Volume 3 — DISEASES OF THE RESPIRATORY SYSTEM. (continued 15)

The disease pursues a rapid course, and ends fatally whenever acute tuberculosis supervenes. This may occur in the early part of the chronic phthisical affection or at any period during its course. The supervention of the acute disease sometimes follows a profuse hæmoptysis. The characteristics are high fever, frequency of the pulse, cyanosis, prostration, and death within a few weeks or even a few days. The physical signs which denote a large extent of solidification of lung and the consequent destructive changes are wanting in these cases.

A small proportion only of cases of pulmonary phthisis fall in the category either of galloping consumption or of the supervention of acute tuberculosis. In by far the larger proportion the disease is chronic from the beginning to the end, and a fatal termination takes place after a period averaging from two to three years, the period sometimes extending to many years.

An important distinction, as regards the history of the disease, is expressed by the terms progressive and non-progressive. The disease is progressive when the local and the general symptoms denote more or less activity in the tuberculous process, the physical signs generally showing progressive extension of the pulmonary affection. It is non-progressive when symptoms and signs having the significance just stated are wanting. The disease may become non-progressive early or late, and at any period during its continuance. A stationary condition may continue indefinitely. The symptoms and signs may show processes of restoration—namely, disappearance of the tuberculous product, diminution in size, and the cicatrization of cavities. The disease is then said to be regressive. A regressive course is not extremely infrequent. It is more or less slow and may or may not end in recovery. A stationary condition, regression having taken place to a greater or less extent, is not infrequently observed. This condition may remain because the pulmonary lesions are too great to admit of restoration. In most cases the disease is not steadily progressive. It ceases from time to time to progress, the periods of non-progression varying much in duration. With each renewal of progress the physical signs generally show an addition to the tuberculous product. As a rule, this product does not increase continuously, but, as it were, by successive eruptions after intervals of time which may be either short or long.

Pulmonary phthisis in some cases ceases to progress, and regression continues, recovery taking place from an intrinsic tendency—that is, irrespective of any measures of treatment. This highly important fact has not hitherto been distinctly recognized by medical writers and practitioners. I have established it by having recorded a series of cases in which recovery took place without medicinal or other treatment and without any material change in habits of life.¹ In these cases the disease may be said with propriety to be self-limited.² The weight of this fact in its bearing on prognosis and treatment is obvious. That non-progression and regression ending in recovery may be brought about by judicious measures of management cannot be doubted; in other words, the disease may be arrested in a certain proportion of cases when non-progression and recovery would not have resulted from an intrinsic tendency or self-limitation.

¹ Phthisis, in a Series of Clinical Studies, by Austin Flint, M.D., 1875.

² Vide "Self-limitation in Cases of Phthisis," by Austin Flint, M.D., N.Y., Archives of Medicine, June, 1879.

Pulmonary phthisis proves fatal by undermining more or less slowly the powers of life. The appetite and digestion fail. There is progressive loss of weight and of muscular strength. A greater or less degree of pyrexia is persistent, with diurnal exacerbations and night perspirations, forming what is known as hectic fever. Muco-purulent matter is expectorated in abundance, with fatiguing cough. The respirations are accelerated, and there is often suffering from dyspnoea. The pulse becomes more and more frequent and weak. Oedema of the lower limbs is of frequent occurrence. The patient dies by slow asthenia, the mental faculties usually remaining intact and the patient hopeful of recovery to the last.

The history of the disease in many cases embraces tuberculous affections elsewhere than in the lungs, and other complications. The duration is often shortened by some of these. The more important are tuberculosis of the intestines, tuberculous peritonitis, perforation of lung giving rise to pneumo-hydrothorax, pneumorrhagia, pulmonary gangrene, tuberculous meningitis, and chronic laryngitis affecting deglutition. The less important affections are pleurisy with effusion, thrombosis of the femoral or the iliac vein, a circumscribed non-tuberculous acute pneumonia, chronic laryngitis not affecting deglutition, intercostal neuralgia, and perineal fistula. Profuse hæmoptysis is sometimes a grave event, and may prove the immediate cause of death.

It is impossible to divide the course of pulmonary phthisis into sharply-defined stages based on anatomical changes. Often after death the lungs present in different situations all the changes which intervene between a fresh tuberculous product and cavities. The division into a stage of crudity of the product and a stage of softening is of no practical utility. There are no symptoms nor signs which are reliable for determining when softening has taken place. The existence of cavities can generally be determined by means of the cavernous physical signs, and the disease may be considered as advanced phthisis when cavities are discovered. The term incipient phthisis is used to designate an early period of the disease. Having passed the incipient or early period, and before reaching the advanced stage or stage of excavation, cases may be conveniently grouped according to the amount of the tuberculous affection. In different cases and at different periods in the same case the affection is either small, moderate, considerable, or large. Exact chronological divisions are impracticable.

ETIOLOGY.—Pulmonary phthisis, as a rule, is developed irrespective of any antecedent affection of the lungs. The researches of Louis established the fact that the phthisical affection is very rarely preceded by bronchitis, either acute or chronic.³ My clinical studies have led to the same result.⁴ That a neglected cold may eventuate in phthisis is a traditional popular error, unfortunately held also by some medical writers and practitioners. The error is to be regretted because it often interferes with hygienic management in cases of phthisis. The name chronic catarrhal phthisis proposed by Niemeyer was based upon this etiological error. It is a matter of common clinical observation that persistent bronchial inflammation leading to pulmonary emphysema, and often accompanied by asthma, involves no liability to phthisis. The long-continued inhalation of coal- and stone-dust, of the oxide of iron, and particles of other substances gives rise to bronchitis and interstitial pneumonia (pneumonokoniosis, anthracosis, siderosis, etc.), but is rarely followed by the common form of pulmonary phthisis. It is common for phthisical patients to suppose, as a matter of course, that their disease originated in a cold. In giving the previous history they often say that they took cold at a certain time. The analysis of carefully-recorded cases shows that very rarely does the disease follow directly upon an attack of bronchitis, notwithstanding that the frequency of the latter, from the law of chances, would involve an accidental concurrence in a certain proportion of cases. Acute lobar pneumonia or pneumonic fever has little or no tendency to eventuate in phthisis. This statement is sustained by the researches of Louis and by my clinical studies. In the rare instances in which phthisis follows either acute pneumonia or bronchitis, the latter diseases act only as auxiliary causes of the phthisical affection if the sequence be more than an accidental connection. This statement applies also to pleurisy with effusion. In certain of the few instances of phthisis apparently having been preceded by pleurisy it is probable that the former was the antecedent disease, occurring early in the history of the phthisical affection and retarding or arresting the progress of the latter. It may be added that there is no ground for supposing that phthisis is ever produced solely by traumatic causes acting upon the chest.

