique médicale, vol. ii. p. 664, 2d ed.]

Many exciting causes are assigned by patients in explanation of a dreaded {279} event, and some are otherwise misinterpreted. Their mode of action is not intelligible unless we keep in view the anatomical, physiological, and pathological data heretofore given. Numerous cases occur where no exciting causes can be found, such as those coming on in the quietude of sleep. The insidious agencies of the predisposing causes must be responsible. A study of many cases will show that the alleged causes have become operative only after a considerable time has elapsed, during which a congestive or inflammatory condition has appeared, the expression of a latent tendency. Dancing in a warm room or speaking long in the open air, followed in twenty-four hours by bleeding, are such instances. The physical effort was only so far instrumental as it gave a chance for the development of a potential diathetic condition. It was not the direct cause. Falls, frights, blows on the chest, heavy lifting, playing on wind instruments, and emotional excitement are sufficient to bring on a hemorrhage by direct influence, and by so increasing arterial tension as to overcome the resistance of vessels already weak. It is not intended to maintain the impossibility of rupture of healthy vessels under some circumstances, but the large provision made in the great distensibility of the pulmonary vessels and in the supplementary functions already alluded to make it necessary to be cautious in such admissions. The fact that hemorrhages from the direct causes are sometimes not followed by phthisical effects does not necessarily disprove their diathetic origin.

The effect of blows on the chest in producing hæmoptysis and phthisis has been the subject of medico-legal examinations in suits for damages. In all of such cases within our knowledge there has been the element of fright or great emotional excitement, and hence a complexity of causation. An hereditary tendency to phthisis was also present--a fact which diminished the force of the plea that the blow was alone responsible for the injuries to the health of the parties concerned.

Diseases or injuries of the brain may be mentioned as causes of pulmonary hemorrhage, which may occasionally be shown by hæmoptysis. Experimental pathology has recently thrown much light on these cases. (See PULMONARY APOPLEXY, infra.)

It may be worth while, in view of recent researches, to refer to a form of hæmoptysis closely associated with a newly-discovered parasite, named Distoma Ringeri,[45] after Ringer of Tamsui, Formosa, who discovered the parasite, but did not at once recognize its etiological relation to the endemic hæmoptysis. In a post-mortem of a man dead from rupture of an aortic aneurism he found the parasite lying on the lung-tissue, probably escaped from a bronchus. There were some small deposits of tubercle, no cavities, and slight congestion of the lungs. Manson found that these parasites were associated with a frequently-recurring hæmoptysis. Baely of Tokio[46] discovered the parasite, probably before any others. It is quite common in North Formosa and through Japan. Manson says:[47] "Endemic hæmoptysis can be readily diagnosed. There is a history of irregular, intermitting hæmoptysis, associated with a slight cough, and in the intervals of more active bleeding the expectoration once or several times a day of small pellets of viscid, brownish mucus. Examination of a small portion of the sputum with the microscope at once settles the diagnosis, sometimes as many as twenty parasites being found in a single field." Further examination is necessary to determine the manner in which this parasite produces the hæmoptysis.

[Footnote 45: The Filaria sanguinis hominis and certain New Forms of Parasitic Disease in India, China, and Warm Countries, p. 134, by Patrick Manson, Amoy, China.]

[Footnote 46: London Lancet, Oct. 2, 1880.]

[Footnote 47: Ibid., p. 143.]

The association of bacilli tuberculosis with hæmoptysis is proven by a number of examinations. These will be referred to in their diagnostic relations at another page. It is not intended here to imply an etiological relation, {280} because as yet our knowledge does not point to the blood-vessels as being the special or usual habitat of bacilli or the place of their most destructive efforts.

Hydatids of the lung are a cause of hæmoptysis which may come from congestion accompanying their growth, or from their rupture and consequent opening of blood-vessels.

Before proceeding farther we shall refer more fully than before to the conditions prepared by heredity, age and sex, etc. for the action of the exciting causes. The agencies were stated to be the peculiar vulnerability of the vascular and epithelial structures of the lungs. When the morbid imminence is reinforced by an infective element, as in phthisis, certain results follow which make easy the action of the incidental causes. Because of the enormous vascularity and great delicacy of structure of the lungs, and their liability to external influences, slight external irritants in such constitutions produce more than what follows in other cases. Instead of a transient hyperæmia or mild catarrhal inflammation, we may have that fluxionary hyperæmia of which an early outcome is hæmoptysis. Experimental pathology explains such occurrences by demonstrating that while a normal vessel, as in the mesentery, will require a pressure of seventy millimeters of mercury to produce extravasation of its contents, an inflamed one will not stand more than twenty-five millimeters. If catarrhal pneumonia proceed in its phthisical form, it adds its elements of danger.

After its early stage of congestion we have the initiative processes extending from the epithelial structures of the bronchi and alveoli to the alveolar wall, which becomes thickened. By means of the double pressure of abundant epithelial and fibrinous products retained within the alveolar cells, and of the increased growth in the alveolar walls, obliterative endarteritis and obstruction of blood-supply follow, the final result of which may be destructive changes opening the way for softening and ulceration, and consequent hemorrhage.

The same early hyperæmia accompanies the development and growth of tubercle, whether it come from the bronchioles, the blood-vessels, or alveolar walls. Trasbot[48] says: "A tubercle is found to be developed along a small artery, most frequently at the angle formed by a terminal division of the vessel--some around a capillary, around which it forms a kind of bead, or in the network of an anastomosis, which envelops it on every side. Vessels are more numerous in the tissues round the nodules and in the septa or interstices of the large masses than in the healthy connective tissue: there the vascularity is often so great as to be mistaken for inflammation."

[Footnote 48: Quoted by Creighton Bevine, Tuberculosis in Man, p. 133.]

Hamilton,[49] speaking of the formation of tubercle in the alveolar wall and cavity, says: "Capillary blood-vessels, filled with blood-corpuscles, are drawn into it, and in this stage are distinctly visible. They are all much engorged, and occasionally minute extravasations are visible, the blood-corpuscles being thrown into the alveolar cavity." The chance of an earlier obliteration of vessels is greater under these circumstances than where the process begins in any other structure. The final result is that combination of catarrhal and tubercular products characteristic of mixed phthisis.

[Footnote 49: The Pathology of Bronchitis, Catarrhal Pneumonia, Tubercle, etc., 1883.]

As increased vascularity accompanies and surrounds the nascent tubercle, so vascular neo-formations accompany or are intermixed with the obliterated zone of vessels, as long since described by Guillot and recently substantially confirmed by Ewart. The former says:[50] "There result numerous and inextricable anastomoses, which extend incessantly, and of which the whole forms a mass of vessels proportional in extent to the age of the tubercles and cavities that they entirely surround."

[Footnote 50: L'Expérience, vol. i. p. 553.]

{281} There ensues a connection between this system and that forming on the false pleural membranes, and a supplementary function of supply for regions outside of the area of obliterated vessels and for walls of cavities is established. Considering the want of vitality of new formations generally, it is quite probable that these become sources of hemorrhage occasionally. Successive extensions of the diseased regions reduce the amount of this supply, so that the converse follows--comparative anæmia of the lung involved and diminished tendency to hæmoptysis in some of its forms.

These observations, involving considerations of predisposition and its tangible forms, do not apply to the important class of cardiac hæmoptysis. The factors here are increased venous tension, pulmonary hyperæmia of mechanical rather than vital origin, sclerosed or atheromatous vessels, capillary ectasis, and embolic obstruction of the pulmonary artery with resultant infarction, etc.

SYMPTOMS.--The definition requires that the blood be pure or unmixed, yet the coarse physical appearances may vary a good deal. The color is usually a bright red, but may be dark or venous in hue. There is sufficient inconstancy in color to prevent its being reliable in distinguishing the special source of the bleeding, though usually the bright color is of bronchial and the dark of pulmonary origin. If bright red at the onset, it loses some if not the whole of its brightness as the attack progresses or is subsiding, sometimes because of retention in the air-passages. The mass is more or less frothy, and varies in density and specific gravity, in diffluence or adhesiveness, the latter quality increasing in proportion to congestive or inflammatory conditions, whether in the early or later stages. This is dependent on the increase of the plastic, fibrinous, or reactive elements in the blood and adjoining tissues. The mass may lie in a circumscribed or in a splashy form in the bottom of the vessel, circumstances of distance and force of ejection, as well as of physical quality, producing the variations. The quantity varies greatly, both as to the amount at each act of expectoration and as to the amount during all of them. The whole amount throughout an average attack of initial hæmoptysis might be placed at about one and a half to two ounces. Such would be called moderate but decided hemorrhage. The extremes would range between a teaspoonful and several pounds, and the time consumed in the attack may vary between the time taken up by one or two ejections and several months. The intervals between the successive ejections will vary from a few minutes to twenty-four hours or more in a case lasting a week. The manner of ejection is sometimes by a single effort of hawking or throat-scraping or clearing, sometimes by a slight hacking cough or by a vigorous effort of expulsion; at other times the outflow is so rapid through the mouth and nostrils that it resembles vomiting and may suggest a hemorrhage of the stomach.

The effect which a severe attack may have on the patient is often notable. He becomes pale out of proportion to the amount of blood that he has lost; the pulse is full, bounding, and corresponds to what is called the hemorrhagic pulse. This is sometimes due to the mental shock, but again it is independent of any excitement on the part of the patient, or of even any sort of constitutional disturbance, as fever. We have seen it in full development in connection with a profuse hæmoptysis and a temperature of 105°. It has been noted also as part of the phenomena of hemorrhage produced by septic influences upon the vaso-motor system. Walshe's dictum is no doubt true, that there is a calm and excited variety quoad cardiac action.[51] In the former there is little vascular or mental excitement or debility, and the patient does not willingly yield to the necessary restraint.

[Footnote 51: Diseases of the Lungs, p. 330.]

Feebleness is an accompaniment, sometimes to a degree disproportionate to the amount of blood lost, and is an element in the shock which the patient {282} feels at so unexpected an event. The early part of the attack is usually without fever. This comes on later as a part of the reaction phenomena, and becomes then a very important prognostic symptom. We have known it, however, to range as high as 105° before the hemorrhage appeared, and without any reduction by a most obstinate continuance of the depletion.

Many cases occur without premonition. In a proportion there are symptoms precedent to the outbreak. The significance of these is often not perceived until the hæmoptysis appears. Certain subjective symptoms are common. A sense of burning, which is substernal or unilateral, corresponding to that lung which is then or shall afterward show itself affected; soreness within the same bounds; dyspnoea, rarely grossly objective; slight hacking cough for variable periods, and, more immediately antecedent, a salty taste in the mouth,--are some of these. They have their origin in a state of hyperæmia or irritation which has its outcome in catarrhal processes or hemorrhage. Which it may be will depend on certain predisposing as well as the immediately operative causes already mentioned.

Of the objective states, some importance may be attached to characteristics of the individual, such as the brunette complexion, dark hair and eyes, or to external correspondences with others of the family known to have been similarly affected.

More than the usual care is necessary in the physical examination, particularly in the use of percussion. Palpation and auscultation can be safely applied, but there might be greater difficulty in getting the patient into a good position for the actual examination. In the hæmoptysis of incipient phthisis the physical signs most usually found are deficient expansion and resonance and vesicular murmur at either apex. These are evidences of causes that had been in operation before the hæmoptysis, and indicate important physical changes at the region where they may be found. Yet they do not necessarily indicate that the bleeding has its origin at that place. Add moist bubbling râles, and the presumption becomes almost a certainty that you have found the locality of the hemorrhage. If these subside as the amount of blood expectorated gets smaller, the inference is still stronger. Successive increments of physical signs would indicate that the bleeding had been correctly located and that the lesion which gave origin to it was progressing. A proportion of cases occur where no physical sign can be found even after careful examination, so that it happens sometimes that at the period of most importance for diagnosis physical signs are not available, and when they are most distinct in the advanced cases the diagnosis is already established. They may even become embarrassing by their abundance. The true significance of the physical signs cannot be determined until the attack has subsided entirely. The termination of an attack is usually by disappearance of the congestion of which the symptoms related were the expression. The soreness and oppression beneath the sternum, the dyspnoea and fever, are relieved. The persistence of cough would not necessarily augur badly, because there is apt to be some catarrhal secretion which necessitates it. The general result is relief. If the termination is to be unfavorable, there will be an evident increase of constitutional symptoms, especially of fever, as in the case alluded to above with the high temperature. There will be a slower return to the pre-hæmoptic state and an increase of the physical signs, and you may have apparently a case of phthisis ab hæmoptoe. The impetus in a large majority of cases is from the constitutional elements which initiated the symptoms, rather than from the local cause, blood within the air-passages. Clinical experience proves that there are cases where serious and rapid injury to the lungs has followed closely upon an hæmoptysis. It is admissible to classify such as phthisis ab hæmoptoe only, in the sense that the effusion of blood in the remote parts of the lungs has brought about catarrhal pneumonia, which in those predisposed {283} ends in phthisis. Sommerbrodt's[52] experiments proved that the healthy animals recovered from the catarrhal pneumonia.

[Footnote 52: Virchow's Archiv, vol. lv. p. 192.]

To determine the genuineness of any such special case, we should be able to include inherited or acquired predisposition; to prove priority of the hæmoptysis to cough, dyspnoea, and fever, and that these followed soon after the bleeding; and to show that the age at the time of the occurrence was not the phthisical age. If a direct or mechanical cause can be found for the bleeding, the proof would be still stronger. Most of the cases depended on to prove phthisis ab hæmoptoe or hemorrhagic phthisis (Powell) do not answer to these requirements. In the 8 cases reported by Sokolowski[53] are summarized these features, and they give strong support to the conception of a phthisis ab hæmoptoe. The mode of termination by sudden death is by syncope, and suffocation cannot be said to be very frequent. There have not been more than 3 suddenly fatal cases (within a half hour) in the Cincinnati Hospital records in a period of fifteen years: 22 cases are given in the second medical report of Brompton Hospital, where the cases of phthisis are very numerous; Powell's table[54] has 15 cases, which happened at the Brompton Hospital between February, 1868, and November, 1870. The cases which we have collected as occurring since that amount to about 20. T. Williams[55] says that of 198 patients who died, 4 died of profuse hæmoptysis. Thompson[56] says that of 383 deaths occurring in the hospital (Brompton) during three years, 26 were from fatal bleeding--a percentage ranging between 2 and 6 in the two series.

[Footnote 53: Berlin. klin. Wochenschrift, 30 Sept., 1878.]

[Footnote 54: Vol. xxii., Lond. Path. Soc. Tr.]

[Footnote 55: Med.-Chir. Trans., vol. liv.]

[Footnote 56: Loc. cit., p. 115.]

The symptomatology given above is a general one. Looked at with reference to the varieties of hæmoptysis, the assignment would be to the earliest or initial attacks. Assuming five varieties--1, the simple or idiopathic; 2, the congestive; 3, the ulcerative; 4, the cavernous; 5, the extra-pulmonary--it would belong to the simple or to the congestive form.

Under the first may be included those cases which occur without any heredity or traceable cause, are not accompanied by fever, soreness, dyspnoea, or physical signs, and which further observation shows are not followed by pulmonary disease. Such cases are rare, yet clinical records afford them. Time is so important an element in the diagnosis that the presumption would be against such a classification at the time of the call for treatment. They have probably developed the hemorrhagic element of phthisis, and by otherwise vigorous constitutions are protected from its further evolution.

The congestive form is the one with which we most often meet, and is essentially the expression of the predisposing element mentioned as one of the agencies of heredity. Unlike the idiopathic variety, it has its positive symptoms, so familiar to the practitioner. Special clinical forms, as the hæmoptysis of pregnancy, the so-called vicarious cases, the earliest attacks in the hemorrhagic variety of phthisis, the hæmoptysis of plastic bronchitis (which has a phthisical element in it), that of hydatids of the lung preliminary to the opening of the hydatid, and probably others, such as cancer of the lung, may be placed in this category. Hysterical hæmoptysis is a term of doubtful propriety, because facts show that the tubercular diathesis has close affinities with the neuropathic heredity,[57] and hence that the hæmoptysis arises from the tubercular and not the neuropathic element. From this point of view it has its congestive origin, and can be properly classified under this head.

[Footnote 57: J. Grasset, Brain, vols. vi. and vii.]

The ulcerative form is familiar to us in the second stage of phthisis. It is more subordinated to the constitutional features, fever, hectic, and debility, to the purulent expectoration, and to the easily-determined physical signs. {284} Notwithstanding the apparently increased chance of profuse hemorrhage, the quantity of blood is often quite small and apt to be accompanied with a mixed sputum. It is not so florid as in the congestive form. Some of the most copious hemorrhages in this stage arise from the presence of the hemorrhagic diathesis or are found in persons of full and plethoric habit. They will recur at intervals of once or twice a year for many years, and some of them finally cease, with a remainder of physical signs. The physical signs usually indicate nothing more than consolidation of the lung for a long time. They are dulness, bronchophony, bronchial breathing, and mucus or crackling sounds over a limited area in the upper part of the chest. In the slow cases of pulmonary fibrosis there is now and then a small amount of ulcerative action to produce hæmoptysis. We have seen cases fatal by a suffocating quantity without discovery of the actual source.