³ Recherches sur la Phthisie, 1825.

⁴ Phthisis, in a Series of Clinical Studies.

It is an old doctrine that bronchial hemorrhage may be causative of phthisis. This doctrine has been recently revived by Niemeyer and some others. It is disproved by the following clinical facts: in two-thirds of the cases in which hæmoptysis antedates phthisis the development of the latter is after the lapse of a considerable period—weeks, months, or years. The instances are few in which phthisis immediately follows the hemorrhage. The occurrence of hæmoptysis during the course of phthisis, as a rule, is not followed by any increase of the phthisical affection. On the contrary, the local symptoms are not infrequently relieved by the hemorrhage. It is, however, to be remarked that hæmoptysis as a forerunner of phthisis is of much significance. In the larger proportion of cases phthisis follows its occurrence sooner or later. It is to be added, in view of the recent discovery by Koch, that bronchial hemorrhage may proceed from the same local cause which afterward leads to the development of phthisis—namely, the presence of a special micro-organism.

The etiology of pulmonary phthisis not involving any antecedent affections of the lungs nor any appreciable local causes, it would seem to follow that the disease involves either a predisposing or a causative agency elsewhere within the organism; and as, with our present knowledge, the source of this intrinsic agency cannot be localized, it is customary to say that the disease has a constitutional origin. This use of the term constitutional here, as in other instances, expresses an important fact—namely, that the disease is not purely local; that is, attributable solely to extrinsic or any appreciable causes acting on the affected part. At the same time, the term is a confession of the imperfection of our knowledge, inasmuch as it does not specify the nature of the causative or predisposing agency, nor its origin, beyond the statement that it is not local. That the constitutional agency has a special character is a logical inference from the fact that the disease may be said to have such a character. The term vulnerability does not fully express the special character of the constitutional agency. The condition of the constitution which stands in a causative relation to the disease is something more than an undue susceptibility to morbific influences of any kind—a susceptibility giving rise to diseases the nature and seat of which are accidental. The condition is one which has relation both to the character and the situation of the pulmonary affection. Such a condition is expressed by the term cachexia.

It remains to inquire whence arises this phthisical or tuberculous cachexia.

A congenital predisposition or diathesis exists in a certain proportion of cases. This is to be inferred from the number of instances in which several or many members of a household, brothers and sisters, become affected with phthisis. There may or may not be evidence that this predisposition is inherited. An inherited predisposition is to be inferred from the number of the cases in which parents or grandparents were phthisical. While statistical facts show undoubtedly heredity as involving a causative agency, making due allowance for the law of chances, it is important for the physician to bear in mind that a tuberculous parentage involves only a certain measure of liability to phthisis in the offspring. The progenitors of many healthy men and women have been phthisical. There are instances of large families of children in which many have died with phthisis, leaving, however, some who escape this disease and are in all respects healthy.⁵ The question arises whether in cases of phthisis where there is lack of evidence of a congenital predisposition the diathesis may not be innate. The affirmative answer seems probable in view of the inability oftentimes to find any rational explanation on the supposition that the diathesis has been acquired. Positive data bearing on this question are of course not available.

⁵ For data on which these statements are based, vide Phthisis, in a Series of Clinical Studies, by the author.

Age has a decided influence on the development of phthisis. Cases in which the ages of patients are between twenty and thirty years greatly preponderate over the number in any other decade of life. Next in order as to the number of cases are the ages between thirty and forty years. The form of tuberculous disease under present consideration is rare under ten years and also in advanced life. All that can be said with our present knowledge in explanation of the influence of age is, that either an existing diathetic condition tends intrinsically to the development of the disease or that the diathesis is likely to be acquired at certain periods of life more than at other periods. Of these two explanations the former is the more rational.

Statistics show that occupations which involve sedentary habits, confinement within doors, especially in small, illy-ventilated rooms, poor or insufficient food, and prolonged mental depression, increase the liability to phthisis. The disease is developed either during or shortly after gestation in a sufficient number of cases to show that pregnancy has a causative agency. Facts appear to show a less degree of prevalence of the disease in most cold and tropical climates than within the temperate zone. It is, however, true, as stated by Ruehle, that "there are regions in all zones which are free from the disease, and, on the other hand, there is no zone in which it is not very prevalent." The prevalence is less in high than in low altitudes. Humidity of the soil has been shown by Bowditch, Buchanan, and others to enter into the etiology. In order to determine how far purely climatic agencies exert an influence either for or against the prevalence of the disease, it is necessary to take into account other associated agencies, together with an innate predisposition; and the latter especially does not admit an exact estimation.

Certain general diseases seem to involve a liability to phthisis as a sequel. This is true of rubeola and pertussis. In cases of diabetes mellitus, phthisis is considered as occurring sufficiently often to show a causative connection. In my own clinical experience, however, phthisis has not been of frequent occurrence in that disease. Typhoid fever in some cases appears to favor the development of phthisis. Some, however, have contended for the reverse of this statement. Certain affections are apparently antagonistic in their influence. In this category are pulmonary emphysema and obstructive or regurgitant valvular lesions at the mitral orifice of the heart. The disease is rarely developed in chlorotic patients. Facts go to show that alcoholism opposes its development. In opposition to current belief, my clinical studies lead me to conclude that they who have had scrofulous disease of the cervical glands in early life are not likely to become phthisical in after years. Contraction of the chest from deformity diminishes the liability to the disease.

The communicability of phthisis is a doctrine dating as far backward as the history of medicine extends. Distinguished physicians in every age have held that the disease may be communicated under circumstances which involve close proximity, as from husband to wife or vice versâ, and from patients to nurses or attendants. The contagion is supposed to be contained in the expired breath. The clinical evidence in behalf of this doctrine is the number of instances which seem to be striking examples of communicability. It is easy to collect a considerable number of such examples. But in order to constitute clinical proof of the doctrine of communicability the number must be so large as not to be accounted for on the ground of mere coincidence. A collection of isolated instances gathered from medical literature or reports from different physicians does not establish the doctrine. Owing to the great frequency of phthisis, mere coincidence suffices to account for a certain number of instances. Moreover, long-continued proximity to cases of phthisis generally involves causative agencies other than a contagium—namely, confinement within doors and mental anxiety. In my collection of 670 recorded cases of phthisis, the number of instances in which there was room for the suspicion of the disease having been communicated either from the husband to the wife or from the wife to the husband amounted only to 5. In one of these instances, a wife, who became phthisical after her husband, had lost two sisters, one of whom was a twin sister, by the disease. It must be admitted that the analysis of these cases, without disproving the doctrine of communicability, fails to lend to it support, for the reason that in such a large collection of cases the number of examples of apparent communicability are so few.