In cavernous hæmoptysis there are striking facts which give this class a great interest. It includes most of the suddenly fatal cases which shock families or hospital inmates. It comes from rupture of small aneurisms in the walls of old cavities. A less dangerous form is that from small granulations or vessels in the walls of recent cavities or from small vessels in their trabeculæ. The elucidation of hemorrhage and death from pulmonary aneurism is of the later acquisitions in our knowledge.[58] A distinction between the ulcerative and pulmonary aneurism forms is not always practicable. A detection of the aneurism by auscultation has not been recorded, though it is at times quite large. In the latter form you may have, as in the former, repeated attacks of hemorrhage before this fatal one. The most decisive indication in favor of the aneurismal source of the bleeding, besides frequent and abundant hemorrhage, would be the proofs of a chronic cavity. In Powell's[59] 15 cases of fatal hæmoptysis 3 were without discoverable source; of the other 12, 3 were immediately fatal; in the remaining 9 the previous attacks of hæmoptysis occurred at periods varying from eighteen months to two days. The aneurisms were all in the left lung except 2: 6 occurred in individuals with family histories of phthisis; 3 with such histories; 2 are negative or doubtful of fatal hæmoptysis.

[Footnote 58: Williams says that Peacock and Fearn of Derby were the first to record instances of pulmonary aneurism in England. Stark in his works edited by J. C. Smyth, 4th Lond. ed., 1788, p. 31 (quoted by Young, loc. cit., p. 331), relates a case of diseased lungs in which sudden death took place from the bursting of an aneurism of the pulmonary artery.]

[Footnote 59: Vol. xxii., Path. Soc. Trans., London.]

We have a table of cases collected from reports made since Powell's--in all 21. In 10 the aneurisms were in the left lung, 8 were in the right, and in 3 the place of the aneurism was not designated; 16 were in males, 4 in females, and 2 not noted. The relation of heredity to phthisis was not noted, except in 1, which was affirmative. In 2 there was no previous attack of hæmoptysis. The longest interval between the first and fatal attack was four years: 7 were immediately fatal. From both collections we have 33 aneurisms of the pulmonary artery in cavities, 20 being in the left lung; 10 were in the right. Most of the aneurisms were situated in the upper lobes, as might naturally be expected. Powell's opinion was that there were good grounds for saying that the more chronic and quiescent the cavity, and the more unilateral the disease--the more nearly, in short, it approached the type of fibroid phthisis--the more probable it was that the hemorrhage, if it occurred in any quantity, proceeded from a pulmonary aneurism. Taking 15 cases from our list the duration of which could be fairly named, the average was about seventeen months. The average duration of Powell's cases was about twenty-four months. Most of our cases were bilaterally affected, and only 2 were positively stated to have been of the fibroid variety. Yet, practically, {285} the clinical features enumerated by Powell form the best standard by which to determine the source of the fatal hemorrhage. Copious hæmoptysis, with great chronicity and quiescence of phthisis and cavernous physical signs, points to aneurism of the pulmonary artery within the cavity.

In the class of extra-pulmonary hæmoptysis are included those cases of ulceration and rupture of aneurisms of the aorta and its branches into some portion of the air-passages, and the necessary discharge of blood therefrom. Experience justifies a classification of this kind. Cases have occurred where the pulmonary symptoms and signs have been so prominent as to have obscured those of the coexistent and causal aortic aneurism until the fatal hæmoptysis revealed the mistake. Still others of simultaneous tubercular disease of the lungs and aortic aneurism are reported. J. W. Ogle[60] reports a case where the patient had had cough for seven years, at first attended with hæmoptysis, dyspnoea, and palpitation, and afterward consolidation of the left lung, and where death was produced by rupture of aortic aneurism into the right bronchus. Bronchitis and pneumonia have been treated without suspecting the real cause until a similar event occurred. Janeway and Loomis[61] also give instances of aortic aneurism and phthisical deposits with doubtful diagnoses in the same persons. We have seen an instance where illness began with cough, frothy and then purulent expectoration, then loss of flesh and strength and pain in side, fever to 102, dulness below right clavicle, and then a number of large hemorrhages, and finally a fatal one, all of the hemorrhages depending on an aneurism of the internal carotid artery discharging into the mouth. The chances of these irregular clinical associations must, then, be borne in mind. Careful examination only will enable us to eliminate the doubtful features.

[Footnote 60: Lond. Path. Soc. Trans., vol. xvii. p. 104.]

[Footnote 61: N.Y. Med. Rec., vol. vii. p. 304.]

In a collection of 33 aortic aneurisms discharged through the air-passages, 9 had histories of hæmoptysis previous to the last one. These discharges were more or less copious, and, considering the physical signs of phthisis obvious in some, and recollecting that aneurisms were not recognized, the clinical features were such as to produce if not justify a diagnosis of intrapulmonary hæmoptysis. Of the 33, 16 opened into the left bronchus, 14 into the trachea, 2 into the right bronchus, and 1 is given without special designation of the point of communication. Of 2 aneurisms of the arteria innominata, both opened into the trachea. Aneurisms of the subclavian have also been known to have discharged through the apex of the lung. These clinical and anatomical facts point to a large predominance of symptoms and lesions connected with the left lung where the pulmonary organs are at all affected. In our own table, while 18 had marked lesions and symptoms pertaining to the left, only 6 had them connected with the right lung. These figures are too limited to be decided, but so far as they go they tend to prove a greater amount of left-lung lesion in extra-pulmonary than in cavernous hæmoptysis.

So far we have considered the symptoms and classification of phthisical hæmoptysis. There remain those other forms of pulmonary hæmoptysis connected with cardiac disease and hemorrhagic infarction. Practically, these are reduced to the first variety, as cardiac disease is the question we have most frequently to consider in this connection. We are justified in assuming the parenchymatous origin of cardiac hæmoptysis, because it rarely appears until chronic valvular disease has prepared the way for its occurrence by its well-known degenerative effects on the pulmonary circulation whereby thrombosis appears, and because at those advanced periods emboli are often injected into the pulmonary artery capable of producing hemorrhagic infarction and consequent hæmoptysis. This latter is accompanied by aggravation of symptoms already serious--increase of dyspnoea, cardiac perturbation, and probably cough. If the hemorrhage be copious, shock may appear, and varies {286} according to the size of the obstructed vessel and the amount of hemorrhage. The patient may have some premonitions, but not of the kind noted in the initial hæmoptysis of phthisis, such as the superficial soreness, burning, or pain localized in the substernal regions. The hæmoptysis, after it has begun, continues more regularly, at shorter intervals, and for a longer time, with the coarse appearance of the blood already mentioned, such as dark, non-aërated, coagulated sputum. The quantity may equal that from the most typical bronchial or broncho-pulmonary hæmoptysis in phthisis; usually it is not copious. Fever is not an ordinary accompaniment, but may develop in consequence of increased structural lesion, as from pneumonic infiltration around a large infarction. It has not then the typical range of ordinary pneumonia, seldom going beyond 100 or 101. The physical signs exclusive of the primary cardiac lesion are those pointing to limited infiltration of lung-tissue about the middle or lower region of the lung. We have limited areas where percussion is dull, almost as much so as over pleuritic effusion, and where the respiration is very feeble or suppressed, and later a bronchial breathing adjoining as a consequence of pneumonic complication. There may be several of these areas, varying in size. Sometimes the localization by physical signs is impossible because of the hemorrhage or infarction being small and deep-seated. Pain becomes a localizing symptom when the infarction is superficial and the pleura becomes involved. The form of valvular disease most likely to produce hæmoptysis is mitral disease, especially mitral obstruction disease.

Beside infarctions originating in cardiac disease there are others of peripheral origin, as in the puerperal condition from phlegmasia dolens. Hæmoptysis is a rare symptom in such cases, but when it does appear it has the same basis. It is seldom severe, and soon merges into an expectoration of pneumonic character, with the clinical forms of embolic pneumonia, or possibly of abscess or gangrene of the lung.

PATHOLOGY.--Incidentally, the pathological relations of hæmoptysis have been already indicated as being connected with phthisis and cardiac disease--principally with the former. If phthisis be an infectious or specific disease, as a large and growing professional opinion claims, hæmoptysis has its specific relations with it. Few symptoms have greater differentiating force than it has. Its occurrence, outside of well-known cardiac or dyscrasic disease, removes any case of primary pulmonary disease from the category of simple inflammation. There may be much more congestion in bronchitis, more catarrhal products in simple catarrhal pneumonia, and more fibrinous or croupous exudation in pneumonia, than in the primary stages of phthisis, and yet no hæmoptysis appear. The mechanical conditions are present in greater degree, but the infective element is wanting. Its closest affinity is with apex pneumonia or alveolar catarrh, yet probably most of such cases occur without it. A blood-dyscrasia contributes an important element in the pathogenesis of hæmoptysis.

In cardiac hæmoptysis the pathology is more simple. Extreme mechanical conditions of obstruction and reversal of the circulation are reinforced by nutritive changes of the vessels and heart, until the so-called cardiac cachexia is established. There is no infective element, and such cases are seldom if ever followed by phthisical destruction.

MORBID ANATOMY.--Reference has already been made to anatomical changes having direct or indirect relation to hæmoptysis, such as those in the blood-vessels. The anatomical basis of the slight hemorrhages of the early stage of phthisis is seldom if ever discoverable. The belief in vascular fragility and congestion with special origin rests much more upon clinical reasoning than demonstration. The large hemorrhages are now and then fatal within short periods of time or instantly, and we then have the opportunity of noting the general appearance of the lungs.

{287} It is notable that cases are not very frequent where the source of the bleeding has not been found by the most careful search. The general appearance varies according to the length of time that has elapsed since the bleeding which preceded death.

In the cases immediately fatal the tubes are filled with fresh blood, which has stained the mucous membrane and has changed the general surface of the sections of lung into a dark, mottled, or patchy color. The greater amount of blood is to be found in the lung from which it has primarily come, but in the more profuse hemorrhages, and particularly where there has been time for the struggles of the threatening suffocation, much blood may either overflow or be inhaled into the other lung and carried into the extreme portions of the air-sacs. If the flow be not overwhelming, the patient may survive long enough to allow other effects from the blood, which has by gravitation or insufflation been carried into certain parts of the lung. We are indebted to Reginald E. Thompson[62] for the most important study of the secondary effects of the blood thus remaining. He says that the relics of blood are to be found in the presence of hard nodules, often deeply, though not always, pigmented. They are mostly found at the summit and middle part of the upper lobe, the middle axillary region, between the third and fifth ribs, close to the pleura, the anterior inferior border, and the middle part of the base corresponding to the summit of the arch of the diaphragm. "Absorption, decoloration, and fibrination go on; the outlying portions of the blood disappear; the central nodules become hard and white, and alone remain to show what has taken place." They are in some cases of varying color, slight red or of an ivory white, mottled with old blood-pigment, around the bronchioles especially, and in the shape of small black granules. Microscopically, they consist of "a group of alveola firmly packed with a semi-opaque, homogeneous fibrinous material, and there is some thickening of the alveolar tissue and also of the interlobular tissue, which thickened tissue forms the limiting capsule."

[Footnote 62: Op. cit., p. 46, etc. These researches are an important epoch in the history of hæmoptysis.]

The ultimate fate of these nodules is variable. Sometimes they go on to formation of cavities, or softening occurs around the periphery or in the centre, and leads to general liquefaction of the nodule, or they may separate from the surrounding tissue by traction. Sometimes the effect of retention of the blood in the air-passages is a catarrhal pneumonia, with the ordinary anatomical proofs of it referred to in the paragraph on modes of termination of hæmoptysis.

Accepting the observations, we have the demonstration of a phthisis ab hæmoptoe.

The morbid anatomy of cases fatal from rupture of aneurisms of the branches of the pulmonary artery has been made prominent by the researches of Rokitansky and Rasmussen.[63] He describes small sac-like aneurisms and ectasias situated in the vessels running along the wall of the cavity. The aneurisms have the shape of a bag and an even surface. The walls of the unbroken aneurisms are of great thickness, and those of the broken ones thin. The opening is always found on the most protruding part of the sac; the edges are thin; their size varies from a pea to a small orange. Powell[64] says a microscopic section taken from a specimen in an early stage shows new connective-tissue elements, causing induration affecting the whole thickness of the wall and obscuring the distinction between the coats. The wall is brittle, becomes thinner from want of support, and yields to an inciting cause, with rupture and death as the result.

[Footnote 63: Edinburgh Med. Journal, 1868-69.]

[Footnote 64: Trans. London Pathological Society, vol. xxii. pp. 54, 55.]

{288} The morbid anatomy of cardiac hæmoptysis is found mostly in two conditions--that of degenerated, atheromatous, varicose blood-vessels, brought about by the condition of chronic obstruction and increased venous tension in valvular disease; and in that of pulmonary infarction.

The first prepares the way for diapedesis or rupture, and consequent hæmoptysis. The rupture takes place in the parenchyma, or, as the anatomical details formerly given make probable, from the blood-vessels of the bronchial mucous membrane also.

Pulmonary infarction is recognized by a dark, dense, pyramidal or wedge-shaped area of varying size situated at the surface of the lung, with the base of the pyramid coming to the pleura. It is found oftener in the lower lobes and in multiple form. It is caused by an embolic obstruction of a terminal branch of the pulmonary artery; sometimes by a thrombosis or by both. A venous reflux from the neighboring districts is supposed to fill the empty vessel, and after a certain time has elapsed changes are supposed to have occurred in their walls by which the blood escapes into the air-cells and interstitial tissue. Litten's[65] explanation, sustained by his experiments, is that the venous reflux, after a closure of the pulmonary artery, is by no means necessary to the formation of an infarction. The infarction fails if the pulmonary artery and the bronchial artery, and those arteries lying outside the lungs, but in circulatory connection with them--the pleural--are simultaneously shut off. If the whole arterial supply be thus taken away, but a living connection be maintained by means of the veins, an infarction does not follow, while it immediately follows if, at the same time with the open veins and closed pulmonary arteries, the collateral or supplementary circulation be kept free. A venous reflux cannot occur so long as a circulation in the capillaries of the lung is sustained by collateral arterial branches. The explanation is that in an unobstructed circulation the entire resistance which is offered to the blood-stream in the capillaries of the lung is overcome by the pressure existing in the pulmonary artery, which, corresponding to the greater width of the capillaries, is much less than the pressure in the corporeal arteries. If the pulmonary artery becomes suddenly impermeable, the pressure in the collateral arteries, which originates partly from the bronchial artery, and partly from those outside of, but in connection with, the lungs, as the pleural, etc., is sufficient to prevent a venous reflux, but not sufficient to overcome the entire resistance in the lungs and to drive the blood beyond the capillaries into the left auricle. Then follows an accumulation and stasis of the blood in the capillaries and smaller veins, and hence results at first a hyperæmia and later a diapedesis. Litten makes another important change in Cohnheim's doctrine: he maintains that the hemorrhage appears before the integrity of the vessel-walls is impaired.

[Footnote 65: Zeitschrift für klin. Med., vol. i. p. 148, Berlin, 1880.]

Other fatal cases find their anatomical basis in the softening and ulcerating processes, which while forming cavities are liable to open vessels of greater or less size in their walls or trabeculæ.

The condition of the heart in phthisis is one which has an effect in influencing the occurrence of hæmoptysis. The general statement by Peacock, that the weight of the heart in phthisis, though less than in acute diseases, is greater than that in other chronic diseases, needs to be modified somewhat, as he did not make a distinction between different forms of phthisis. The more the case approaches the fibroid variety the more likelihood of some increase of size, particularly in the right ventricle. Spatz,[66] a later authority, gives as the result of his examination that phthisis diminishes the size of the left ventricle--that an absolutely compensatory hypertrophy of the right ventricle, which is apparent in special cases, does not as a rule exist, although {289} the resultant decrease does not throughout stand in relation to the decreased weight and volume of the whole body in phthisis. The ratio between the depth of the left ventricle and circumference of the aorta is diminished; and, as this is not compensated for by hypertrophy of the walls of the ventricle, arterial tension diminishes and the pulse becomes soft and small. The chance of rupture of weak vessels by relatively excessive tension is thus much weakened in the later stages of phthisis.

[Footnote 66: Deutsches Archiv für klinisch Med., vol. xxx. p. 154.]

Another element capable of modifying the hæmoptysical features of phthisis is claimed by Jaccoud[67] as existing in the insufficiency of the tricuspid valve, which compensates the increased tension in the field of the pulmonary artery arising from obstruction of a considerable part of it. The amount of blood passing from the right ventricle is thus, by a reflux, proportioned to the area of obstruction in the artery, and the tension is reduced so as to prevent rupture of the weak vessels. His conclusions are based on 18 cases of measurements of the tricuspid orifice. They varied from 111 to 130 millimeters. The evidence obtainable during life was a systolic murmur heard at the ensiform cartilage and cervical venous reflux.

[Footnote 67: Clinique médicale, vol. ii. p. 346, etc.]

DIAGNOSIS is mostly called for with regard to the chances of hæmatemesis. Inspection of the blood is naturally an early point for attention. Its bright-red color, frothy look, freedom from extraneous matter, and its coming up by coughing are strong evidences easily acquired of its pulmonary origin. Corroborative circumstances are the family history of phthisis or hæmoptysis, the presence of pulmonary, or in fewer instances of cardiac, physical signs, the immediately premonitory symptoms spoken of before. Fever, the age of the patient, and the continuance of the discharge of blood in its later gradations of color and mixture of catarrhal elements, inspection of the mouth, fauces, and larynx, would exclude those possible sources. Each has its limitations, but together they are conclusive as against hæmatemesis. Recent and accumulating experience attributes some diagnostic value to the presence of bacilli tuberculosis in the expectorated blood. Hiller[68] reports 6 cases of hæmoptysis in which the blood showed in bacilli: 3 were completely initial. The bacilli were easily demonstrated by preparations and also by inoculation on guinea-pigs. They have also been found in the blood of cases of acute tuberculosis by Weichselbaum.[69] Resort may be had to the well-known tests for the presence of the elastic tissue of the lung in sputum.

[Footnote 68: Centralblatt für die med. Wissenschaft, March 24, 1883.]

[Footnote 69: Wiener med. Wochenschrift, No. 13, 1884.]

As positive data for hæmatemesis we have the dark color of the blood, its firmer clotting, greater density and want of aëration, acid reaction, the presence of extraneous matters of food and drink, their ejection by vomiting, and pain or uneasiness at the epigastrium. As corroborative we have the less frequent occurrence of hæmatemesis, the individual history of gastric disease, such as ulcer of the stomach or presence of hepatic cirrhosis from intemperate habits, and the history of a blow on the abdominal surface: discharges of blood from the bowels are more likely to occur in hæmatemesis.

Hæmoptysis may be simulated, as by scratches or cuts on some part of the internal surface of the throat or mouth. The blood is then likely to be thinned by secretion from the mouth. Inspection would detect the imposture. The chance of blood from an epistaxis being swallowed and afterward ejected by vomiting is to be remembered. Cardiac hæmoptysis is distinguished in most cases by the presence of symptoms and physical signs of valvular, usually mitral, disease in a considerable degree of advancement. These are so pronounced as to exclude phthisical disease. Other and fewer cases occur where the hæmoptysis is the first evidence of the cardiac disease, and they require a careful exclusion of all the features of tubercular disease, so as to be able to {290} arrive at a correct conclusion. There are no conclusive considerations pertaining to the amount and character of the blood. In the severe and copious hemorrhages there is likely to be present a marked shock.

PROGNOSIS.--Hæmoptysis usually implies phthisis existing or imminent, and yet it has in general a favorable effect on its course. This applies more to its first stage than subsequently, and more to the small than to the large hemorrhages. The gravity of the small ones increases in proportion to their frequency. The family and personal equation is of more importance than the mere quantity. We may have a slight hæmoptysis and a large increase of the morbid condition following it, and the reverse, the result depending on the individual tolerance of and susceptibility to reaction. As in the second stage the reactive elements are more potent, the small hemorrhages then are less beneficial. They are the index of activity in the destructive lesions, and yet may relieve the accompanying congestion. The easiest appreciable symptom of the progress of the disease is the fever. We may fail to properly interpret physical signs because of want of familiarity with the individual case before us. If besides more fever there be more cough, dyspnoea, and debility, the prognosis increases in gravity. These remarks will apply with more force to the large hemorrhages than the smaller ones, and are guides for prognosis in all the clinical forms of hæmoptysis. In the special clinical form, the hemorrhagic variety of phthisis, bleedings recur often and in large quantities during years, and some of the cases end with final recovery. The fever and constitutional irritation give way under seemingly very unfavorable conditions. The fact that a great part of them have no history of heredity, and that they come on at a late period of life, may account for this, because they thus escape the influences which heredity and age are known to impose upon the other classes of phthisical subjects. Some interesting conclusions have been drawn from the history of cases of profuse hemorrhages. Pollock[70] thinks that they shorten the duration of the first stage and lengthen the duration of the second and third. Out of his 351 cases, 204 occurred in the first three months of illness: 45 had remained in the first stage when examined, 142 having undergone softening, while 164 had cavities. Of 286 cases of profuse hæmoptysis classified by Williams,[71] the number of cases in the first stage was 187, and the percentage of deaths was 13.95; 65 cases were in the second stage, and the percentage of deaths was 24.61; 31 were in the third stage, and the percentage of deaths was 67.74, showing increased effect of hemorrhages upon pulmonary structures advancing in destructive processes and upon constitutions being progressively undermined by them. In other clinical varieties the symptom is so clearly subordinated to the general process that it loses its prognostic importance in the established disease. There is an imminence of fatal hemorrhage in many of them, as in fibroid phthisis, cancer, abscess, gangrene, and hemorrhagic infarction of the lungs. In extra-pulmonary hæmoptysis or in that from rupture of pulmonary aneurism there is seldom opportunity for prognosis.

[Footnote 70: Elements of Prognosis in Consumption, p. 139.]

[Footnote 71: Pulmonary Consumption, p. 150.]

If the condition be recognized, we can but say that the fatal attack is liable to come at any moment. In cardiac hæmoptysis the hemorrhage is an event coming toward the close of organic and obstructive changes which are not much within our control. There are minor degrees, as shown by expectoration of single small masses of dark coagulated blood and by the absence of marked aggravation of the symptoms, which do not prognosticate unfavorably for the immediate, but do show impending dangers of a future, attack. Morbid anatomy shows traces of a recovery from a number of premonitory threatenings. The elements of a serious prognosis are the appearance of a shock, increased dyspnoea, a large amount of hæmoptysis, increased perturbations in the heart-action, and increased areas of dulness or râles at certain parts of {291} the lung other than the usual sites of consumptive disease. These and other evidences of constitutional initiation are not as available as in the other varieties mentioned.

TREATMENT.--In the cases of the mildest form very little more need be done than to keep the patient quiet. His apprehensions may require attention. They may be allayed by assuring him that the hemorrhage will be more of a security than a danger, because it is the expression of a local congestion that will be relieved by the discharge. We have found that a large dose of quinine (ten or fifteen grains) will answer the double purpose of a nervous sedative and of controlling the congestion and hemorrhage if the latter object be necessary. This suggestion becomes still more applicable in the severe forms of hæmoptysis. The dose may be repeated within twenty-four hours if needed. If congestion be manifested by its symptoms of substernal heat, soreness, oppression, dyspnoea, and cough to a greater degree, and if the hemorrhage is becoming copious and the hemorrhagic pulse developed, and the temperature elevated, the necessity of a more active interference is evident. Absolute quiet in bed, fresh air, a calm and equable behavior on the part of the family or friends in attendance so that no excitement may be reflected to the patient, are essential. The medicines selected should be such as may control the vascular excitement, and hæmostatics. Ergot will fulfil such indications. It has its limitations in its unpleasant taste, but it should be pushed to the points of tolerance. Of the fluid extract one teaspoonful should be given every hour or two until some effect is observed in slowing the pulse or checking the hemorrhage. If the stomach rebel, ergotin pills may be substituted in doses of three to five grains at the same interval. Should all the resources of ergot medication be required or the above mode of use fail or disagree, hypodermic injections may be added. Two to three grains of the extract of ergotin would form a proper dose, to be repeated every one or two hours. It has been quite the exception in our experience to have serious irritation follow the use of it in this way. Failure in this and other uses of ergot will follow because we do not administer it with sufficient freedom.[72] Another most valuable hæmostatic is turpentine. It should also be given freely. From ten to thirty drops in an emulsion or in sugar may be given every two to four hours, according to tolerance and to the threatening character of the case. The ergot and turpentine are best alternated at intervals of one to three hours, according to the requirements of the attack. Some preparation of opium is often required to quiet cough--morphine or codeine, one-fourth grain of the former and one-half grain of the latter, repeated at intervals until their effects are obvious. By adding the use of broken ice and the external application of cold compresses frequently repeated, and, if time and strength permit, the inhalation of persulphate of iron spray twenty or thirty minims in half an ounce of water, we get a plan of treatment adapted to the urgent cases. Some recent reports have confirmed the confidence of the ancients in the use of ligatures. They may be applied to both lower limbs. A dozen dry cups may be applied to the chest. There is no occasion or time for the use of many medicines, but if a general plan, such as the above, must be changed, acetate of lead in doses of two grains every two hours would be an excellent substitute, due regard being had to the possible toxic effects from too long continuance of it in such doses; it is usual to add a little opium to it. Gallic acid is an effectual remedy for the control of different kinds of hemorrhages. Like ergot, it is usually given in too small quantities. Twenty to thirty grains must be given every two to four hours. {292} It is better borne by the stomach, and can often be continued longer, than the medicines above mentioned.

[Footnote 72: A medical friend, T. C. Minor of Cincinnati, has in his own case used three or four drachms of the fluid at a dose, with the effect of reducing his pulse twenty beats in a few hours.]

We have already noted ipecacuanha as one of the survivals of ancient practice. It has had warm advocates among modern physicians. Graves places vivisection first and ipecacuanha next in his plan of treatment. Trousseau strongly recommended it. Peter and the French practitioners also strongly endorse its use in the severe forms. We have no doubt of its efficacy. It is important to exclude if possible the existence of a pulmonary aneurism or any such source of blooding, as there are no special means by which this can be done. It is a good rule to use the ipecacuanha in the cases of early or first-stage hæmoptyses. We would give it as it is given in dysentery. Precede its administration half an hour with thirty drops of laudanum, then give ten grains in water. If vomiting comes on, repeat it in an hour, and again, if hemorrhage continue, in two hours. The usual experience is that tolerance is established after two or three doses. It has also an application in small doses of one-quarter to one-half a grain in the milder forms, with irritative cough and slight fever.

Graves calls attention especially to the excellent effect of opium in all kinds of passive hemorrhage, hæmoptysis as well, but insists that it should be given only after vivisection has been performed or when the hæmoptysis has become rather passive, or in scorbutic and similar cases. His direction on one occasion to a physician, in a case of protracted bleeding of the gums, was, "Go home and give two grains of opium immediately, and then half a grain every hour until the bleeding stops." A combination applicable to the persistent bleeding recurring day by day is the sulphate of magnesia made soluble in rose-water by the free use of dilute sulphuric acid--one teaspoonful of the former, fifteen drops of the acid, one-half to one ounce of the rose or plain water. Many other remedies might be mentioned, and among them atropia. After the bleeding has ceased it is necessary to be assured as to the condition in which the lung has been left, and to counteract, if needed, any persistence of irritation. Fever is the most valuable evidence as to this point. If it exist, the use of quinia and ergot had better be continued freely. A three-grain ergotin pill about three times daily, and five grains of quinia morning and evening, can be tolerated two or three weeks. Local irritation should be applied if physical signs or pain warrants it.

{293}

PULMONARY APOPLEXY.

BY WILLIAM CARSON, M.D.

DEFINITION.--Escape of blood into the pulmonary parenchyma, with laceration of its substance.

SYNONYMS.--Hemorrhage (pulmonaire) foyer (Jaccoud); Diffuse pulmonary apoplexy or Diffuse pneumorrhagia (Fleich); Diffuse pulmonary apoplexy (Loomis); Pneumo-hemorrhagie (Gendrin), etc.

HISTORY.--Latour[1] is quoted as being the first to use the words, "apoplexie du poumon."[2] Yet Duguet[3] also quotes from Frank that Dolocus had a long time before employed it. It is known that cases had been described long before this, as by Corvisart in 1808, Allan Burnes in 1809, among those of this century, and by Prosper Martiano, Bonet, Morgagni, Haller, etc., among the more ancient authors.[4] Again, Laennec gives the weight of his authority, and establishes Latour's use of the name, until, as the synonyms show, modern usage has almost abandoned it. Among the multitude of those who have treated of pulmonary apoplexy, we will have filled the requirements of this brief historical statement by mentioning Virchow and his pathological investigations into embolism, and also Cohnheim,[5] and later Litten's[6] studies on infarction, which have some indirect connection with pulmonary apoplexy.

[Footnote 1: Histoire philosophique et médicale des Hémorrhagies, 1815, passage misquoted in L'apoplexie pulmonaire by Duguet.]

[Footnote 2: Op. cit., pp. 220, 222, and 224.]

[Footnote 3: Op. cit., p. 11.]

[Footnote 4: Duguet, p. 10, etc.]

[Footnote 5: Untersuchungen über die Embolischen processe, 1872.]

[Footnote 6: Zeitschrift für klinisch Medicin, Erster Band, 131.]

ETIOLOGY.--Predisposing Causes.--The male sex affords predominance of cases, because of greater liability to accidents, to the various forms of ulcerative destruction of lung-tissue, and to aneurisms of the aorta and pulmonary artery.

The adult age is most exposed for similar reasons. Ogston's statistics[7] support in a general way, but not with strictly technical force, their quotation by Herz.[8] Omitting the last 4 of his 20 cases (2 of which were from poisoning, 1 from fracture of skull by a fall down stairs, and 1 from drowning), the average for males (12) was 56.4, and 55.3 for females (4).

[Footnote 7: Brit. and For. Med.-Chir. Rev., vol. xxxvii., 1866, p. 459.]

[Footnote 8: Ziemssen's Handbook, vol. v. p. 298. Ogston says (p. 465) it did not appear, however, that any distinct rent of their substance had taken place--to any extent, at least. "When we consider that the area of the extravasation was sufficient to involve often one or two entire lobes, and that death was in most of them very sudden, the cases may be adopted as showing the action of causes similar in kind, if not in degree, to those operative in undoubted pulmonary apoplexy."]

As more efficient predisposing causes than either age or sex, may be mentioned aneurisms of the aorta and pulmonary artery, amyloid degeneration of bronchial and pulmonary vessels, the influence of Bright's disease in producing disease of blood-vessels, and atheromatous diseases of the pulmonary artery.

Exciting Causes.--Penetrating and contused wounds of the chest by their {294} direct mechanical effect, and diseases and injuries of the brain through the medium of the nervous system, may produce pulmonary apoplexy, the result in the latter case being usually an infiltration or small infarction.

SYMPTOMATOLOGY.--Pulmonary apoplexy is the least common of the two forms of distinctive pulmonary hemorrhage, the other being pulmonary infarction, already treated of under HÆMOPTYSIS. A proportion of cases is associated with mitral disease in its most advanced stages. At that time we may expect pneumorrhagia, but whether from infarction or apoplectic laceration even the event can only occasionally determine. In the latter, if hemorrhage makes its appearance it will be copious and generally overwhelming; at other times the hemorrhage may not appear, and the patient dies suddenly with possibly other indications of the internal flow. The physical signs cannot be relied on, for often the pulmonary tissue is already changed by the long-continued obstruction of circulation. Rupture of aneurism, particularly of aorta, in the great majority of cases takes place into a bronchus, and not into the parenchyma. In case of wounds of the contused variety a laceration of parenchyma occurs at times sufficient to produce marked hæmoptysis. If the blood be not ejected, there are no certain indications of what has happened. If the case be seen immediately after the accident, such physical signs as moist bubbling râles on the margin of an area of feeble or suppressed vesicular murmur, possibly attended with a dull, high-pitched percussion note over that area, would afford a strong presumption in favor of ruptured lung and consequent hemorrhage.

The same signs later might be due to a limited traumatic pneumonia. If the internal hemorrhage, whether traumatic or spontaneous, has made its way through the pleura, then, if the patient live long enough for examination, besides such symptoms as great oppression and exhaustion, the physical signs peculiar to pleural effusion may appear to a limited degree. This opportunity seldom occurs, as such a rupture produces almost invariably a fulminant and rapidly fatal result.

COURSE, DURATION, AND TERMINATION.--The course of the lighter cases is much like that of pulmonary infarction, and that of the severe forms too brief for observation. As to termination, it is quite possible there are cases of laceration so limited as to allow complete recovery, but clinical experience shows that pulmonary apoplexy is usually fatal.

PATHOLOGY AND MORBID ANATOMY.--With branches of the pulmonary vessels weakened by long-continued heart disease, or with such vessels as are found with chronic nephritis, a sudden increase of tension in them from unusual effort or excitement will precipitate a fatal rupture. Sometimes the progress of the degeneration is so insidious and complete that a rupture may occur without obvious exciting cause. This is also the natural history of aortic aneurism. An examination soon after the laceration will show a mass of blood, usually coagulated, sometimes partly fluid, lying in an irregular cavity with walls of the lacerated lung-tissue. After a longer time the lung-tissue beyond the walls of the hemorrhagic focus becomes oedematous to a certain extent. A contraction of the cavity, with change of contents, may proceed to the extent that an encapsuled mass of very small size will remain as the final result (Rokitansky).

DIAGNOSIS from bronchial hemorrhage by the probable existence of phthisical conditions and history. The quantity of blood ejected may be profuse in either case, and therefore be no criterion. From pulmonary infarction, as the other form of pulmonary hemorrhage, by the larger amount of hæmoptysis. If there be no hæmoptysis, a presumption would exist in favor of apoplexy in case of extreme dyspnoea or a fatal result. The associated diseases or causes being similar, no inference from the medical history would be reliable except in case of injuries.

{295} PROGNOSIS.--As we meet with it in recognizable form, the result is almost invariably fatal. A qualification is allowed because of the experience of such a pathologist as Rokitansky, who describes a process of cure in a few cases. The prognosis in such would be determined partly by the severity of the antecedent or accompanying disease, as in heart lesions, and partly by the increased respiratory distress, pain, exhaustion, and hemorrhage.

TREATMENT.--As has been before intimated, a case of pulmonary apoplexy distinctive enough to be diagnosed is usually one that is beyond the reach of treatment. Remedies that may relieve dyspnoea, exhaustion, and hemorrhage are those to be relied on. External irritants, as turpentine-stupe stimulants, ergot, turpentine internally, and such other remedies as are of known effect in the treatment of the associated heart troubles and of the incidental pulmonary infarctions.

{296}

ABSCESS OF THE LUNG.

BY WILLIAM CARSON, M.D.

DEFINITION.--A circumscribed suppuration of the lung, resulting in a cavity.

SYNONYMS.--Abcés du poumon; Lungenabscess.