A new and strong impetus was given to the discussion of the doctrine by the discovery of the inoculability of tuberculous disease. Villemin in 1865 demonstrated the fact that this disease could be communicated to rabbits and guinea-pigs by inserting beneath the skin portions of the tuberculous product. The experiments of Villemin and many others have shown conclusively that the insertion of fresh undecomposed tuberculous matter beneath the skin or within the pleural and the peritoneal cavity, or in the anterior chamber of the eye, is followed by an eruption of tubercles in these animals within two or three weeks. If tuberculous matter taken from an animal in which the disease has been produced by inoculation be inserted in another animal, the disease is transmitted to the latter. These results of inoculation, which have been abundantly confirmed in all countries, prove indisputably the communicability, by that mode, of tuberculous disease in certain animals which have a peculiar susceptibility thereto. The fact that the disease is not readily communicated to dogs, cats, and other animals shows a peculiar susceptibility to be an important factor in the successful results of inoculation. The conclusion drawn by Villemin and others from these experiments is that the disease is communicated by means of a specific virus, a term implying the existence of a contagium.

Opposed to this conclusion are experiments which appear to prove that tubercles may be produced in rabbits by inoculating them with various kinds of non-tuberculous matter. By those who adopt the doctrine of a specific virus it is contended either that true tubercles are not produced in these experiments, or that, if followed by the development of true tubercles, the production of the latter is attributable to the derivation of the virus from the laboratories in which tuberculous animals had been confined or to a contagium received directly from these animals. The introduction of non-tuberculous matter was found by Cohnheim and Fraenkel never to be followed by tuberculous disease when the experiments were repeated in places where tuberculous animals had not been confined and the animals on whom the experiments were made were isolated from those affected with tuberculosis. Cohnheim states that inoculation with portions of indurated lung, or of the nodules resulting from peribronchitis, or of the contents of bronchiectasic cavities, will not give rise to true tubercles, for the reason that, although taken from phthisical lungs, they do not contain the tuberculous virus. This distinguished pathologist, at first an opponent of the doctrine of a specific virus, afterward became a strong advocate therefor. He was led to regard a successful inoculation as affording the only criterion and reliable test of tuberculous disease; that the etiology of tuberculous disease invariably involves the presence in the system of this virus; that it exists in a latent form whenever there is an innate predisposition to phthisis; and that it may enter the system in different directions—namely, with the inspired air into the lungs, and even within the skull through the foramen of the ethmoid bone, into the small intestine by deglutition, and into the uterus with the semen. Becoming developed in any situation, the virus may remain localized, or it may be disseminated more or less extensively by means of the lymph and blood. The behavior of the tuberculous virus, according to Cohnheim, corresponds closely to that of syphilis.

Experiments made by Gerlach, Bollinger, Aufrecht, Chaveau, Leisering, Harms, Gunthern and others, have shown that the disease may be communicated by incorporating tuberculous matter with food. Rabbits, guinea-pigs, dogs, calves, swine, sheep, and goats have been rendered tuberculous by these experiments. Klebs, Tappeiner, Parrot, and Puech claim to have communicated the disease by combining with the food the matter of expectoration from phthisical patients. Gerlach and Klebs have seen the disease in animals fed with milk from cows affected with the so-called pearl disease (perlsucht), which is considered to be identical with phthisis. Finally, the disease appears to have been produced by exposing animals to an atmosphere impregnated with fine particles of tuberculous matter by means of an atomizer, and by blowing into the trachea this matter reduced to a fine powder.⁶

⁶ For a summary of the experiments relating to the communicability of tuberculous disease by inoculation, by the ingestion of tuberculous matter, and by its inhalation, and for reference, the reader is referred to an article by Wm. P. Whitney in the Boston Medical and Surgical Journal, July 28, 1881; to the article on "Tuberculosis" by Frederick C. Shattuck in supplement to Ziemssen's Cyclopædia of the Practice of Medicine, 1881; to the "Cartwright Lectures," by William T. Belfield, M.D., published in the New York Medical Record in February and March, 1883; and to an article by Surgeon George M. Stemberg, U. S. Army, in the American Journal of Medical Sciences, January, 1885.

It is noteworthy that tuberculous disease may be produced by inoculating with the infiltrated product, with matter from miliary tubercles, or from scrofulous glands in the neck. The identity of these morbid products is thus made evident, assuming that the fact of communicability involves the existence of a specific virus.

The practical importance of the facts already ascertained respecting the communicability of phthisis is obvious. They constitute the foundation for a reasonable supposition that the disease may be communicated to man by means of the meat of tuberculous animals, by milk, and by breathing an atmosphere charged with particles of tubercle. That the instances in which the disease is communicated, however, are rare seems to be a rational inference from the difficulty of obtaining clinical proof of communicability. That susceptibility is an essential factor is made evident by the well-known predisposition pertaining to certain periods of life. It is to be considered that while the communicability of the disease to certain animals is abundantly shown by the experiments to which reference has been made, the existence of a special virus or a contagium is not as certainly established by these experiments. They leave to be settled, by further investigation, the question whether or not the communicability of the disease involves only the agency of a septic matter devoid of the special character expressed by the terms virus and contagium. Without waiting for data sufficient to settle this important question, prudence would dictate the propriety of all practicable precautionary measures.

Still more recently, and since the foregoing remarks on the communicability of phthisis were written, have appeared the remarkable experimental researches of Koch of Berlin. Koch claims to have demonstrated the constant presence in tuberculous products of a specific organism which he calls the bacillus tuberculosis, and that it is not found in non-tuberculous products. This parasite he has isolated, and by cultivation carried through several successive generations. By its introduction, after, as well as before, cultivation, into the pleural cavity, the peritoneal cavity, the anterior chamber of the eye, and in other situations, he produced tuberculous disease, not only in rabbits and guinea-pigs, but in dogs and rats, the latter animals being less susceptible than the former to tuberculous infection. In his experimental observations, animals not inoculated, placed under the same external conditions as those inoculated, did not become tuberculous. The same parasite, alike capable of infecting healthy animals, he found in miliary tubercles, in the cheesy tuberculous deposit, in scrofulous glands, and in the sputa from tuberculous patients. The parasite was found not to have lost its vitality in dried sputa.⁷

⁷ For the details of Koch's researches vide his report in the Berliner klinische Wochenschrift, April 10, 1882; vide, also, Verhandlungen des Congresses für Innere Medicin, Erster Congress gehalten zu Weisbaden, 20–22 April, 1882.