HISTORY.--The ancients described abscess of the lung, and placed it among the terminations of the inflammation of that organ. They believed that if the inflammation did not resolve itself by the fourteenth or twenty-first day its termination was to be by suppuration. Hippocrates, Van Swieten, and others are mentioned among those who maintained these views and consequent frequency of such cases which prevailed until physical methods and pathological investigation proved their incorrectness. J. P. Frank, Bayle, and Cayol[1] are given credit for a partial reversal of this opinion. Avenbrugger,[2] a pupil of Van Swieten, in describing vomicæ, divides them into two kinds--the ichorous and the purulent. By the purulent vomica he means an encysted abscess of the chest resulting from the conversion of an inflamed spot into a white, thick, glutinous, fatty matter. When these communicate with the bronchi and discharge any of their contents by expectoration, they are called open; otherwise, close or shut. He gives symptoms and signs belonging to the respective varieties. Corvisart, in his comments on these propositions, says: "In fact, the purulent vomica is always the result of an inflammation, more or less acute, of the lung." He makes distinctions between the various kinds of purulent vomica and the ichorous vomica. Laennec, as in many other subjects of which he treated, has the credit of placing this one on its modern basis, at least so far as the frequent termination of pneumonia in abscess is concerned. Among English writers Stokes deserves especial mention. Abscess was the fifth and the last of the stages of pneumonia, according to his classification. He treated largely of the perforating abscess. Traube, Trousseau, and Leyden are among those who have contributed largely to the elucidation of the subject. The latter has especially claimed for this subject a more prominent place in the literature of practical medicine, and has strongly enforced his views.

[Footnote 1: Nouv. Dict. de Méd. et de Chirurgie, tome xxix. p. 394; and Leyden, "Ueber Lungenabscess," Sammlung klinische Vorträge, von Richard Volkmann, Nos. 114, 115.]

[Footnote 2: On Percussion of the Chest, a translation of Avenbrugger's original treatise by John Forbes, with comment by Corvisart, 1761-1808, pp. 38, 43, etc.]

ETIOLOGY.--Predisposing Causes.--Everything tending to debilitate the constitution may become a factor in the production of abscess of the lung. Senile constitutions, Bright's disease, chronic alcoholism, diabetes mellitus, and insanity are some of the predisposing causes.

Exciting Causes.--These may be divided, as in the case of gangrene, into the pulmonary, or those originating in the lung or pleura, and the intra-pulmonary, or those originating outside of the lung or pleura. Among the former are included pneumonia and empyema, perforating and discharging into the {297} lung, or one variety of Stokes's perforating abscess, pulmonary apoplexy, and suppurating bronchial glands, opening up a passage through the lung and bronchial tube. Either croupous or catarrhal pneumonia may be associated with or terminate in pneumonia. Among the latter, or extra-pulmonary class are included cases of embolism from the right heart, producing infarction, or from the systemic veins. These emboli carry with them the productive capacity of suppuration. Abscess external to thoracic walls, as in deep-seated mastitis, will at times perforate the walls and enter the lung. Abscesses of the liver not infrequently perforate the diaphragm, and are discharged through the lung.

Foreign bodies in the bronchi may ulcerate through them and produce suppuration of the lung, which may finally open a way externally through the chest-walls.

SYMPTOMATOLOGY.--The symptoms of abscess of the lung, as may be inferred from the enumeration of causes, are divisible into two categories--one including those symptoms with which the abscess may be associated, but which do not necessarily prognosticate it; and the other including the symptoms which indicate the abscess as a fact accomplished. In the simplest and most frequent clinical form, that following pneumonia, the early symptoms would be those of a severe and irregular form, as shown by very troublesome and uncontrollable cough or unusual pain or respiratory embarrassment, high fever, but at that time fairly typical pneumonic temperature, great prostration, etc. These may all diminish in due time, and mostly do without suppuration following. A return of pain, dyspnoea, fever, and general distress should awaken suspicion, yet they may be the result of an extension of pneumonia to other portions of the lungs. Rigors and sweats and increased depression would point to a suppurative process and under such circumstances to the lung as the locality. We cannot, then, positively predict an abscess. It is suspected when a more or less copious eruption of purulent discharge occurs suddenly, and sometimes the discharge is so abundant and pus-like that any other alternative than abscess is very remote; at other times the discharge is small in quantity. The proof of physical cavernous signs is the final step. This is often difficult. A slightly greater increase of lung-density, probably at the middle or upper part, with imperfect bronchial breathing, the appearance of a few moist râles or crepitus, the gradual increase of these and merging into coarser crepitus, and revelation of more or less of the cavity signs, is the physical history of many cases of abscess of the lung. Others have a much more pronounced course, such as the cases of so-called gangrenous abscess--a sort of connecting link between gangrene and abscess of the lung. The breaking down of tissue is ostensibly very sudden, and the cavernous signs are very soon unmistakable. Other clinical forms are the pyæmia, to be distinguished by the antecedent history, which will reveal a source for infectious emboli. The abscesses are usually multiple and small, so that their precise locality cannot be made out. The proof of infectious transportation is sudden pneumonic symptoms, as pain, tinged and finally purulent expectoration. Rupture into pleura may occur and produce empyema. Rupture of hepatic abscess and discharge through the lungs is also a clinical form shown by this antecedent event, pointing to hepatic inflammation. The egress of the pus is sometimes through a narrow track, and not by a reservoir within the pulmonary tissue; at other times the lung is really excavated. The discharge of pus is usually copious and paroxysmal. Leyden recognizes as his third class a form of chronic abscess, or one coming on during a case of chronic pneumonia and bearing great resemblance to a variety of phthisis. Its general symptoms are much the same as in the acute variety, differentiated by the element of time.

COURSE.--It may be said, in a general way, that the etiology has much to {298} do with its course. If the cause be pneumonia, the course will be such as the detail of symptoms already given shows. In some unknown way the natural course of the disease is interrupted, and what promises to be an average case is followed by the characteristic features of abscess. If pyæmia be the precedent condition, a peculiar form of pneumonia, embolic in origin, appears, and abscesses again follow. Greater septicity and rapidity of destruction are probable sequences. The perforating abscesses are subject to modifying influences of mechanical effect, such as gravitation and the resistance of tissues, and have their peculiar course, which is often marked by great chronicity.

TERMINATION.--In the course of seventeen years the reports of the Cincinnati Hospital show that there have been 6 cases of abscess of the lung treated there. Of these 4 died and 2 were discharged as improved. These figures show the infrequency of such cases, and also represent a greater mortality than probably occurs in the non-hospital class. We know of no large statistics which show what is the percentage of recoveries. Our own experience in private practice gives a majority of recoveries. They were cases following typhoid fever, croupous and catarrhal pneumonia, and hepatic abscess. A termination in a chronic cavity now and then happens: perforation of the pleural cavity, with subsequent pyo-pneumothorax, discharge externally through an intercostal space, or even extension into the abdominal cavity, are among the actual events of such abscesses.

DURATION.--The duration of an ordinary case is subject to wide variations between one and six months. A few cases are recorded of several years' duration. Previous constitutional condition has much to do with this element. The degree of infectiousness in the pyæmic class is important as to time. The abscesses become a subordinate condition in the fate of the case. In this connection we may also refer to Leyden's third variety, a so-called chronic abscess.

PATHOLOGY.--A close parallelism, etiologically and otherwise, is observable up to certain points between gangrene and abscess of the lung. Both are products of, or associated with, pneumonia. That which finally determines whether the result shall be gangrene or abscess is unknown to us. In the article on GANGRENE OF THE LUNG some investigations are referred to which point to a probable solution in the existence of specific forms having special pathogenetic force. The tendency of experimental and clinical investigations is to connect the suppurative process closely with the product of specific germs. Ogston in 65 cases of acute abscess found micrococci present in all of them. Obstruction of blood-vessels in the centre of the pneumonic area or on the margin of the abscess walls is an important anatomical element in the production of abscess, and it is claimed that it is often due to colonies of micrococci within their calibre; so that it is probable that there are both mechanical and biological or chemical influences at work. If the view of the zymotic and infectious character of pneumonia be tenable, the contingency of an abscess developing in its course would seem not very remote. Yet the proportion of cases of abscess from pneumonia is not more than 2 per cent. Leyden's high authority supports the idea of the essential and specific differences in the chemical and morphological peculiarities of gangrene and abscess of the lung, but the subject is as yet on a hypothetical basis.

MORBID ANATOMY.--The fresh cavity, generally in the upper lobe, has rough, ragged, and irregular walls, and may have bridles of the more resistant structures, as bronchi and vessels, crossing it. Such a cavity is quite likely to contain portions of undissolved parenchyma or more or less malodorous pus. The older cavity becomes smoother walled, and of more regular limits and cleaner contents. A gradation from granular hepatization through congested to crepitant tissue is almost uniform in the varieties of abscess, {299} whether simple or pyæmic. In addition, some peculiarities are observable in the latter. These are usually several, varying in size from a pea or less to a walnut, some round and others wedge-shaped; others lying superficially and forming slight elevations on the pleural surface. In proportion to the curative progress the cavity will contract and disappear, occasionally leaving behind a cicatricial mark. A lining pus-secreting membrane will sometimes form, resulting in such a limitation of morbid action and such a disappearance of reactionary symptoms as to make the disease entirely local, but quite chronic.

DIAGNOSIS.--The more or less sudden and copious expectoration of pus, without a specially offensive odor, in the course of a case having up to that time the history of a pneumonia, would be considered as due to the development of an abscess in the lung. Some degree of fetor in breath and expectoration is observed, but it is far different from that of gangrene. The detection of the débris of lung-structure in coarse particles, and the microscopic discovery of elastic lung-tissue, are important diagnostic points in contradistinction from the solution of tissue that gangrene usually effects upon the parenchyma of the lung. According to Leyden's[3] very complete investigations, the microscope reveals fatty crystals, mostly in roundish fragments, of the size of the epithelium of the lung and of a brilliant structure; pigment-débris of a yellowish-brown or brownish-red color; hæmatoidin and bilirubin, which Traube thought were due to hemorrhagic infarction, but which Leyden has observed in all of his cases; and, lastly, micrococci, in the well-known form of the round, granular micrococci colonies, which differ from those in gangrenous fragments in that they show very little movement and do not give the iodine reaction.

[Footnote 3: "Ueber Lungenabscess," Volkmann's klin. Vorträge, p. 994.]

Difficulties of diagnosis arise in the case of an empyema discharging through the bronchi, or of an encysted empyema discharging through the third or fourth intercostal space in front; also, between abscess of the superior portion of the liver and one in the base of the lung, or between the latter and a pyo-pneumothorax. Very careful study of the history in each case is of the first importance. Where this is not attainable the difficulty is often much increased. In the case of the empyema the discharge is more profuse at each time, the whole amount in a given period is much greater, and the time of opening is much delayed beyond that of the pneumonic abscess. Trousseau gives the case of a child who brought up for more than six months 200 grammes of pus daily. He makes children an exception to the rule as to the late opening of the pleural abscesses. In the encysted empyema discharging either internally or externally the difficulties are greater. A portion of the lung-tissue may be so near behind the deposit of matter as to make the physical signs confusing if the pus has opened externally. Some of these and of the interlobular deposits it is almost impossible to diagnose.

In hepatic abscess opening into the lung and bronchi the discharge is copious, dirty brown, paroxysmal, and will generally, on careful observation, show the bile color or its chemical reactions or some microscopic débris of the liver. In Leyden's third class, or the chronic abscess arising in the course of chronic pneumonia, the history is so much like that of some forms of phthisis as scarcely to serve in diagnosis. He thinks there are some macroscopic and microscopic appearances which may serve for diagnosis. There are in the expectoration dark and compact pieces of greenish-black color, not unlike plugs of pus, and larger, black-pigmented fragments of parenchyma, from a pin's head to a hempseed in size. Microscopically, they consist of a close and strongly-pigmented parenchyma, which seldom reveals alveolar structure. They show fatty degeneration and cholesterin plates. This class of cases is mostly without fever. The application of the bacilli-tuberculosis test would seem to offer some assistance in diagnosis.

{300} PROGNOSIS.--A grave prognosis may be formulated if there be a history of feeble constitution, and especially if it be further impaired by habits of intemperance, if the patient belong to either extreme of age, if there has been a recent debauch, or if there be wide variation from the typical form of pneumonia. Variations will be shown in such a complexus of symptoms as follows: fever of low grade, subject to extremes in range; feeble and frequent pulse, but not so marked as in gangrene of the lung; dyspnoea, objective and subjective; typhoid depression; tongue dryish; delirium; copious and fetid or difficult expectoration; physical signs of extensive lesion, such as a large cavity with a large outlying pneumonic area. A favorable prognosis would be conditioned on the appearance of a fewer number of these symptoms or on their evolution in a milder form.

The capacity of the patient to endure a long-continued suppurative discharge is principally determined by his natural vigor and his ability to assimilate food, other elements, such as extent of injury to the lung, being the same. A well-defined superficial cavity would be more favorable, because within surgical relief.

In the pyæmic variety the force of the infectious element will determine largely the result. Chills and sweats are important prognostic elements in such a case.

In the secondary abscesses of either the empyematous or hepatic variety prognosis is grave--more so in the latter than in the former, because surgical procedure would be more promising in the former, and because of the implication of an organ so liable to destructive inflammation as the liver. A long and tedious course of suppuration is possible in either. The dangers in an established abscess arise from liabilities to septic infection and exhaustion consequent on want of reparative power and persistent suppuration.

TREATMENT.--The treatment of abscess differs little if at all from that of gangrene of the lung. The tendencies of the two diseases toward exhaustion and infection are similar, but are less pronounced in the former. The same remedies are necessary in both, such as stimulants, tonics, antiseptics, anodynes, and expectorants internally, inhalations and drainage externally; brandy and malt liquors as stimulants; nourishing and concentrated food at frequent intervals; quinine as tonic and antiseptic; carbolic acid and turpentine as most valuable antiseptics (the latter being also an excellent stimulant); eucalyptus in cases of profuse as well as fetid discharge; carbonate of ammonia, senega, as expectorants; morphine and codeine or anodynes to control cough; carbolic acid for inhalation; and in cases of definitely localized cavities a free opening to be made with antiseptic injections.

Successful cases of surgical interference are reported, and such treatment is now recognized as proper when the system is giving way under septic poison, evinced in chills, sweats, and great prostration, where the purulent discharge is fitful and imperfect, and where the physical signs are clear enough to show the locality of the abscess.

{301}

GANGRENE OF THE LUNG.

BY WILLIAM CARSON, M.D.

DEFINITION.--Putrid necrosis of the lung-tissue.

SYNONYMS.--Lungenbrand, Gangrene du poumon, Gangræna pulmonum.

HISTORY.--By common consent, Laennec has the credit of first identifying, naming, and classifying gangrene of the lung as a distinct disease; yet Lieutaud[1] in 1707 describes imperfectly a case of gangrene of the lung in a child: "the right lung, within and without, appeared entirely putrid." Bayle[2] is considered, in his section on his fourth variety of phthisis (phthisis ulcereuse), to have described a rather chronic form of gangrene of the lung. Morgagni, Boerhaave, Stoll, J. Frank, and Cullen considered gangrene as one of the terminations of peripneumonia.[3] Laennec's development of the subject has only in a few directions been enlarged. His classification is universally adopted. His description is adopted generally as the most complete. There have been, however, controversies on different points, such as the relation of pneumonia and of the obstruction of the vessels to gangrene of the lung.

[Footnote 1: Historia Anatomica Medica, 1787, Obs. 329, cited by Louisa Atkins, 1872.]

[Footnote 2: Bayle, G. L., Recherches sur la Phthisis pulmonaire, 1809-10, p. 30.]

[Footnote 3: I. Straus, Nouv. Dict. de Méd. et de Chir., p. 403, etc.]

In the pathology and etiology of gangrene Virchow's investigations on embolism and thrombosis opened up important relations; in diagnosis, Traube and Leyden and Jaffee; in medical treatment, also Traube; and in surgical treatment, Haley and Lawson (1879),[4] S. C. Smith (1880), E. Bull (1881), Fengar and Hollister (1881), Mosler and Voght (1882). The antecedent development of pulmonary surgery, through important work done by Mosler, Pepper, and others, had prepared the way for special applications of it to gangrene and abscess of the lung. Spencer Wells claims to have suggested similar proceedings nearly forty years ago.

[Footnote 4: Lungen Chirurgie, Mosler, xx. p. 67.]

ETIOLOGY.--Predisposing Causes.--Constitutional weakness is a common predisposing influence: it may be a primary condition, but is more often secondary or dependent on some recently-acting debilitating cause, as typhoid fever, chronic lung disease, diabetes, etc. Chronic alcoholism is a cause which, besides its effect on the system at large, may add a special one on the lungs in producing hyperæmia or drunkard's pneumonia.

Of 46 cases we have collected mostly from the Vienna Hospital report, the youngest was nineteen years old and the oldest was forty-seven years. Lebert[5] has collected altogether 60 cases, 32 of his own and 28 of others: 19 occurred between twenty and thirty years, and 1 between thirty and forty. Huntington[6] gives 32 cases from the Massachusetts General Hospital Record between 1857 and 1875: 9 were between twenty and thirty years, and 12 between thirty and forty; the youngest was ten years old and the oldest sixty-four. It is noticeable that these figures coincide largely with those {302} showing the incidence of phthisis. Louisa Atkins[7] gives, as the youngest ages among all the varieties, one of three months and another of two months.

[Footnote 5: Klinik der Brustkrankheiten, vol. i. p. 827.]