The researches of Koch had been continued for two years before the publication of the results in March, 1882. Moreover, his ability as a skilled experimental observer in the study of micro-organisms, and his sincerity as a truth-seeker, are universally admitted. Naturally, the publication of the results of his researches excited at once great interest in all countries. At the present moment (April, 1885) questions connected with the bacillus tuberculosis are more considered than any others relating to medical pathology and etiology. Thus far, the observations of competent medical mycologists are confirmatory of the results of the researches by Koch. It seems to be established that the so-called bacillus tuberculosis is uniformly present in tuberculous products, and as uniformly absent in other morbid products; that it is generally present in the sputa of phthisical patients, and never present in the sputa of non-phthisical patients; and that tuberculous disease in animals may be produced by inoculation with this organism after cultivation has been sufficiently continued to eliminate all else pertaining to the tuberculous product. On these data are based the conclusions that phthisis is an infectious disease—in other words, that it involves in its causation a specific agent capable of self-multiplication; that it is a communicable disease, and that the agent of the communication is the bacillus tuberculosis—that is, this agent is the contagium. The supposition that the presence of the bacillus is secondary to the tuberculous affection is not tenable in view of the fact that the affection is produced by the introduction of this organism after it has passed through several generations by culture out of the body.

As has been already seen, clinical experience fails to furnish positive proof of the communicability of phthisis. There are many striking instances which, taken by themselves, render it probable that the disease was communicated; but, on the other hand, there are so many cases of its development under circumstances not pointing to contagion, and of the number of persons in close proximity to tuberculous patients the proportion of those who become affected is so small, that it has seemed impossible to establish the doctrine of contagion by clinical evidence.

The insufficiency of clinical proof, however, cannot invalidate the demonstration by inoculation. Assuming it to be demonstrated that the disease involves a specific agent, and that this agent is proven to be a contagium by its capability of producing the disease when introduced into a healthy body, the conclusion as to communicability is not to be shaken by the lack of corroborative clinical evidence or by inability to explain certain facts which seem to be inconsistent with that conclusion. Having accepted a demonstrated truth, the endeavor should be to reconcile therewith facts which do not sustain it and which may appear to be opposed to it. It remains to inquire in what way the communicability of phthisis by means of a contagium vivum is to be reconciled with facts furnished by clinical experience.

If we accept the conclusion that a particular parasitical organism is the primary and efficient causative agent in the production of phthisis, the development and multiplication of this organism must require certain local conditions. Without these the parasite is innocuous. The conditions are to its development and multiplication what the peculiarities of soil are to the production of different vegetables. Of the nature of these conditions we are at present ignorant. When they exist the bacillus develops and multiplies; when they are wanting the parasite is incapable of development and multiplication. This dependence of specific morbific agents upon particular conditions is exemplified in other infectious diseases. For example, the contagium of the eruptive fevers, received into the system ever so abundantly, is inoperative in some persons, and, as a rule with rare exceptions, it is never operative after the disease which it occasions has been once experienced. In these instances it is not the contagium itself which has lost the capability of producing the disease, but the conditions for its activity are wanting. Of the nature of these conditions we know as little as of those which are essential to the development and multiplication of the bacillus tuberculosis. The inoculation of animals with tuberculous matter shows that the disease is produced in some species of animals much more readily than in other species, and some animals of the same species much more than others are susceptible to this contagium. These facts are to be explained by variations in different species of animals, and in different animals of the same species, as regards the conditions required for the efficiency of the morbific agent.

The facts in the clinical history of phthisis which denote a constitutional predisposition thereto or a tuberculous cachexia are explicable by reference to the conditions requisite for the development and multiplication of the parasite. A predisposition which may be innate, inherited, or acquired involves the existence of these conditions. The latter may be greater or less in degree. The causative agencies of confinement within doors, humidity of soil, pregnancy, etc. operate by either giving rise to or increasing these conditions. If this view be correct, it is evident that the curative influence of climatic changes, alteration of the habits of life, and other hygienic agencies must be by means of an effect exerted upon these conditions; and probably it is in this way chiefly that remedies are useful. Of the essential nature of these conditions we know neither more nor less than of what consists the tuberculous cachexia. We are, of course, as ignorant of the one as of the other if it be assumed that they are identical—that, in other words, the different expressions have the same meaning. The only difference is this: If phthisis be an infectious and a communicable disease, a contagium enters into its etiology; whereas if the existence of a contagium be denied, it follows that the cachexia is itself sufficient for the causation of the disease.

In connection with the etiology of phthisis a theory which of late years has found favor with many should be referred to. It is, that this disease may be a result of the absorption of caseated non-tuberculous morbid products in different parts of the body. This theory of autochthonous infection derives but little support from clinical observation. In much the larger proportion of the cases of phthisis it is impossible to discover anywhere caseated morbid products which may be supposed to have a causative connection with the disease. To assume that, when not discovered, foci of infection nevertheless are concealed somewhere within the organism is evidently begging the question. On the other hand, how often do suppurations, necroses, and degenerated morbid products occur in different situations without being followed by phthisis!

SYMPTOMATOLOGY AND COMPLICATIONS.—Giving under this head a fuller account of the symptomatology and complications than has been already given in sketching the history of the disease, it will be a convenient arrangement to consider these topics in their relations to the different anatomical systems of the body—namely, the respiratory, circulatory (including temperature), hæmatopoietic, digestive, nervous, and genito-urinary systems.

Symptoms, etc. referable to the Respiratory System.—The dry cough which is the earliest pulmonary symptom in typical cases is to be regarded as an effect of the local irritation caused by the presence of the tuberculous product. This product, increasing and extending, gives rise to circumscribed bronchitis which causes increase of cough with expectoration. The expectoration represents this secondary bronchitis prior to the occurrence of ulceration, the escape of liquefied tuberculous product, and the existence of cavities. The quantity and the characters of the matter expectorated depend on the degree and the extent of the bronchial inflammation, the latter depending on the extent of the phthisical affection. Different cases present wide variations in these respects. The frequency and severity of the cough depend in a great measure on the quantity of the matter of expectoration and its adhesiveness. The matter expectorated, at first semi-transparent mucus, becomes muco-purulent, the characters pertaining to mucus and pus being combined in varying proportions, as in cases of chronic bronchitis. Nummular sputa—so called from the resemblance in form to a coin when lying on a flat surface, the edges often serrated—are considered as casts of small cavities formed by dilated bronchi. A microscopical examination of the sputa may show elastic yellow fibres. The presence of these is almost pathognomonic of phthisis, and denotes either the process of ulceration or exfoliation of tissue from within cavities.⁸ Liquefied tuberculous product appears in the matter of expectoration as a puriform fluid. It sometimes contains small semi-solid tuberculous masses. The lining membrane of tuberculous cavities furnishes a veritable purulent matter of expectoration. It is stated by Buhl that the presence of alveolar epithelium in the sputa is distinctive of phthisis; hence the name proposed by him, desquamative pneumonia. It is, however, stated by Frischl that the alveolar epithelium is found in the matter expectorated in cases of oedema and congestion of the lungs.⁹ There is sometimes notable fetor of the matter of expectoration, due to putrescent decomposition of the purulent contents of cavities or to small sloughing portions of pulmonary tissue. The varieties of sputa which have been mentioned may be accompanied by a serous liquid in more or less abundance. Calcareous masses varying in size from a pin's head to a pea are expectorated in some cases. I have known several hundred to be expectorated in a single case. In the instances which have fallen under my observation these pulmonary calculi have been expectorated when the symptoms have denoted arrest and regression of the disease; and it is consistent with this fact to regard them as obsolete tubercles. They are not to be confounded with the small solid bodies sometimes formed in the follicles of the tonsils, the latter consisting of a sebaceous-like product, which is crushed, without crumbling, by pressure, and emits a fetid odor. Since the discovery of the bacillus tuberculosis by Koch microscopical examinations of sputa in a large number of cases by different observers have shown that this parasite is generally, but not invariably, present. Its abundance in the sputa appears to correspond to the rapidity with which the tuberculous affection is progressing, and examinations with reference to its presence and its abundance are of much practical utility in diagnosis and prognosis.

⁸ In order to discover the elastic fibres readily, Fenwick advises as follows: "Prepare a solution of caustic soda, about twenty grains to an ounce of distilled water. Collect all the patient has expectorated in twelve or twenty-four hours, from ten at night to ten the next morning being the best period. Pour this, previously mixed and well shaken with an equal quantity of the soda solution, into a glass beaker, and boil it over a gas or spirit-lamp, stirring it occasionally with a glass rod. A test-tube does not warm as well as a beaker. As soon as it boils pour it into a conical glass, and add four or five times the amount of cold distilled water. If the mucus is still gelatinous after boiling, you have either added too little soda or not boiled it sufficiently. The cold water carries down to the bottom of the glass any lung-tissues that may be present, where they form a slight deposit in about a quarter of an hour; if no deposit is visible, put the glass aside for two or three hours. Remove the deposit with a dipping-tube, place it in a glass cell, cover it with a piece of thin glass, and examine with a one-inch object-glass. The lung-structures will be often found clinging to hairs and other foreign bodies present in the sputa" (Guide to Medical Diagnosis).

⁹ Vide Niemeyer by Seitz, tenth ed.

Hæmoptysis occurs in a large proportion of the cases of pulmonary phthisis. It occurs much oftener in the early than in a later period of the disease. As regards the number of attacks, their duration, the intervals between them, and the amount of hemorrhage, there are wide variations. Prior to the formation of cavities the hemorrhage is from the bronchial tubes (bronchorrhagia). After cavities are formed the blood comes from the interior of these. As a rule, bronchial hemorrhage is not followed by the evidence of any increase of the phthisical affection. Not infrequently a sense of relief follows. The analytical study of a large collection of cases shows that the occurrence of bronchial hemorrhage does not diminish, but apparently increases, the chances of arrest and of tolerance of the disease. This statement holds true with regard to cases in which the hemorrhage is often repeated and profuse, as well as to those in which it is slight and infrequent.¹⁰

¹⁰ Vide Phthisis, in a Series of Clinical Studies, by the author.

Cavernous hemorrhage may be due to rupture or ulceration of parenchymatous bands which traverse cavities, but often it is caused by the bursting of small aneurisms in their walls. It may be so profuse as to prove fatal. Cavities sometimes become filled with coagulated blood, which, if life continue, becomes decomposed and gives rise to a grumous, fetid matter of expectoration. Bronchial hemorrhage is supposed to be caused by a circumscribed hyperæmia at the situation where the blood escapes. In a case under my observation in which death took place shortly after a profuse hæmoptysis, there was congestion limited to the middle lobe of the right lung, and the bronchial tubes in this situation contained bloody mucus, none being found elsewhere. A circumscribed hyperæmia, however, must depend upon some local cause. Probably in most instances this anterior local cause is the tuberculous product. That the escape of blood involves a change in the coats of the vessels from which it escapes is probable.

A rare event occurring in connection with hæmoptysis is the coagulation within the bronchial tubes of fibrin which may be expectorated in the form of casts of the tubes, analogous to those which characterize fibrinous or plastic bronchitis. I have met with an instance, and also with a case in which after death the bronchial tubes of an entire lobe were found to be filled with solidified fibrin. The death in this instance followed quickly a profuse hæmoptysis. There is not the danger connected with the gradual disintegration and expectoration of the coagulated fibrin which was surmised by Niemeyer.

The presence of the tuberculous product in the lungs and the processes to which it gives rise, inclusive of the secondary bronchitis, occasion no pain. Patients often strike the chest with violence, as affording to them evidence that the organs are sound. But in most cases, from time to time during the course of the disease, sharp stitch-like pains occur. They are sometimes slight or moderately severe, but they may be sufficiently intense to confine to the house or even to the bed. They last, usually, but a few days, and recur at variable intervals. They are referred generally to the upper part of the chest, often beneath the scapula. Patients are apt to imagine that the pains are rheumatic. They are symptomatic of successive, circumscribed, dry pleurisies, which are very rarely wanting in cases of phthisis, leading to the pleuritic adhesions constantly found after death. These pleurisies are secondary to the phthisical affection, and recur at epochs when new developments of the latter take place. There is no reason to suppose that they contribute in any way to the increase of the phthisical affection. On the other hand, they protect against one important event at least—namely, perforation of lung, and, as consequent thereon, pneumo-hydrothorax. In this point of view they are conservative. These pleuritic pains are to be discriminated from those of intercostal neuralgia. The neuralgic pains generally are situated lower, and the diagnostic criterion of intercostal neuralgia is available—namely, the tenderness on pressure in the intercostal spaces near the median line in front, the axillary line, and the spinal column.