[Footnote 6: Boston Med. and Surg. Journal, vol. xcv. p. 486.]

[Footnote 7: Gangræna Pulmonum bei Kindern, 1872.]

Of the 46 Vienna Hospital cases, 43 were male and 3 female. Huntington's cases were males 24, females 8. Of Lebert's own 32 cases, 22 were males; of the 32 others summarized by him, in 4 sex was not mentioned, and of the remainder 17 were males and 11 females. These figures show the large predominance of males in the liability to attack.

Exciting Causes.--They may be classified as pulmonary and extra-pulmonary. The influence of the alcoholic habit has been referred to above among predisposing causes: debauches are a frequent antecedent, especially in hospital cases, by means of resulting pulmonary hyperæmia and drunkard's pneumonia. Its association with croupous pneumonia may be assumed as settled after some warm disputes. The pneumonia of Bright's disease and putrid bronchitis are occasionally causative; bronchiectasies result in it not unfrequently. Extension of diphtheritic inflammation from the tracheal and bronchial mucous membrane is another form. The catarrhal pneumonia secondary to measles may produce it in children.

Embolism is the most frequent cause in the class of extra-pulmonary causes. It may be mechanical or infecting. A bronchial artery may be plugged so as to produce a gangrenous slough from mechanical cutting off of nutrition. Embolism of the pulmonary artery branches is more frequent, and by bringing about infarction and apoplexy may produce gangrene. Of the infecting variety may be mentioned emboli from the peripheral veins, as in surgical or uterine phlebitis, or from cerebral sinuses secondarily involved from otitis. Other causes acting from without on the lungs are foreign bodies, as particles of food passing beyond the trachea into the lungs, as in case of the insane or drunkards, and blows on the walls of the chest. These latter are capable of producing not only the ordinary phenomena of contusion-pneumonia[8] but gangrene, and without evidence of external injury or fracture of the ribs.

[Footnote 8: M. Litten, p. 26, vol. v., Zeitschrift für klinische Medicin.]

SYMPTOMATOLOGY.--Gangrene of the lung is the termination of a process the beginning and progress of which are not declared or cannot be followed through characteristic symptoms. Even its final occurrence may remain unknown if a communication be not established with a bronchus, which event is followed by the true symptoms, the expectoration and its odor. Whatever symptoms occur previous to that event may occur independent of it. Adopting Lebert's dictum,[9] gangrene of the lung is not a pathological unit. As its pathogenesis varies, so does its symptomatology. A feature common to its several varieties is marked constitutional depression and variations from the typical form of the disease in which it occurs. If pneumonia, croupous or catarrhal, be the precedent or associated disease, it will be marked by soft and feeble and frequent pulse, restlessness, dulness or distress of countenance, more or less cyanosis, cool and relaxed skin, possibly delirium, dry tongue, unusual dyspnoea and pleuritic pain, copious prune-juice expectoration, irregular or non-typical temperatures. Along with these functional variations occur some in physical signs, as a lesser amount of dulness or of bronchial breathing, indicative of less structural density and corresponding exudation. A case with such an evolution may afford a presumption of an outcome in gangrene, but appearance of the characteristic expectoration and fetor is necessary to exclude it from irregular forms of pneumonia, which have no such termination. The same general remark applies to the cases of gangrene in bronchiectasic cavities. Perhaps some aggravation of the general condition may excite apprehension, but the characteristic phenomena of expectoration, odor, etc. must decide. If the cause be of embolic origin, we {303} may expect some suddenness and perhaps shock in the beginning, and later the evidences of a more limited inflammation of the lung-tissue, such as circumscribed dulness and modified respiratory sound, which finally end in those indicating destruction of lung-tissue.

[Footnote 9: Op. cit., p. 803.]

The macroscopic characters of the expectoration are those of a putrid or fetid liquid of varying shades of color, ashy gray, dirty green, or greenish-yellow, prune-juice, or more or less hemorrhagic. The odor, which is at first so fetid and penetrating, often disappears after the expectoration has been standing a while. It is separable, as first described by Traube,[10] into three principal layers. The uppermost, covered with a layer of foam, consists of, first, dirty green, crumbling, confluent lumps; second, of larger, homogeneous, green muco-purulent masses; and, third, of whitish-gray, transparent, mucous masses. The second layer is formed of a colorless fluid. At the bottom is a fine yellowish-white sediment. Microscopically are found fat-acid crystals, many large fat-drops, and finely granular débris, masses of free, black pigment. It is said elastic tissue is nowhere to be found, but to this statement there are no doubt exceptions. Other bodies have been found by Leyden and Jaffee,[11] which they named Leptothrix pulmonalis. Kannenberg,[12] besides the above forms, found constantly infusoria of the family of monads in the sputa of 11 out of 14 cases of pulmonary gangrene. He considers them peculiar to the processes of decomposition in the lungs.

[Footnote 10: Gesammte Beiträge zur Pathologie und Physiologie, Zweiter Band, p. 452, etc.]

[Footnote 11: Deutsches Archiv für klin. Med., Band ii. pp. 488, etc., "Ueber putride Sputa."]

[Footnote 12: Virchow's Archiv, Band lxxv.; Zeitschrift für klinische Med., Band i. p. 228.]

PROGNOSIS in general is unfavorable. Individually, the gravity of the case is determined by the evidence bearing on previous habits and constitution; by the violence of the onset, as shown in prostration, severe pain in the chest, dyspnoea, persistent and violent cough, delirium, feebleness and softness of the pulse; by the variations from the typical standards of croupous, or especially catarrhal, pneumonia, such as greater amount of septic or infectious or typhoidal element, non-typical and low temperatures in the early stages and also in the stage of disintegration; by the amount of the latter as shown in the physical signs of extensive lesion and in the amount of gangrenous sputum; and by the irritant effect of this in producing bronchial catarrh, and consequent catarrhal secretion, which may of itself become an element of danger in a system already much prostrated. Favorable prognosis is allowable when these conditions are being gradually reversed.

PATHOLOGY.--The pathology of gangrene of the lung is scarcely more settled than it was forty years ago, when Stokes[13] published his eighteen propositions, embodying his experience. Obstruction of vessels and inflammatory exudations are present as important pathological conditions, but of themselves are not pathogenetic of gangrene. Other, as yet unknown, elements of putrefactive agency are present. Leyden and Jaffee's observations and those of Kannenberg have been mentioned[14] as efforts to throw light upon the pathogenesis of gangrene of lung, but how far the bodies described by them precede, coincide, or follow the familiar clinical phenomena are undetermined questions. Filehne,[15] in his experiments to determine the reason of the almost universal absence of elastic fibres in the expectoration of patients with gangrene of lung, comes to the conclusion that there is a ferment which, acting under alkaline conditions, destroys the fibres. The agents of this ferment he does not try to determine. Stokes anticipates the tendency of modern experimental pathology by announcing as an alternative proposition that "a process of putrefactive secretion precedes in many cases the death of lung." The constitutional debility which is so early a symptom prepares the way for such {304} an invasion. In reference to the relation between the septic material and thrombosis in gangrene, Kohler[16] affirms that the septic material produces the fibrin-ferment, and thereby capillary thrombosis. Recklinghausen thinks that a special material capable of exciting coagulation has not yet been found in gangrenous substances, but that there may be several factors, such as anæmia, changes in the vessel-wall, imbibition with foreign substances, etc. Other experiments[17] and views point toward the conclusion that there are substances formed in various diseased conditions which have the power of ferments and of producing coagulation of blood in the lesser circulation.

[Footnote 13: Dublin Quarterly Journal Med. Science, Feb. 1, 1850.]

[Footnote 14: Op. cit.]

[Footnote 15: "Sitzungsbericht der Phys. Med. Soc." in Erlangen Schmidt's Jahrbucher, 1877, No. 7.]

[Footnote 16: Recklinghausen's Handbuch der Pathologie, p. 136.]

[Footnote 17: Wooldridge, Du Bois-Reymond, Archiv Centralblatt für med. Wissenschaften, No. 41, vol. xi. 1874, p. 734.]

MORBID ANATOMY.--The circumscribed variety, as it usually appears, is a cavity irregular in outline, with ragged walls, made so by the unequal invasion of the lung-tissue by the gangrenous process. Sometimes the cavity itself contains loose fragments of lung-tissue, or the contents may be of a dirty, greenish, or brownish color, with some of the odor of the expectorated matters. If the case has been a chronic one, the walls are smoother, with a more or less formed lining membrane and the contents of a less characteristic color or odor. The cavity is usually in the right lung, and in the middle or lower portion. There is much variety of statement on this point. The tissue immediately adjacent to the gangrenous walls shows more or less of the products of catarrhal pneumonia. The vessels terminating in the walls are obstructed by coagula. If the gangrenous part come to the pleural surface, belonging to what Fournet calls the superficial variety, it may produce adhesions there, or it may result in perforation, with the result that we have the products of pleuritic inflammation united with the contents of the gangrenous cavity. In multiple foci, some will show the less advanced stages of disease, such as incomplete softening and local inflammatory lesions. In the diffused variety the lesions are sometimes described as being the same except in extent. The demarcations, however, from surrounding tissue are not as well marked; the tissue is soft, breaking easily under pressure, sometimes oedematous, dark or dirty black on surface or on section of lung; at other times the surface is mottled with lighter-colored patches. A secondary result is the production of bronchitis by the contact of the irritant expectoration from the gangrenous cavity.

DIAGNOSIS.--Abscess of the lung is the disease most likely to be confounded with gangrene of the lung. In the former you do not have the same amount of profound constitutional depression; the symptoms have a more frank expression, as it were, because of better precedent conditions usually; the first eruption of matter from the abscess is more copious and sudden than the usual manner of expectoration of gangrenous sputum; the appearance of the contents of the abscess is that more nearly of healthy pus, though the latter has at times a dark dirty brown or hemorrhagic look; the separation into layers is not apt to occur; the odor is usually not so fetid; microscopically, elastic fibres are much more abundant in abscess than in gangrene of the lung. The cavernous physical signs are not reliable in either disease. There are cases in which it is impossible, and in which it is of no practical importance, to make a diagnosis between gangrenous abscess and pulmonary gangrene. Gangrene supervening in phthisical cavities is distinguished by the history of a chronic pulmonary disease in which a cavity has been previously marked. It is phthisis advanced to the destruction of tissue plus the unknown gangrenous element which has found a lodgment in a favorable place. Stagnation of cavity contents, depression of system, etc. are favoring conditions. The same remarks apply to bronchiectasic cavities and putrid bronchitis, physical signs in the latter being additional points of difference.

{305} Our experience proves that the essential SYMPTOMATOLOGY of gangrene of lung, except the débris of lung-structure in the sputum, can occur where there was no gangrenous destruction, either circumscribed or diffuse, no bronchiectasic cavities or bronchial dilatations, and no phthisical cavity. In the case alluded to the gangrenous odor and general characters of the sputum and the separation into layers and the consolidation of tissue were present, but the post-mortem afforded no explanation of the fetid expectoration. It was a case of debauch and alcoholic excesses and exposure.

COURSE, DURATION, AND TERMINATION.--The course of this disease is essentially an acute one. Whatever the early condition be, the gangrenous element hastens its progress, as in cases beginning with the phenomena of acute pleuro-pneumonia. A pre-existing phthisical cavity will take on acute phases, also the septic element will be reinforced, and, as indicated in the enumeration of symptoms, clinical irregularities will be introduced. The early prostration is increased, and the patient dies from exhaustion after a period varying from three days to six weeks from the time the gangrene became manifest. Various complications, such as pleuritis and perforation of pleura and pneumothorax, hemorrhage, or extensive, diffused gangrene may cut short the patient's life within the average period. Occasionally the gangrenous cavity becomes chronic and the patient may live for months in imperfect health. The termination of the circumscribed variety is usually death. Diffuse gangrene is invariably fatal.

TREATMENT should be directed, first, to the known precedent states of constitutional weakness, bad habits, etc., which lay a foundation for unhealthy inflammatory processes, and for the pathogenetic elements that bring about the gangrenous and septic and exhausting conditions; second, to the special symptoms, such as severe pain in the side, harassing cough, dyspnoea, etc. Remedies of the first class are quinia, turpentine, early alcoholic stimulation, carbonate of ammonium, antiseptics, as carbolic acid, etc. An anticipation from the beginning of any irregular form of acute pulmonary disease of its termination in gangrene is impossible, and hence early treatment is necessarily general. It would be properly confined to the use of quinia, which would be useful, either before or after the gangrenous element had developed, in small doses frequently given, unless high temperature or the septic process indicate the use of large ones. Turpentine internally is desirable in proportion to the infectious or typhoidal character of the attack. Its use by inhalation is beneficial when gangrenous destruction has already taken place. Brandy or whiskey in moderate and frequent quantities, one-half to one tablespoonful every three hours, and carbonate of ammonium, meet the requirements which the tendencies to debility indicate. Milk, milk-punch, beef and chicken extracts should be given in the intervals between the administration of medicines. This general plan is applicable throughout the pre- and post-gangrenous stages. In the symptomatic treatment pain and a general respiratory distress often demand attention. Opium is then useful, both in relieving pain and moderating dyspnoea and cough. As these symptoms are often urgent in the later stages of gangrene of the lung, the treatment of the disease harmonizes both in its constitutional and symptomatic aspects. Prescriptions can also be readily prepared which contain remedies that have a decided effect in correcting the fetor of the breath and expectoration, and thus evincing an influence on the putrefactive process or ferment, which has become the prominent feature of the disease. The author recommends that carbolic acid, in the dose of one grain every four hours, be given for that purpose, and also its use by inhalation. Assistance can sometimes be given by putting the patient in such a position on the side as to promote the emptying of the cavity.

Tapping a gangrenous cavity and the introduction of drainage-tubes may be successfully resorted to. The cases suitable for such surgical treatment have {306} been described by Fenger and Hollister[18] as those where, "the presence of a gangrenous or ichorous cavity having been ascertained, it is found that notwithstanding an outlet through the bronchi for a portion of the contents of the cavity, it steadily fills up again; the partial evacuation does not relieve the patient; the infection of the healthy portions of the lung from the decomposed contents of the cavity has commenced or is evidently about to take place; the breath and expectoration continue fetid; absence of appetite; increasing weakness, with or without fever, etc." For the steps of the operative procedure reference may be made to the complete directions given by the same authors or to works on surgery. The double opening advised by the above authors would be the most efficient plan.

[Footnote 18: Amer. Journ. Med. Sci., Oct., 1881, p. 385.]

{307}

CROUPOUS PNEUMONIA.

BY ALFRED L. LOOMIS, M.D.

SYNONYMS.--English and American: Acute sthenic exudative pneumonia; Primary lobar pneumonia; Vera peripneumonia; and Pneumonitis. Fr. Fluxion du poitine and Fièvre pneumonique; Ger. Pneumonia lobaris and Lobäre Lungenentzündung.

DEFINITION.--Croupous pneumonia is an acute general disease with a characteristic local pulmonary lesion. Anatomically considered, it is an acute inflammation of the vesicular structure of the lungs, resulting in infiltration of the alveoli, with inflammatory products, which renders them impervious to air. This condition is known as hepatization.

HISTORY.--Until the time of Laennec, pneumonia and pleurisy were described as one disease. Hippocrates said that pleurisy was "a disease quickly fatal, and characterized by sputa of various colors." Although these two diseases were undifferentiated, accurate descriptions of the lesions and objective signs of pneumonia have come to us from the earliest medical writers.[1]

[Footnote 1: Thucydides, The Plague at Athens, B.C. 430.]

Much of the early history of this disease is interwoven with the detailed accounts of a great variety of pulmonary symptoms which occurred in the epidemics and plagues which prevailed in Eastern Europe in the centuries just preceding the Christian era, and in Western and Southern Europe during the sixteenth and seventeenth centuries. The black death has been regarded by some as an epidemic of pneumonia. While it is probable that in most of these epidemics the lung was early involved, and that its implication hastened death, yet no proof exists to sustain the belief that they were other than epidemics of typhus fever, dysentery, and those (as yet unknown) fevers which collectively were named plagues. That many of these plagues were complicated by pneumonia there is scarcely room for doubt.

French investigators were the first to separate the pneumonic process from all other morbid processes which occur in the thoracic organs. Valsalva, Morgagni, and Boerhaave gave accurate descriptions of pneumonia, but they did not sharply distinguish it from pleurisy. Bichat and Pinel separated collapse of the lung attending pleuritic effusion from inflammation of the lung-substance.[2] Laennec was the first to draw the line sharply between pneumonia and pleurisy, and to him, more than to any other observer, is due the credit of describing pneumonia as a distinct disease. With his labors begins a new era in the history of pulmonary inflammations.

[Footnote 2: Nos. phil., ii., Pinel.]

Grisolle's work[3] is especially valuable in statistics relating to the climatic element in the development of pneumonia and its comparative frequency among different races. The elaborate treatise on the geographical distribution of pneumonia by Ziemssen has furnished data for a more accurate knowledge of its geographical boundaries. Following in the footsteps of Laennec, {308} Chomel, Stokes, Addison, and many laborers of our own day have furnished the material from which the clinical and pathological history of pneumonia is now being constructed.

[Footnote 3: Traité de la Pneumonie.]

Recently, Jürgensen has strongly advocated the infection theory of pneumonia, and has presented strong arguments in support of his opinions. Sturges of London and Cohnheim[4] advocate the use of the term pneumonic fever, and the former gives a most interesting general comparison between it and the affections which he regards analogous to it. Careful pathological experiments have recently been made by Heidenhain, Sommerbrodt, Schuppel, and Klebs[5] with a view to establish the germ-theory of pneumonia.