The respirations are more or less frequent in different cases and at different periods in the same case according to the impairment of the function of hæmatosis by the pulmonary affection and the increased frequency of the heart's action. A sense of the want of breath as implied in the term dyspnoea is, however, seldom sufficient to occasion much suffering. Even when the respirations are considerably increased in number it is rare for the patient to complain of the want of breath when at rest. A degree of muscular weakness which prevents the patient from freeing the bronchial tubes and cavities of morbid products may give rise to distressing dyspnoea. A sudden increase in the frequency of the respirations, with dyspnoea and cyanosis, when not attributable to filling of the bronchial tubes nor to pneumothorax nor pleuritic effusion, points to the development of miliary tubercles in abundance—in other words, to the supervention of acute tuberculosis.

Important complications referable to the respiratory system are laryngitis, non-tuberculous pneumonia, pleurisy with effusion, perforation of lung with pneumo-hydrothorax, pneumorrhagia, and pulmonary gangrene.

Dysphonia and aphonia, the voice being husky or hoarse and the whisper stridulous, denote laryngitis. These diagnostic symptoms are never wanting, and the laryngeal complication may be excluded if they be absent; but the extent to which the larynx is affected is of course determinable by means of the laryngoscope. The affection in some cases extending to the epiglottis, paroxysms of cough and spasm of the glottis are produced by the act of swallowing food and drinks. The interference with deglutition may be so great as to restrict seriously alimentation, and in this way may hasten a fatal termination of the disease. In the majority of cases, however, deglutition is not interfered with. There is very rarely laryngeal obstruction to respiration. The affection involves little if any liability to the supervention of acute laryngitis or oedema of the glottis.

In most cases the laryngitis occurs at a considerable period after the commencement of the pulmonary affection, this period, in a proportion of more than one-third, being from two to four years. In some instances it seems to occur coincidently with, and in some to precede, the pulmonary affection. In the latter instances it is probable that latent tuberculous disease of the lungs preceded the laryngitis. The diversity as regards the interval of time between the date of the pulmonary affection and of the occurrence of the laryngitis, the apparent coincidence in the occurrence of both in some instances, and the want of any uniformity in different cases as regards the amount of pulmonary disease and the stage of its progress when the laryngitis occurs, render it a rational conclusion that laryngitis is not dependent on the disease of the lungs, but that it proceeds from the same cause which determines the latter.

Excluding the instances in which the laryngitis involves the epiglottis and interferes with alimentation, clinical experience teaches that this complication does not diminish the chances of arrest or recovery from the pulmonary affection, and that it has no untoward influence on the duration of the disease in the cases which sooner or later end fatally.¹¹ As a rule, in cases which recover the voice remains permanently more or less affected.

¹¹ Vide Phthisis, in a Series of Clinical Studies, by the author.

Acute lobar pneumonia or pneumonic fever is sometimes an intercurrent affection in cases of phthisis. The cases are so rare as to show absence of any predisposition to that disease derived from the phthisical affection. The pneumonia ends in recovery in a proportion of cases sufficiently large to show that, as a rule, the prognosis is not unfavorably influenced by phthisis, and, as a rule also, the course of the latter is not influenced unfavorably by the pneumonia. A circumscribed pneumonia is an occasional complication of phthisis. Its non-tuberculous character is shown by the rapidity and completeness of the absorption of the intra-vesicular product. This circumscribed pneumonia gives rise to physical signs which appear to denote a rapid and considerable increase of the phthisical affection. The disappearance within a short period of the added dulness on percussion, bronchial respiration, and bronchophony, is the evidence that these signs represent a circumscribed pneumonia occurring as a complication.

Pleurisy with serous effusion is not an infrequent complication at an early period in the course of the disease. There is very little if any liability to its occurrence at an advanced period, except as associated with pneumothorax from perforation of lung. It is probably secondary in certain of the cases in which the phthisical affection appears to follow the pleurisy. The pleuritic effusion appears to retard the progress of the phthisical affection. Clinical experience shows that this complication, if it be unilateral, is not an untoward event. A double pleurisy with effusion is evidence of the existence of phthisis.

Perforation of lung, giving rise to pleurisy with effusion and pneumothorax, is an event which belongs, with some exceptions, to an advanced period of the disease. The perforation is caused by rupture of the wall of a cavity superficially situated where pleuritic adhesion from circumscribed dry pleurisy had not taken place. In most instances the occurrence of the perforation is quickly followed by acute pain and orthopnoea, with notable disturbance of the circulation, fever, and prostration, these symptoms being due to the sudden entrance of air into the pleural sac, the development of acute inflammation, and rapid serous effusion. The recognition of the pneumo-hydrothorax by means of physical signs is easy. The suffering of the patient becomes less after twenty-four or forty-eight hours. In the great majority of cases death takes place within a short period; that is, within a few days or weeks. The duration of life depends on the amount of phthisical disease, together with the condition of the patient as regards strength, etc. In some instances, the perforation taking place when the phthisical affection is small and accompanied by favorable symptoms, the pneumo-hydrothorax is tolerated for a long period. The accumulation of liquid within the pleural sac sometimes causes the air to disappear, and the pneumo-hydrothorax is converted into simple pleurisy with large effusion.

Pneumorrhagia and pulmonary gangrene are very rare complications of pulmonary phthisis. The analytical study of nearly 700 recorded cases furnished but a single example of each of these complications.

Symptoms and Complications referable to the Circulatory System, including Temperature.—More or less acceleration of the pulse and elevation of the temperature of the body belong to the clinical history of pulmonary phthisis. It may be stated that the pulse and temperature are never normal if the disease be progressive. A persistent normal pulse and no elevation of temperature therefore denote arrest or non-progression of the disease. It may also be stated that the acceleration of the pulse and the increase of temperature form a good criterion of the rapidity or otherwise of the progress of the tuberculous disease, provided inflammatory complications be excluded. The disease is progressing rapidly in proportion to the frequency of the pulse and the increase of temperature.

If the disease be progressive daily exacerbations of fever take place. They occur in the afternoon usually, and continue into the evening or the nighttime, ending in perspiration which is more or less profuse. The exacerbations are often, but not always, preceded by chilly sensations, and sometimes by a well-pronounced chill which may be accompanied by rigors. During the febrile exacerbations the cheeks frequently present a circumscribed flush and the eyes have a glistening appearance. The term hectic fever has long been applied to the febrile exacerbations which characterize progressive phthisis.

The febrile exacerbations sometimes occurring prior to the development of marked pulmonary symptoms may be supposed to be malarial manifestations. Recurring daily at or near the same hour, they may simulate closely the paroxysms of intermittent fever. A differential point is the existence of more or less fever between the exacerbations in cases of phthisis, whereas after a paroxysm of intermittent fever there is apyrexia. Another point is, the occurrence of exacerbations in cases of phthisis is generally after mid-day, whereas in the majority of cases of intermittent fever the paroxysms occur earlier. But of course the existence of phthisis is to be ascertained by means of the diagnostic symptoms and the physical signs. It is, however, to be borne in mind that phthisis and intermittent fever may be associated.

The profuse night-sweating which is a source of great discomfort in cases of phthisis has no fixed relation to the intensity of the fever which precedes it. The fever may be high and very little perspiration follow, and vice versâ.

Acceleration of the pulse and elevation of temperature may arise from an inflammatory complication, such as pleurisy, pneumonia, or peritonitis, and from the supervention of acute miliary tuberculosis.

To endeavor to explain the rationale of the acceleration of the pulse and the rise of temperature would require the consideration of the general pathology of the febrile state. The absorption of septic matter is probably a factor, but is hardly sufficient for a full explanation, and it would not be easy, with our existing knowledge, to explain the modus operandi of this morbific agent. The difficulty here, however, is not greater than in explaining the phenomena of fever when occurring in other pathological conditions. Here, as in other instances, there is no uniformity in the relative degree of acceleration of the pulse and the increase of temperature. The latter may be high without a proportionate disturbance of the circulation, and the reverse. Clinical experience shows a connection between a persistent high temperature and the waste of the body, and in proportion as the vital powers decrease the action of the heart is enfeebled, and a notably small and weak pulse denotes that death by asthenia is not far distant.

Thrombosis of the iliac vein on one side or on both sides is an occasional event in cases of advanced phthisis (marantic thrombosis). The effect is a considerable oedema of the lower limb or limbs. Oedema of both lower limbs, however, occurs as an effect of feebleness of the systemic circulation. If, as is sometimes observed, there be general dropsy, it denotes a renal complication, which is generally the waxy variety of chronic Bright's disease. Under these circumstances the urine is found to be albuminous.

Symptoms and Complications referable to the Hæmatopoietic System.—Pallor of the face is generally more or less marked from an early period in the history of phthisis, and it becomes, as a rule, more and more marked as the disease progresses. There is considerable variation in this respect in different cases. Impoverishment of the blood is in a great measure to be explained by the diminished ability to ingest and assimilate food. It is not, however, in all cases proportionate to defective alimentation, and therefore it is a fair inference that the disease in some other unknown way interferes with the blood-forming processes. Exceptionally, in some cases in which the disease is progressing, pallor is wanting. The complexion sometimes retains for a long time a rosy color. This is probably due to the condition of the vessels, and is not evidence of a normal condition of the blood. It is a noteworthy fact that notwithstanding the appearances denoting anæmia in cases of phthisis the venous hum in the cervical veins is, as a rule, wanting.

That the impoverishment of the blood is an effect of the disease, and that it does not contribute to the progress of the tuberculous affection, may be inferred from the fact that anæmic patients are not likely to become phthisical. This fact, which has already been stated, is established by clinical observation. Nor do the diseases relating to the hæmatopoietic system, anæmia being a prominent feature in all—namely, leucocythæmia, Hodgkin's disease, pernicious anæmia, and Addison's disease—involve any special liability to phthisis. Other intercurrent affections occasion death in these diseases when it is not due exclusively to the latter.

Symptoms and Complications referable to the Digestive System.—The opinion has been held that the development of phthisis is preceded and accompanied by appreciable disorder of the digestive system. This opinion is not sustained by the analysis of carefully-recorded cases. In many, and perhaps the majority of, cases at the time of the commencement of the phthisical affection the appetite is not notably impaired and the digestive functions appear to be well performed. Sooner or later, however, the appetite fails. This symptom may be marked when the food which can be taken does not occasion evidence of indigestion. Different cases differ very much as regards the degree of anorexia. It is marked in the cases in which there is notable increase of temperature and acceleration of the pulse. It is often invincible; that is, not only is the desire for food wanting, but there is a degree of repugnance which renders it impossible for the patient to take it. It is intelligible that in these cases emaciation and exhaustion must be progressive. It is not more easy to give a pathological explanation of anorexia as an effect of phthisis than when the symptom occurs in connection with other diseases not involving either inflammation or any ascertained structural affection of the digestive organs. The symptom is probably connected with morbid changes within the gastro-intestinal or peptic glands.

Vomiting is a rare symptom in cases of phthisis, except it be produced sympathetically in paroxysms of coughing. As thus produced it is not rare. It is of importance from its interference with alimentation.

Diarrhoea is a frequent symptom. It may be due either to intestinal indigestion or to a subacute enteritis or colo-enteritis thereby induced. A waxy or fatty affection of the liver may conduce to diarrhoea by interference with the digestion of certain alimentary principles. If, however, the diarrhoea be persistent, it points to intestinal ulcerations. These are usually seated in the Peyerian and solitary glands within the small intestine, but not infrequently they are found after death in the large intestine, and in the small intestine above the portion in which the Peyerian glands are situated. The number and extent of the intestinal ulcers found after death do not always correspond to the prominence of diarrhoea as a symptom. They cannot be excluded by the fact that this symptom is not prominent. The presence of pus and blood in the dejections is evidence of ulcerations. If the ulcers be situated high up in the intestinal tract, the pus and blood may have undergone changes which render them unrecognizable by the naked eye, and the microscope is necessary to demonstrate their presence. The diarrhoea is often accompanied by griping or colic-like pains. In proportion as diarrhoea is prominent it contributes to emaciation and exhaustion. These effects are expressed by the term colliquative, which has long been applied by medical writers to exhausting diarrhoea and perspirations occurring in cases of phthisis.