[Footnote 4: Leçons de Chir. méd., 1877, p. 17.]

[Footnote 5: Arch. für experiment. Pathol., p. 420.]

The literature of the past ten years is richer in the development of facts and experimental investigations than all the centuries that have preceded; and these recent experiments, combined with modern statistics and the results of the microscope in pathological histology, have given to croupous pneumonia a separate and distinct place in the list of pulmonary diseases.

MORBID ANATOMY.--Anatomically as well as clinically, there are three recognized stages in croupous pneumonia: 1, Stage of engorgement or congestion; 2, Stage of red hepatization; 3, Stage of gray hepatization, resolution, or purulent infiltration (suppuration).

It has been claimed that the stage of engorgement is preceded by a dry stage, or "stage of arterial injection," in which the lung-tissue is dry and of a bright-red color. It is evident that congestion of the minute branches of the pulmonary artery would not give to the lung-tissue a bright-red color, and if such a condition exists it must be due to injection of the bronchial vessels. It is by no means proven that such injection ever precedes pneumonic engorgement. In the stage of engorgement that portion of the lung which is involved in the pneumonic process does not collapse when the thoracic cavity is opened. The affected portion of lung is distended and firmer than normal lung-tissue, and when pressed upon crepitates less, often remaining indented after the pressure is removed. The lung is not entirely airless, for by pressure the air can be forced from one portion of it to another. Its color is darker than normal, usually being of a brownish-red or purple. There is an increase not only in its actual weight, but in its specific gravity. On section a thin, frothy, blood-stained serum exudes, and sometimes on pressure flows freely from the cut surface; occasionally this exudation is tenacious. When alcohol is added to this fluid, it coagulates into a granular, amorphous mass.

The capillaries around the air-cells are distended, and dark blood oozes from their divided ends. Occasionally, upon close examination, there may be seen beneath the pleura and between the air-sacs small points of blood-extravasation. A portion of lung in this stage, when placed in water, does not float as near the surface as healthy lung-tissue.

When examined with the microscope, the lumen of the alveoli are seen to be diminished by the encroachment of the varicosed and tortuous capillary vessels. As a rule, the air-sacs are uniformly dilated; some, however, may be collapsed--a condition probably due to pressure during the early period of the pneumonic process. The epithelia of the alveoli are swollen, and contain a granular protoplasm with free nuclei. The air-vesicles also contain exfoliated epithelial cells and white and red blood-corpuscles. The serum which escapes into the alveoli from the distended capillary vessels is the fluid in which these cell-elements float. Since the enlarged epithelia often suffer a division of their protoplasm, embryonic mono-nucleated cells are intermingled with the other elements. It is still a disputed question whether the bronchial or the pulmonary capillaries are the chief source of the pneumonic exudation.

Physiology teaches that lung-tissue is nourished by the blood in the {309} ramifications of the bronchial arteries, and that the pulmonary capillaries are the passive media for the interchange of gases. Hence it is claimed that the bronchial capillaries only are implicated in the inflammatory process. Virchow has shown that the pneumonic process can be completely established in places where pulmonic capillaries cannot be traced on account of the plugging of a large branch of the pulmonary artery;[6] yet even he admits that secondarily the pulmonary vessels have much to do in the inflammatory process.

[Footnote 6: Ges. Abhang., p. 369, Virchow.]

On the other hand, it is claimed that in the early stages of the pneumonic process the parts that are supplied by the bronchial capillaries are not reddened or injected, as they would be were these vessels primarily concerned in the inflammatory process. Reasoning from the above, it would seem that both sets of vessels are involved, but that usually one set is implicated at the very commencement to a greater extent than the other.

It is often difficult, and sometimes impossible, to differentiate between the anatomical appearances produced by pulmonary congestion and oedema and the first stage of pneumonia. In pulmonary congestion and oedema the fluid in the alveoli is serum, and contains none of the pathological cell-elements found in the first stage of pneumonia. The alveolar capillaries are turgid, and in this respect resemble the capillaries in pneumonic congestion, but when a stream of water flows over a portion of lung in the first stage of pneumonia its dark color remains, while in hyperæmia of a non-inflammatory character this is not the case.

On account of its color and its resemblance to liver-tissue the name red hepatization has been given to the second stage of croupous pneumonia. The lung in this stage has a dark liver or mahogany color, and is slightly mottled, the mottling becoming more marked the farther advanced is the hepatization. The color is of a brighter red when the lung is first removed from the body than after it has been exposed to the air.

The volume of the lung is increased--at times so as to bear the impress of the ribs. It is solid and firmer than normal; pressure does not indent but tears it; it is very friable, and its torn surface presents a granular appearance. Its specific gravity is increased. It is airless, and there is an entire loss of crepitation.

Upon section it is seen that the granular appearance of the cut surface is due to the pneumonic exudation which fills the alveoli. This granular appearance is not so well shown on the cut as on the torn surface. The granules can be readily removed from the air-cells by means of a fine needle. A dirty, red, viscid fluid slowly oozes from its cut surface, which is more apparent after the lung has been exposed to the air for twelve or twenty-four hours and has undergone post-mortem changes. At any time this viscid, rusty-looking material may be scraped from the cut surface, or it exudes when a portion of the lung is firmly compressed. A portion of the inflamed lung quickly sinks in water, and small spots of blood-extravasations may be seen scattered here and there throughout its substance. When a stream of water is poured over the cut surface of the implicated lung the color changes from a maroon to a gray or yellow-gray, the usual color of fibrillated fibrin.

Not infrequently the material in the infundibula and air-cells extends into the minute bronchi, but these tubes are rarely completely filled with the pneumonic exudation. When examined under the microscope the alveoli are found filled with a solid material composed of a network of fibrillated fibrin, in whose meshes are leucocytes, red blood-globules, and changed epithelia. These latter are in various forms, usually round or oval. They may, however, become quadrangular, triangular, or irregular. They are granular, and may contain a single nucleus, a nucleolus, or multiple nuclei. These cells finally become granular, and fat-globules accumulate in them. {310} They also become discolored from imbibition of blood-coloring matter, so that in the latter part of the process there is quite an accumulation of pigment-granules, not only in the free cells, but in the fixed epithelia. The larger cells discharge their nuclei into the accumulation of corpuscular elements, and the whole contents of an alveolus present a more or less round shape. The alveolar walls remain unchanged, or are slightly thickened by the capillary turgescence. All of these different cell-elements have been regarded by different observers as characteristic of pneumonia. The red globules give the color to the consolidated lung. The pus-cells are always numerous.

The transition from red to gray hepatization is never well defined. The mottling gradually becomes more marked, so that the affected portion of lung assumes a marbled or granite appearance. As the deep-red color of the second stage fades the density of the pneumonic consolidation becomes less and less, until it is a mere pulp, breaking down under slight pressure. The decoloration is due to the pressure on the blood-vessels, to decoloration of the blood-corpuscles that were present in the second stage, and to fatty degeneration of the other cell-elements which occupied the air-sacs.

The weight and density of the affected lung-tissue are diminished, and toward the end of this stage the lung crepitates. On section a nearly uniform dirty-gray, bloodless surface is exhibited, from which flows spontaneously or upon slight pressure a dirty-white or reddish-gray puruloid fluid. The granular red hepatized look has disappeared or is very indistinct. The amount of oedema in the affected portion of the lung varies in different cases. When it is excessive a large quantity of serum exudes from the cut surface, which then exhibits a smooth, non-granular, glistening appearance, and it does not so readily break down when pressed upon as do other forms of gray hepatization. When examined under the microscope, the alveoli are seen to be filled with numerous round mono-nucleated cells, the intercellular fibrils that bound the elements together having disappeared; in other words (the fibrillated having become granular fibrin), the alveoli are filled with a fluid or semi-fluid mass in which numbers of discrete oil-globules and protein granules are freely mingled.

The granular and fatty elements are due to the rapid degenerative changes that occur in the cell-elements. In this stage leucocytes still emigrate from the blood-vessels. The masses that occupy the alveoli are now shrunken, and between them and the alveolar wall is a layer of fluid, so that in a thin section the contents of the air-sacs are readily lifted out by a camel's-hair brush. All of the affected portion of the lung is rarely in the same stage of the inflammatory process, and to distinguish red from gray hepatization, or the latter from the beginning of some of the conditions next to be mentioned, is often impossible.

The changes which take place subsequent to the stage of gray hepatization, and the modifications due to age, remain to be considered.

Croupous pneumonia may terminate--1, in resolution [recovery]; 2, in suppuration, purulent infiltration; 3, in abscess; 4, in gangrene; 5, and very rarely, in chronic (fibroid) pneumonia.

1. During resolution the lung is moist, lighter than in the stage of hepatization, has a yellow or yellowish-green color, and still shows a marked loss in elasticity. On section, the lung appears to be non-granular, and a tenacious, puruloid fluid escapes when the section is pressed upon. Some oedema may still remain. When examined under the microscope the alveolar capillary vessels are seen to have returned to their normal calibre; the alveolar epithelium is restored; the cells in the air-sacs are degenerated, broken down, and resolved into a detritus. The degeneration of these cells is both fatty and mucoid, and the coloring matter of the blood gives origin to the granular {311} pigment which is scattered throughout the disintegrated and liquefied mass. Some of the pigment is supposed to come from the connective tissue between the alveoli. In this condition the alveolar contents are either expelled by expectoration or undergo absorption, the lung being finally restored to its normal condition.

2. When purulent infiltration or suppuration of the lung occurs, its surface becomes yellow--more so than in any of the preceding conditions; it is soft, moist, and friable, and gives somewhat the sensation of an abscess. It is well described as miry.[7]

[Footnote 7: Pneumonia, Sturges, 1876, pp. 110, 113.]

On section, a diffluent, purulent fluid exudes from a surface whose yellow color is due both to the large number of cells which are undergoing fatty degeneration, and to the anæmia which results from over-distension of the alveoli with these cell-elements.

When examined under the microscope, the cells are found not only crowding the alveoli, but infiltrating the inter-alveolar tissue. This corpuscular infiltration of the alveolar walls may so interfere with their nutrition that they will undergo softening and degeneration. Whether these cells (in all respects resembling pus-cells) have emigrated from the blood-vessels or are the result of epithelial changes is still unsettled. Reason and analogy seem to point to a dual origin. Now and then these cells are pigmented. Occasionally the alveolar walls become thinned, indistinct, and finally rupture.

There has been much discussion over the term suppuration of the lung, but the appearances reported by those who uphold, as well as by those who protest against, the term are identically the same, all agreeing that the "lung is filled with pus."

3. Abscess of the lung, as a termination of croupous pneumonia, is exceedingly rare, and is always preceded by extensive cellular or interstitial oedema; small abscesses are formed by the rupture of several of the alveolar septa. It may follow purulent infiltration. These abscesses vary in size from that of a pea to one which may occupy the greater part of a lobe. They may have a thick, well-defined, irregular wall, their interior being crossed by shaggy shreds of broken-down lung-tissue, or they may form irregular excavations in softened lung-tissue. They may be single or multiple. Several abscesses are often found in the same lobe. They increase in size by peripheral growth or by fusion of several small abscesses.

Abscesses are more common in the upper than in the lower lobes; their frequency is variously estimated as 1 in 30 or 60 cases. These pus-cavities, if of small size, may ultimately close by cicatrization, in which case they may open into a bronchus of sufficient size to allow of the discharge of their contents. Under such circumstances the contents of the abscess are expectorated; interstitial inflammation is set up around their site, which after a time encloses them in a firm connective-tissue wall; contraction ensues, and finally only a line of cicatricial tissue marks their former situation. Or if no such bronchial opening occurs, the abscess becomes encapsulated in firm cicatricial tissue, and the contents undergo cheesy and calcareous transformation. Sometimes these abscesses perforate the pleura and discharge their contents into the pleural cavity, causing pyo-pneumothorax. External fistulous openings have occurred, but they are a rare termination of pulmonary abscess.

4. Gangrene is said to be a termination of croupous pneumonia in about 2 per cent. of cases, but this estimate is based on too few statistics to be wholly reliable. It is met with in bad constitutions where there is very great vital depression, in chronic alcoholismus, and in cases of intense septic poisoning. Interference with the blood-supply, causing the formation of pulmonary or bronchial thrombi, leads to its development.[8] While usually limited to a {312} small area of lung-tissue, it may invade large tracts, and be either circumscribed or diffuse.

[Footnote 8: Huss, Pneumonia; Carswell, Ill. El. Forms of Disease.]

The gangrenous portion of the lung is changed to a dark, dirty, pulpy mass, sometimes wanting the fetor of gangrene. When the mass has become diffluent, a sort of cavity is formed, in which are found fetid fluid and shreds of gangrenous lung-tissue. Around the gangrenous mass there is a zone of gray hepatized, friable tissue, which in turn is bounded by a zone of red hepatized tissue. When the above-named zones are not present in diffused gangrene, the cavities are large, and shreds of tissue and vascular bands traverse the cavity, which swarms with bacteria. Such a gangrenous mass may lead to sloughing of the pleuræ. It has been denied that a croupous pneumonia can terminate in gangrene, but modern pathologists all support the opposite view. It may be mentioned that gangrene in croupous pneumonia of the horse is of frequent occurrence.

5. Chronic (interstitial fibroid) pneumonia may result when the process of resolution in croupous pneumonia is delayed and the inflammatory process does not advance beyond the stage of gray hepatization. In such cases the walls of the alveoli, and finally the inter-alveolar tissue, become the site of new connective-tissue developments.

The peculiarly hard and oedematous condition that sometimes marks gray hepatization is, by some observers, regarded as an intermediate stage between croupous and interstitial pneumonia. An abundant cell-production in the second or third stage of croupous pneumonia may be followed by shrivelling of the alveolar contents, and subsequent cheesy changes may bring about one form of phthisis. Whether this can ever occur independent of tubercle is still a mooted question. This is called (by those who believe in such an origin of phthisis) cheesy infiltration, and is to be differentiated from tubercular infiltration.

In childhood croupous pneumonia is not of so frequent occurrence as catarrhal. In its anatomical changes it does not differ from croupous pneumonia in adults. In old age the pneumonic changes usually begin in the upper lobes of the lung, and extend downward--the reverse of what occurs in adult life. In the stage of engorgement crepitation is usually wholly absent, and when the stage of red hepatization is reached the color is found much darker than in adults, sometimes being blue or black; the lung is much more strikingly marbled, and on section the granules, in those cases where they are present, are much larger than in adult life. Frequently in senile pneumonia the granular look is absent. Gangrene is a far more frequent termination of croupous pneumonia in old age than at any other period. The highly-rarefied condition of the lungs at this period seems to favor the development of small abscesses.

Croupous pneumonia involves either the whole lobe or a whole lung. Its most frequent seat is the lower lobe of the right lung. Its next most frequent seat is the lower lobe of the left lung, then the upper lobe of the right, the middle lobe of this lung being least frequently involved. Double pneumonia has been variously estimated as occurring in from 5 to 50 per cent. of cases, but in all probability the percentage rarely, even in epidemics, exceeds 12 or 15 (Huss, Grisolle, Barth, Ziemssen). In old age the difference in point of frequency of attack between the two sides is very slight, and some affirm that sthenic is more frequent on the right and typhoid pneumonia on the left side. Double pneumonia is more frequent in the senile period than during adult life.

The average duration of the different stages is as follows: The stage of engorgement lasts from two to three days; the stage of red hepatization, from three to five days; and the stage of gray hepatization, from two to six days. In old age the stages rapidly merge into each other, and suppuration of the {313} lung may occur within thirty-six or forty-eight hours from the onset of the pneumonia, while it is not at all infrequent for complete red hepatization to occur within the first six or eight hours.

The changes in the pleura over a pneumonic lung are quite characteristic. An uneven, thin, downy-looking layer of plastic lymph is spread over the pleural surface, which presents a fine arborescent vascularity. At times this plastic layer may partially conceal the liver-brown color of the pneumonic lung. As the stage of gray hepatization is reached, pleuritic adhesions are apt to be formed, which subsequently undergo absorption, and thus the pleuritic changes follow, to a certain extent, those which are taking place within the lung. The cell-elements in this fibrinous meshwork are chiefly pus- and large endothelial-cells. The pleura itself is opaque, congested, and ecchymotic, and may be so thickened as to give rise to a dull note on percussion after the pneumonia has undergone resolution. If there are adhesions from previous pleurisies, or pleuritic changes that have occurred prior to the lighting up of a pneumonia, they will modify its course and termination.

The right heart is dilated, and on inspection immediately after death it is not unusual to find both ventricles filled with pale, firm clots that insinuate themselves between the columnæ carneæ and sometimes extend into the vessels. The pulmonary vessels running to the affected portion of the lung may be the seat of thrombosis. Pericarditis is so frequently found at the post-mortem of those who die of pneumonia that its occurrence must be regarded as something more than either accident or complication.

The blood is hyperinotic in croupous pneumonia, and, while the amount of fibrin is only slightly increased at the very onset, the amount obtainable goes on increasing until the eighth or ninth day; i.e. as the amount of fibrinous exudation within the alveoli augments, so does the same factor appear in greater quantity in the blood--a circumstance whose opposite condition we should expect to observe. In infectious diseases--e.g. variola--as the temperature rises the hyperinosis increases. In pneumonia, however, the pyrexia and fibrin increase in the blood and bear no relationship to each other. The amount varies greatly in every case; it has reached 10.5 in 1000.

Around the zone of pneumonic inflammation it is not infrequent to discover pulmonary oedema; and in many fatal cases extensive oedema seems to be the direct mode of death.

Temporary compensatory emphysema may occur in the neighborhood of the inflamed lobe or lobes. It may be mentioned that when emphysema has previously existed the pulmonic granules observable in the second stage are of unusually large size.

The bronchial glands are enlarged and congested, and in rare instances they may suppurate. The lymphatics of the lung are choked with fibrin and with red and white blood-corpuscles, and the deeper lymphatics contain products identical with those in the pulmonary alveoli. In both lymphatic vessels and in the lymph-glands (bronchial) at the root of the lung there are always well-marked evidences of inflammation.

The liver and spleen are congested, the latter organ especially presenting the characteristics which are found in it in cases of death from fevers.

Finally, gastro-intestinal catarrh is occasionally observed, and in rare cases it is attended by ulceration and hemorrhage. But there seems no good reason for believing that there is any connection between pneumonia and these intestinal changes. Indeed, most of the observations bearing on this point were made during cholera epidemics. Still, analogous influences might induce both at the same time.

No change in the brain accompanies pneumonia, except congestion. Pus and inflammatory products when found in the meshes of the pia-mater are in {314} all probability due to coexisting meningitis or cerebro-spinal meningitis of an epidemic character.

ETIOLOGY.--The specific cause of croupous pneumonia is as yet undetermined, and the very existence of such a cause is still a matter of conjecture.

Among the predisposing causes age ranks first. There are three distinct periods of life in which the liability to pneumonia is greatest--viz. in early childhood, between the ages of twenty and forty, and after sixty.

Notwithstanding the fact that catarrhal pneumonia is a very common disease in childhood,[9] the statement that croupous pneumonia is rare at this period cannot be received.[10] From a number of statistical tables it appears that it is five times more frequent during the first two years of life than in the succeeding eighteen.[11] It is met with most frequently between the ages of twenty and forty, and after a lapse of twenty years the predisposition to it increases, pneumonia being the most fatal of all acute diseases after the sixtieth year. Nine-tenths of the deaths from acute diseases after the age of sixty-five are from pneumonia. Each year after sixty the liability to it is greatly increased.

[Footnote 9: "Die lobuläre pneumonie ist im Sänglingsalter eine ausserordenich häufige Krankheit" (Vogel, Kinderkrankheiten, p. 222).]

[Footnote 10: "Lobäre pneumonie kommt viel seltener vor" (Vogel, loc. cit.).]

[Footnote 11: Klinik der Kreislaufs u. Athms. org., Breslau, 1856.]

In early life, in what may be denominated the first period, anterior to the second year, males and females are very nearly equally affected. Between twenty and forty, the time when the condition of males and females is most diverse, the proportion is 3 males to 1 female, or at least 2 to 1. After sixty, when the hygienic condition of both sexes again differs very slightly, this proportion is less striking, and the disease is pretty evenly divided between old men and old women; still, the male sex always furnishes more cases than the female. When women work as men do, or when both sexes are huddled together (as in prisons), then the difference between them is lost.

The puerperal state does not seem to increase the predisposition, but pneumonia is more apt to occur at the time of the catamenia.

The general condition of the individual at and before the pneumonic seizure seems to have some predisposing influence, although opinion is divided as to whether the strong and robust or the feeble and sickly are the more predisposed to it. Those who are convalescing from acute and severe illnesses, those who are habitual alcohol-drinkers, and those who are under the influence of malarial poison are far more liable to pneumonia than those who are free from such taints. Enervating habits, poverty, antihygienic surroundings and dyscrasiæ (especially cancerous), and chronic nervous diseases act as predisposing causes. Difficult dentition in children seems to act in a similar manner. Diphtheria, erysipelas, measles, small-pox, and other acute infectious diseases must be ranked as causes predisposing to pneumonia.

Chronic and acute uræmia, pyæmia, septicæmia, and all that class of diseases which depend upon the retention of excrementitious substances in the blood, are also powerful predisposing causes. It is also of frequent occurrence in chronic blood diseases, such as chronic alcoholismus. Suppuration in the abdominal cavity, which opens into the thorax, may lead to a pneumonia. Long-continued, passive pulmonary hyperæmia from any cause becomes a predisposing cause to pneumonia. The pneumonia which frequently occurs during acute articular rheumatism has been regarded by some as metastatic from the joints; but the more reasonable explanation is that the blood-changes in rheumatism predispose to pneumonia.

One attack predisposes to others; as many as twenty-eight attacks have been noted in the same individual, the time between the attacks and the {315} number of them being governed by no rule and subject to the widest variations.

When pneumonia follows a severe blow or injury to the chest or shock from any traumatic cause, the injury (or the shock) must be regarded as a predisposing cause. It is noteworthy to observe how often in the aged fracture of the hip-joint is followed by pneumonia. Within four hours after this injury croupous pneumonia has been established.

The influence of prolonged exposure to intense cold and sudden chilling of the surface of the body as a predisposing cause of pneumonia is still undetermined. Cold does not markedly affect the pneumonia-rate, except in the very old. Nearly nine-tenths of the cases of senile pneumonia occur between November and May. The January and February statistics seldom exhibit the highest pneumonia-rate, as they would were there any direct relationship between pneumonia and cold. In elevated regions north-east winds favor the development of pneumonia, and it is most prevalent in any locality during those periods of the year when there are the greatest extremes of temperature. A continuously low or a continuously high temperature has much less influence in its production than great vicissitudes of temperature. In New York City early spring and winter seem to be the periods when it is most prevalent.

A glance at its etiology shows that it is a disease to which all things predispose that depress the general vitality: this is evidenced by the fact that children and old people are greatly depressed by the intense cold of winter and the chilling winds of March and April. Almost unknown in the polar regions, pneumonia is not an infrequent disease along the Mediterranean coast; and one peculiarity is to be noted here, that in cold as well as in warm climates moderate elevation above the sea-level predisposes to its occurrence.

Rainy seasons or moist districts do not influence the pneumonia-rate to any appreciable degree. Both these conditions have a direct effect in increasing the prevalence of bronchial catarrh, but they do not increase the pneumonia-rate.

The well-established facts that pneumonia occurs oftener among the poor than the wealthy; in the sailor when on shore oftener than when he is on shipboard; in soldiers oftener than among civilians at the same military post,--these are explained on the ground of better hygienic surroundings, better mode of life, nourishment, etc., of the one class as compared with the other. And in studying the predisposing causes of pneumonia one is led more and more to observe that it is the more liable to occur the less resistance individuals are able to offer to some (as yet unknown) specific pneumonic influence, and that depressing influences of whatever kind unquestionably predispose to croupous pneumonia.

The more dense the population in a district, the greater the pneumonia-rate. Hirsch says: "The amount of the mean fluctuation in the mortality from pneumonia is in inverse ratio to the density of the population." When a city has attained a certain size, wind, weather, seasons, and races have but a slight influence in varying the pneumonia-rate. Thus, in New York City from 1840 to 1858 (eighteen years) the mortality from pneumonia was 5.85 per cent., while from 1859 to 1877, inclusive, it was 6.2 per cent.

Before considering the exciting causes of croupous pneumonia, or their relation to its predisposing causes, the question meets us, Is croupous pneumonia an acute specific constitutional (infectious) disease or a local inflammation?[12]

[Footnote 12: Virchow's Archiv, Bd. lxx., Heidenhain.]

That it is not a simple local inflammation appears from the following facts: the experiments with the inhalation of hot air, moist warm air, icy-cold air, {316} vapors of various noxious acids and gases;[13] the tracheal injection of caustic ammonia[14] and mercury; and traumatism,--have all resulted negatively as exciting causes. And these experiments have all the more weight since they have been conducted not only at different times, and in countries distant from each other, but also because they have been repeated by various pathologists, and always with a similar result--viz. the development of lobular or catarrhal, and not of croupous, pneumonia. Section of the vagi certainly produces hepatization of the lungs, but it is not the hepatization of croupous pneumonia. Its distinctive microscopical characteristics are always wanting in the part of the lung consolidated by such experiments. A strong argument of those who adhere to the local theory of pneumonia is, that cold occupies a prominent place in its production. As exposure to cold and to draughts is a common experience, it is easy to ascribe the origin of any disease to cold.

[Footnote 13: Sityl, K. K. Akad. zu Wien, 867, Reitz.]

[Footnote 14: Gendrin, Hist. Anat. des Inflam.]

"Close rooms and bad air," says Squire, "more predispose than does outdoor exposure, unless that be prolonged or the individual resistance weakened by fatigue or intemperance." Both wet and cold invariably heighten the bronchitis-rate and exacerbate catarrhal processes, but neither of these can be proven to influence the pneumonia-rate. Statistics show that croupous pneumonia is more prevalent in our Southern States than in our Northern States. The epidemics in the West Indies are as well known as, and have been more devastating than, those in Iceland and in the Norse countries. The prevalence of pneumonia in this continent progressively increases from the pole to the equator.

Hirsch's statistics and statement, that "the amount of the mean fluctuation in the mortality from pneumonia is in inverse ratio to the density of the population," is a strong argument in favor of the view that croupous pneumonia is due to some specific pneumonic infection, for all acute general diseases increase where there is over-crowding.

It is often stated that pneumonia is a far more frequent disease now than it was twenty years ago. That I might arrive at something definite on this point, I have carefully examined the death-reports of England from 1840, also those of New York City, dividing them into two periods of eighteen years each; and I find that the average mortality from pneumonia in England from 1840 to 1858 was 5.57 per cent.; from 1859 to 1877, 4.77 per cent., an actual decrease of 14.3 per cent. In New York City from 1840 to 1858 the average ratio of mortality from pneumonia to all other diseases was 5.85 per cent., and from 1859 to 1877 it was 6.20 per cent., showing an increase in New York of 15.2 per cent. Thus it is shown that while in England pneumonia is on the decrease, in New York City it is on the increase.

Those who advocate cold as a cause of pneumonia base their argument on the seasons of the year when it is most prevalent. The winter and spring are pre-eminently the seasons of pneumonia, but cerebro-spinal meningitis, diphtheria, influenza, measles, and other diseases of similar general character occur with greatest frequency in the winter months, yet it is not now claimed that cold causes them. While it is not to be denied that cold is to a limited extent an exciting cause of pneumonia, the belief that it is the primary or principal cause must be held in abeyance if not altogether rejected. Again, the symptomatology of pneumonia seems to militate against its being a local disorder.

There is no relationship between the amount of lung-tissue involved and the intensity of the symptoms; high fever, delirium or convulsions, and rapid heart-failure are often as well marked when a post-mortem reveals only one lobe to be involved as when a double pneumonia exists. "The local inflammation in its gradual extension and composite character offers no sort of {317} parallelism to the fever which for a while accompanies it." In local phlegmasiæ there is a direct ratio between the amount of surface involved and the attendant constitutional disturbances.

Rarely does a second chill occur when there is an extension of the pneumonic process. "Small consolidations with high fever and severe constitutional symptoms, and extensive infiltrations with a comparatively slight fever and general disturbance, are the rule and not the exception."[15]

[Footnote 15: Ziemssen's Cyclop. Prac. Med., vol. v. p. 146.]

The absence of regular and constant prodromata, the absence of a known period of incubation, of a typical temperature-range, and of characteristic surface phenomena, and the fact that it is not contagious,--these must not be overlooked when we are tempted to regard croupous pneumonia as an acute infectious disease.

The points of resemblance between croupous pneumonia and the acute general diseases are the following: It has an initiatory chill, an orderly pyrexia, and a somewhat typical course, inasmuch as there are in many cases a day of abrupt crisis and a definite duration. The symptoms follow in regular sequence.

There is a peculiar countenance, and here we note a resemblance to typhus and typhoid; there are usually herpetic eruptions; the kidneys are not infrequently the seat of a nephritis; and catarrhal pyelitis is a common condition. The cerebral symptoms greatly resemble the condition that accompanies the exanthems. The peculiarity of its commencement in the very young and old--convulsions in the former and coma and collapse in the latter--serves to point to an alliance with those diseases where a specific morbific agent acts primarily and principally on the nervous system. Etiologically, it often arises under precisely similar circumstances as those which give origin to cerebro-spinal meningitis and diphtheria, to both of which diseases it is also allied, since the pathological changes are distinct from those of any other inflammation.

Again, the influence of septic, miasmatic, and atmospheric conditions is certainly almost universally acknowledged. A good example of this is the sewer-gas pneumonia so often occurring in New York City, and of which frequent mention is made by English writers. Again, there have been frequent epidemics of pneumonia in certain districts in garrisons and on board ship, where over-crowding, bad ventilation, and general antihygienic surroundings prevailed.[16]

[Footnote 16: In the U. S. Sanitary Commission Memoirs, Russel reports: "The surgeons on duty with the regiments in the barracks (Benton, Mo., 1864) report that men occupying the same bunks with those affected were very much more liable to be attacked than those more remote. Some of the most intelligent surgeons were led to believe that the disease was actually contagious."]

During the winter of 1881-82 I remember three instances where two individuals in the same house were simultaneously attacked with croupous pneumonia.

Pythogenic pneumonia is a form which arises under miasmatic influences, and is contagious.[17]

[Footnote 17: Dub. Med. Journal, 1874, vol. i., Grimshaw and Moore.]

"The epidemic form of croupous pneumonia at certain times bears the distinct characteristics of a specific infectious disease."[18] Miasmatic and zymotic pneumonia are names which have also been given to this form; and indeed it is now generally acknowledged that croupous pneumonia does occur as an epidemic disease when it is, seemingly, dependent upon a specific contagion. Huss thinks that during a typhus epidemic pneumonia is apt to assume the low typhoid form.

[Footnote 18: Berliner klinische Wochensch., 1879, No. 37, A. Kühn.]

Moreover, as in typhoid and cerebro-spinal meningitis, so in pneumonia, we {318} have abortive cases, and forms which are distinguished by the names sthenic, asthenic, malignant typhoid, icteric, etc. Still, a pneumonia epidemic is different from a typhoid or cholera epidemic: it does not sweep over large districts and affect all ages and classes indiscriminately.

Every acute general disease has its complications, and the occurrence in pneumonia of peri- and endocarditis, as well as its cerebral and renal complications, allies it to other acute general diseases.

Cerebro-spinal fever has its characteristic lesion in the membranes at the base of the brain and about the cord; typhoid fever, in the lymph-structures of the intestinal tract; diphtheria commences in and chiefly involves the epithelia; and pneumonia has its characteristic local lesions in the vesicular structure of the lungs. Croupous pneumonia is occasionally met with in intrauterine life, and it is to be remembered that acute general diseases occur far oftener in the foetus than local inflammations. Again, the accepted treatment of pneumonia at the present day is an indication of its specific character. Thus the weight of evidence leads to the opinion that pneumonia is an acute specific general disease caused by a specific poison. The nature and action of the pneumonia-poison may be indicated by the following facts and experiments: Hyperinosis does not seem capable of causing croupous pneumonia; the fibrin increases as the consolidation is completed, and does not antedate either the pyrexia or the hepatization. Excessive bleeding increases the amount of fibrin obtainable from the blood; and when, in pneumonia, we find one lung weighing three pounds more than the other, may not the blood-elements effused into the alveoli have much to do with the hyperinosis?

Pneumonia resembles quinsy[19] in its pyrexia, temperature-curves, duration, its constitutional as compared with its local symptoms, and its rapid and abrupt decline. Both have a similar herpetic eruption, and in both the amount of chlorides in the urine is subnormal, the urea (in both) being increased.

[Footnote 19: Sturges, Pneumonia, loc. cit.]

An analogy has been noted by some observers between pneumonia and acute rheumatism. Trousseau sees an analogy between erysipelas and pneumonia.[20] But apart from their etiology it is difficult to recognize any constant resemblances between them. Sturges places "pneumonia in a middle place between the specific fevers, so called, and the local inflammations," and adds that it has something in common with both. Cohnheim classes croupous pneumonia among the miasmatic contagious diseases.

[Footnote 20: Clinical Lectures, vol. iii. p. 353.]

The idea of its being a specific disease dates from the latter part of the eighteenth century:[21] it is not by any means a modern thought, although it has within the last ten years received a new impulse and given rise to extended discussions.

[Footnote 21: C. Strackius in Nov. Theo. Morg., 1786.]

It seems to me that the resemblance of pneumonia to the acute general diseases is to be found for the most part in its nervous phenomena, and that the complications which render pneumonia dangerous are those which interfere directly with the muscular power of the heart or diminish its nerve-supply.

In order that the influence exerted by an abnormal nerve-supply upon the contractility of the cardiac muscles may be more apparent, let us glance at a few modern physiological facts. When the inhibitory nerve of the heart, the pneumogastric, is cut, the heart beats wildly. When the peripheral cut end is stimulated, the heart stops in diastole. But neither of these phenomena instantly follows the operations, on account of the intervening cardiac ganglia, the part of the vaso-motor system which has its centre in the medulla oblongata. Afferent inhibitory filaments (the depressor branch) of the vaso-motor centre are also in the vagus. Now, by injecting atropine into the blood we so influence these cardiac ganglia (which intervene between the conditions of the vagus and the resulting action upon the heart-beat) that the inhibitory {319} action is entirely checked. Thus an intimate connection is apparent between the local heart-mechanisms, the general vaso-motor system, and some filaments of the vagus. Again, we know that the natural explosive decompositions of the nerve-cells of the respiratory centre may be either augmented or enfeebled according to the condition of the blood supplying this ganglion. Now divide the cervical portion of the pneumogastric, and there results, after a more or less prolonged period, an extensive pulmonary consolidation (hepatization), which is not accompanied by the least sign of heart-failure. It is to be remembered that such pulmonary consolidation has none of the essential pathological characteristics of croupous pneumonia.[22]

[Footnote 22: Michael Foster, Wagner, Goetz, Heidenhain, Du Bois-Reymond, Ludwig, and Pflüger.]

From these experiments the following deductions seem at least reasonable: The tonic influence normally held by the vaso-motor system of nerves over the vascular system is either lessened or destroyed by an altered blood-state or by some morbific agent in the blood introduced from without. The large quantity of blood which would then be retained in the arterioles throughout the body, and which could not be returned to the heart, may cause so great a diminution in the blood-pressure as in itself to cause heart-failure. But in addition, and in connection with this, may not the action of a morbific material in the blood upon the intrinsic cardiac ganglia so interfere with their function, or so act upon the medullary vaso-motor centre itself, that the movements of the heart are deranged and its power is more or less diminished?

It would seem that this materies morbi in the blood may as well act upon both the medullary centre of the vaso-motor system and the ganglia in the wall of the heart as upon either alone. The phenomena of asphyxia are brought about by influences acting solely on the medullary centre. Again, the large amount of urea excreted, the result of excessive tissue-change throughout the body, may also be due to deranged nerve-function.

Klebs[23] even claims that he has found the infectious agent--a monas pulmonale--which can be inoculated, with the result of developing croupous pneumonia. This has been credited so far as to lead to the subcutaneous injection of carbolic acid to destroy the pneumonic germ. Incidentally, it may be remarked that it has been shown that the contagion of the pleuro-pneumonia of cattle, according to Parkes, "has been found in the pus- and epithelium-cells of the sputa." The true nature of the pneumonia poison, if one exists, is as little determined as that of the other acute contagious general diseases. But, whatever its nature may be, its primary action seems to be on the nerve-centres.

[Footnote 23: Arch. für exper. Path. u. Pharm., vol. iv., 1875.]

SYMPTOMS.--The symptoms of croupous pneumonia may be considered under two heads--Subjective, or rational symptoms; and Objective, or physical signs.

Subjective Symptoms.--In only a small proportion of cases are there prodromata. Grisolle found that prodromata occurred in 50 out of 205 adult cases, or in about 25 per cent.; and Fox says that he finds the proportion to be about 28 per cent. In old age they seem to be more frequent, the proportion being about 60 per cent.[24]

[Footnote 24: Durand-Fardel, Mal. des Viellards.]

There may be for a day or two, or even for a week, preceding a pneumonic seizure a feeling of general malaise, accompanied by anorexia, headache, dull pains in the limbs, back, and lumbar region, vertigo, epistaxis, or slight diarrhoea. Sometimes the skin assumes a slightly jaundiced hue, and there may be flashes of heat accompanied by, or alternating with, slight rigors. Flying pains in the limbs and chest and epistaxis are common in senile croupous pneumonia. When prodromes have existed more than three or four days, they will be vague and undefined.

{320} Rise in temperature as a prodrome is by some thought to be caused by a deep-seated and undiscoverable hepatization. But let us take one example from many in support of a contrary view--viz. the case of an inmate of Bellevue Hospital during the winter of 1880-81. For three days preceding the first appearance of consolidation the temperature ranged at 102° and 103° F. During this time there were several slight rigors followed by flashes of heat.

Wilson Fox[25] states that he knows of but one case--the one referred to by Monthus in his Essai sur la Pneumonie double.

[Footnote 25: Reynolds's System, art. "Pneumonia."]

In epidemics febrile symptoms and diarrhoea often precede for some two or three days the first sign of consolidation.[26]

[Footnote 26: The Lancet, vol. ii., 1878, p. 701, Couldrey.]

In the great majority of cases croupous pneumonia is ushered in by a distinct chill. Huss and Grisolle found a chill in 80 per cent. of their cases; Fismer and Louis in about 77 per cent. of theirs; and Lebert in over 92 per cent. of his. In 84 out of 100 cases admitted to my ward in Bellevue Hospital, a distinct chill marked the invasion of the disease.

Generally, the patient retires in his usual health, to be seized with a severe chill during the night. The chill lasts from half an hour to two or three hours. Its abruptness and severity are almost characteristic of the pneumonia.

In children, headache, nausea, vomiting, delirium, and convulsions may take the place of the chill; its onset then closely resembles that of the exanthemata, indicating the action of some irritating poison upon the nerve-centres. When these symptoms are not present there will be more or less anorexia, thirst, and a tendency to stupor. The child will awake in the middle of the night with a burning skin, a bounding pulse, flushed face, and hacking cough. When there are convulsions, followed by a loss of consciousness, the pneumonia is usually at the apex of the lung.[27]

[Footnote 27: Rilliet and Barthez.]

If an old person is seized with a severe chill during the night, it is almost a certain indication that pneumonia is developing. Although the chill of invasion is of less frequent occurrence, it is more significant than in adult life. A protracted fit of shivering and pain in the side are the two diagnostic symptoms of acute sthenic senile pneumonia. They occur in about 50 per cent. of all cases, and from statistics taken from the Salpêtrière it seems that in March and April these two symptoms are almost always present.

In the other half of the cases of senile pneumonia the onset is marked by a frequent, irregular respiration, slight rise in temperature, short hacking cough, and signs of great exhaustion. Nausea, vomiting, diarrhoea, and collapse or a semi-comatose condition may usher in a senile croupous pneumonia.

Durand and Fardel give the following statistics of the mode of advent in 35 cases of senile pneumonia: 7 began with distinct rigors; 8 with rigors and pain in the side; 6 with rigors and vomiting; 8 with pain in side alone; and 6 with vomiting only. When a chill is the initial symptom, either in childhood, adult life, or at the senile period, it is rarely repeated.

In adults, following the chill there is usually pain underneath the nipple of the affected side; sometimes the earliest symptoms following the chill are headache, vomiting, and diarrhoea, dyspnoea, a hacking cough, and pain that simulates that of lumbago. Within twenty-four hours after the invasion the aspect of the patient becomes characteristic: there is a rapid rise in temperature, attended with great prostration; the pain in the side is aggravated by coughing and deep inspirations; and the respiratory movements are accelerated. The countenance assumes a dull or anxious expression, with a tendency to lividity; the pulse is accelerated, full, and soft; there is complete anorexia and great thirst; speech is difficult, and often there is great restlessness. The urine becomes scanty and high-colored, the bowels are constipated, and the tongue is dry and covered with a white coating.

{321} These symptoms either increase in severity or are attended by exacerbations and remissions until the day of crisis, which usually occurs between the third and the ninth day; when, if recovery is to take place, there is a sudden remission of all the pneumonic symptoms; the temperature falls abruptly; the surface becomes moist; the flush of the countenance disappears; the pulse and respiration become normal; and the patient rapidly passes on to complete convalescence.

In some cases the decline in the symptoms is gradual and the disease terminates by lysis and not by crisis. In unfavorable cases signs of heart-failure appear within the first few days, and the patient sinks rapidly into collapse and dies.

With this brief outline of the disease I will pass to an analysis of its prominent symptoms.

Respiration.--The respirations are more constantly increased in frequency in croupous pneumonia than in any other acute disease. In most febrile diseases the respirations increase in frequency with the pulse-rate. In pneumonia there is no uniform ratio between pulse and respiration; this is regarded by some as an important diagnostic sign.[28] In some cases the respirations will be 80, and the pulse only 90, per minute. The acceleration in the respiration is not in proportion to the amount of lung-tissue involved, but seems to be due to a peculiar condition of the nervous system which existed prior to the pneumonic seizure or is caused by a poison acting upon the nerve-centres. Traube[29] thinks that it is due to the pain and to the high temperature. This theory would not explain its occurrence in those cases where the pleura is not involved--i.e. when no pain is present--and yet the shallow, panting, rapid breathing is well marked.

[Footnote 28: Dis. of Lungs, Walshe, 1860, p. 366.]

[Footnote 29: Annal. de Charité]

In other pulmonary diseases, when there is high temperature, as in acute phthisis, the respirations are not so much accelerated as in pneumonia. The character of the respiratory acts is also peculiar: they resemble the panting of a dog. Accelerated breathing may or may not be accompanied by dyspnoea; in many cases the dyspnoea seems to be independent of it, for extreme dyspnoea is often present where the respirations are but slightly increased in frequency.

In children the acceleration of respiration is more marked than in adults, and the ascent of the chest occurs during expiration, and not, as normally, with the inspiration. The diaphragm is markedly contracted with each expiratory act, and the diagnosis will as often be made by the character of the respiration as by the physical exploration of the chest, for in children the early physical signs of pneumonia are often unsatisfactory.

The hurried breathing prevents a young child from nursing; it takes the mother's nipple for an instant, nurses greedily, and then drops back, gasping for breath.

It is to be remembered that in pneumonia in children the pulse and respiration discrepancy will not be so well marked as in adults: the pulse may be 150 to 160 per minute, while the respirations are 80 or 90. In children there will early be noticed the peculiar expansion of the nostrils which comes on late in adults. In senile pneumonia the chest enlarges vertically during inspiration. The whole act has a panting character, and the expiration is prolonged.

In perfectly healthy old people the inspiratory movements are jerky in character. The lungs become fully expanded only after a succession of interrupted efforts. An exaggeration of what is physiological in old age--i.e. catchy breathing--is the most frequent form of abnormal respiration in senile pneumonia.

Dyspnoea, although frequently accompanying accelerated respiration, is by {322} no means a constant attendant of it. When urgent it is not in proportion to the amount of lung involved, since double pneumonia may be accompanied by less dyspnoea than when but one lobe is involved. It can be due only in small degree either to the diminution in the total breathing capacity, to the pain, or to the rapid and destructive tissue-metamorphosis; for on the day of crisis it ceases, although the lung at this time is not relieved of its obstructive exudation. The most intense dyspnoea usually occurs in those cases where there is extensive nervous prostration, and must always be regarded as a symptom of great gravity.

In secondary pneumonias, especially where there is coexistent disease in any part of the respiratory tract, the dyspnoea is usually more marked than in primary and uncomplicated pneumonia. It differs from the labored dyspnoea of general capillary bronchitis. A diagnosis between these two diseases can often be made by the character of the dyspnoea.

When the summit of the lung is involved, the dyspnoea is always greater than when the pneumonia is at the base. In pneumonia of the apex in children the dyspnoea is so great that the nostrils are widely dilated, the mouth is open, and its corners are drawn downward and outward. In senile pneumonia, even when the respirations are 70 per minute, patients do not complain of difficulty in breathing.

When persons over seventy who have been asthmatic or are the subjects of chronic bronchitis develop a pneumonia, they often suffer less from dyspnoea than before the pneumonic attack. They feel exhausted, are unable to move about, and on lying down to rest often suddenly expire.

Immediately after the initial chill pain is present in over 85 per cent. of the cases. It is of a sharp stabbing character, and is usually located over the seat of the pneumonia; it is intensified by coughing, sneezing, and deep inspirations. In some cases there is tenderness on pressure over the seat of the pain. The pain usually disappears after the third or fourth day of the disease; if it continues until the eighth day, it may be regarded as evidence of pleuro-pneumonia. If the pneumonia is central there will be no pain. In old age, even in a pleuro-pneumonia, pain is never severe. It is rather a dull, uneasy sensation referred to the whole chest, or if localized by the aged patient is referred to the pit of the stomach, the nipple, the loins, the hypochondrium, or even to the side opposite to the one involved.

Cough is generally present within twenty-four hours after the accession of croupous pneumonia. At first it is short, ringing, or hacking in character, and increases the pain in the side. It sometimes entirely ceases just before a fatal termination. In children a hacking cough is more constant than in adults. Within a few hours it becomes painful and urgent, and occasionally assumes a paroxysmal character, resembling whooping cough.

Old people with pneumonia often have no cough. When present it is slight, and may escape the notice of the patient as well as of the physician. When an aged person suffering from chronic bronchitis or asthma, who has had a chronic cough, develops a pneumonia, the cough generally becomes less severe, and may entirely cease.

Expectoration.--The sputum in pneumonia is characteristic. During the first forty-eight hours it is simply frothy mucus; then it becomes semi-transparent, viscid, gelatinous, and tenacious, but never opaque. Streaks of blood often appear early, mixed with the sputa. So tenacious is it that the cup which contains it may be inverted without spilling the mass. It can be drawn out between the thumb and finger into thin strings, and its tenacity undoubtedly is one cause of the difficulty in its expectoration. Its color varies: generally on the second day the brick-dust or rusty sputa are observed; still, there are numerous exceptions. The color is due to admixture of blood which extravasates from the capillaries of the alveoli. The rusty sputa are preceded {323} in some cases by a transient brighter red expectoration. In other cases it is of a creamy-yellow color, resembling in this respect ordinary catarrhal sputa; or, again, it becomes dark and of a prune-juice color. A severe pneumonia may have none other than a purulent sputum.

Prune-juice sputa of an offensive odor are indicative of a depraved state, and occur only in grave forms of pneumonia. In alcoholismus and in those markedly septic forms of pneumonia which are to end fatally, the prune-juice or burnt-sienna sputum is usually present. In some instances prune-juice sputa appear before the physical evidences of hepatization.

A watery and blood-stained expectoration indicates pulmonary oedema and congestion, and is an unfavorable symptom. When a case is tending to a fatal termination, the sputa become scanty, less tenacious, more diffluent, and often of a greenish color. But a greenish color may be present during the stage of resolution, and may temporarily occur in the middle period of a pneumonia, without being indicative of serious changes. It is usually present in the so-called bilious pneumonia when there is jaundice.

Pre-existing or complicating lung diseases may mask or alter the ordinary rusty pneumonic sputa. On the day of crisis, when resolution occurs, the sputa usually become abundant and of a creamy-yellow color. But purulent creamy sputa may occur with a complicating abscess and in some cases of purulent infiltration. During the whole course of the disease there may not be a single characteristic sputum, or it may not be present until the fifth, sixth, or even the twelfth day of the pneumonia. Again, the sputa may continue of a brick-dust hue until the ninth or tenth day. There is frequently an entire absence of expectoration in the pneumonia of acute articular rheumatism and in pneumonia of the apex.

Lastly, the sputa may be more or less pigmented, or when venesection or purgation has been extensively practised expectoration may suddenly cease.

In children expectoration is rarely present, but the brick-dust masses may often be detected in the ejected matter after an attack of vomiting. In senile pneumonia expectoration is never an early symptom, and it is liable during any period of the disease to suddenly cease. Rusty sputa occur in only about 33 per cent. of senile pneumonias. They are at first scanty, gray, and frothy, then yellow or catarrhal (sputa cocta). In severe and fatal cases profuse bloody expectoration may be present at the onset. The reason why the viscid (pathognomonic) sputum of pneumonia is so often absent in senile pneumonia is that the stages pass rapidly into each other, and purulent infiltration takes place very early. The day of crisis is not marked by the same changes in the expectoration that mark the crisis in pneumonia of adult life.

A chocolate-looking serous expectoration usually accompanies the so-called typhoid pneumonia.

When examined under the microscope, the sputum is found to contain swollen epithelia, both spheroidal and columnar, red and white blood-globules, minute spherules of fat, and the other elements which were described as filling the alveoli during the stage of red hepatization. (See Morbid Anatomy.)

Walshe affirms that pus-cells are not found in the brick-dust expectoration of pneumonia. The mucoid cells will often be stained by the liberated coloring matter of the blood, and pigment-granules may be found mingled with the granular débris of its resolving stage. In about 75 per cent. of the cases there will be found in the sputa, when floated in water, casts of the alveoli and bronchioles.[30]

[Footnote 30: Diagnost. u. Pathognos. Untersuch., 1845, Remak.]

The chemical constituents of the sputa are albumen, mucus, and mucin. Different observers have found the sputa to contain tyrosin and sugar. There are two explanations of the acid reaction of pneumonic sputa.[31] {324} Verdeil thought it due to the excess of pneumic acid in the inflamed lung. Bamberger claims that it is due to the deficiency in alkaline phosphates.[32]

[Footnote 31: Gaz. méd., 1851, p. 777, Robin et Verdeil; Chem. Anat. Phys., vol. ii. p. 460 et seq.]

[Footnote 32: Wurtzburg Med. Zeitschr., ii., No. 506.]

It may be noticed that the following differences exist between pneumonic and catarrhal sputa: catarrhal sputa contain 10 to 14 per cent. of alkaline earths; pneumonic sputa contain no alkaline phosphates. In catarrh the ratio of the soda to the potash is 31 to 20; in pneumonia the ratio is 15 to 41. There is 3 per cent. of sulphuric acid in catarrhal and 8 per cent. in pneumonic sputa.

Early in pneumonia there is an increase of the fixed salts, notably chloride of sodium, in the serum of the blood. It has been thought that from the rapid and excessive cell-transformation in the lung the chloride of sodium is attracted to that organ. In one case where no sodium chloride was found in the urine 10 per cent. of the solid material of the sputa consisted of that salt. Still, the presence of it in the sputa and blood, and its absence from the urine, are facts that still need elucidation.[33]

[Footnote 33: Beale gives the following analytical table of a case of acute pneumonia:

Chloride of Sodium. Per cent. of Solids. Urine 0. Blood from heart 0.68 Hepatized lung 2.59 Healthy lung 1.43]

The expired air in croupous pneumonia is colder than normal, and, as in many acute general diseases, there is a diminution in the amount of carbonic acid excreted.

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