Peritonitis occurs in phthisis as an acute and as a chronic affection. When acute, it is caused by intestinal perforation incident to ulcerations; this is a rare accident. It is to be inferred whenever the symptoms denote rapidly-developed acute peritoneal inflammation. The peritoneal sac contains intestinal gas. Perforation is excluded if percussion shows dulness or flatness over the site of the liver. The normal hepatic dulness or flatness on percussion is always abolished if the peritoneal cavity contains gas. A tympanitic resonance over the liver, on the other hand, is not evidence of the presence of gas within the peritoneal cavity, inasmuch as this resonance may be conducted from the transverse colon distended with gas. Peritonitis from perforation is speedily fatal. In a chronic form the peritonitis may be preceded by an eruption of miliary tubercles in this situation, or the inflammation may have proceeded from intestinal ulcerations, perforation not having taken place. The local symptoms of chronic peritonitis are often not marked. The diagnosis is to be based on pain, tenderness, muscular rigidity, and the signs denoting liquid within the peritoneal sac. A chronic peritonitis may be associated with a small pulmonary affection which may not actively progress, and under these circumstances the peritoneal complication may be tolerated for a considerable period.

Peritoneal fistula may be reckoned among the complications referable to the digestive system. It occurs sufficiently often in cases of phthisis to show some pathological connection. Analysis of cases in which it occurs affords no evidence of its having an untoward influence on the course of the phthisical disease. On the other hand, there is ground for the opinion generally held that it either occasions or betokens slowness in the progress of the pulmonary affection. It follows that it is unwise to attempt to effect a cure by surgical interference. The characteristic bacilli have been found in the matter derived from peritoneal fistula, showing that this affection is tuberculous in character.

Symptoms and Complications referable to the Nervous System.—The symptoms referable to the nervous system relate to the mind. The mental faculties in most respects remain intact, except that in proportion to the general feebleness there is diminished ability to continue their exercise. The integrity of the intellect, with one exception, often remains up to the last moment of life. A marked characteristic of the disease, however, is a delusion in respect to improvement and recovery. In spite of the progressive emaciation and debility, which are obvious to every one, patients are apt to believe that their condition is becoming more and more favorable and to feel confident of restoration to health. Even medical men affected with phthisis manifest the same delusive ideas. So strong is the determination in some cases to keep up the delusion that the statements of patients in regard to their symptoms cannot be relied upon. They are sometimes offended if the physician feels it to be his duty to intimate danger. On the other hand, when patients are convinced of the nature of the disease, and that they have not long to live, as a rule they become quickly and completely reconciled thereto. Perhaps there is no other chronic disease in which the near approach of death is generally regarded with greater complacency.

Cephalalgia, delirium, and coma are symptoms which are developed in a few cases. They denote tuberculous meningitis. This is a very rare complication in the adult. When it has given rise to the symptoms just mentioned a speedy fatal termination is to be expected.

Symptoms and Complications referable to the Genito-urinary System.—Tuberculous disease of the kidneys, testicles, ureters and the prostate gland is sometimes secondary to pulmonary phthisis. The local symptoms will depend on the situation and amount of the tuberculous product, together with the destructive changes to which it gives rise. The consideration of the anatomical conditions and the symptomatology falls properly under the head of diseases of the genito-urinary system.

As already stated, the variety of chronic Bright's disease known as the amyloid or waxy is an occasional complication in cases of phthisis. The other varieties may coexist, but the coexistence is rare. There is no tendency in phthisis to these affections, and, on the other hand, they do not involve any predisposition to phthisis.

As regards functional disorders of the genito-urinary system, there is nothing noteworthy which pertains to the urine. From the readiness with which often phthisical patients of either sex enter into the marital relation it may be inferred that the disease does not for a considerable period extinguish the sexual instinct. By interrogating a considerable number of patients Louis was led to conclude that in men the disease has an erotic influence.¹² Phthisical women do not readily conceive, but pregnancy is not extremely infrequent. They may give birth to healthy children. During the course of phthisis the menses, as a rule, cease, but they continue in some cases up to a late period in the history of the disease. When suspended early they may return if the disease become non-progressive. That the cessation of the menses has an unfavorable influence on the tuberculous affection is a popular error. Nothing is gained by efforts to bring about their return. Their cessation, however, is not a good omen, and their return has a favorable significance.

¹² Recherches sur la Phthisie.

MORBID ANATOMY AND PATHOLOGY.—In the definition of the common form of pulmonary phthisis were embraced the leading anatomical characteristics of the disease. For a full account of these, together with the changes referable to peribronchitis, periarteritis, endoarteritis, secondary pleuritis, and bronchitis, as well as for histological appearances, the reader is referred to treatises on morbid anatomy. The practical objects of this article will be fulfilled by stating the abnormal physical conditions incident to the morbid changes in different cases and at different periods in the same case, and by a statement of the anatomical points involved in the general pathology. Knowledge of the abnormal physical conditions is essential with reference to physical signs and the diagnosis. It has also an important bearing on the prognosis, and is not without importance in its relations to the treatment.

Certain anatomical facts may be premised, as follows: The pulmonary affection begins at or near the apex of one lung in the vast majority of cases; exceptionally it begins at the base of one lung. The affection extends from the apex downward. The extension is not continuous in respect of time, but a series of tuberculous deposits or eruptions takes place at different epochs after variable intervals. Hence it is that different sections of one lung may show all the changes which intervene between a fresh deposit and tuberculous cavities. As a rule, not long after the affection begins in one lung the other lung is affected. This rule is so constant that, although both lungs are not affected simultaneously, the affection may be said with propriety to be bilateral. The constant occurrence of secondary circumscribed pleurisies and bronchitis has been stated under the head of Pulmonary Complications.

At an early period of the disease the marked changes appreciable by physical signs usually consist of a few hardened patches or nodules varying in size from that of a pea to that of a filbert, situated at or near the apex of one lung. The physical signs are those of slight solidification—namely, some dulness on percussion, increase of vocal resonance, and broncho-vesicular respiration. The presence of the morbid deposit causes circumscribed bronchitis affecting the smaller tubes, and this complication may give rise to subcrepitant râles within the area of the tuberculous affection. The disease may end with no further increase or extension of the local affection, this termination resulting either from self-limitation or from the agency of treatment. Of this fact I have proof from cases not only studied during life, but in which appearances were noted after death. The ending of the disease and recovery after a small tuberculous deposit occur oftener than is generally supposed.

An increase and an extension of the phthisical affection occasion larger areas and also a greater degree of solidification. As the amount of increase and extension within a given period varies very much in different cases, it follows that there is nothing like uniformity in these respects. Generally, the solidified portions of the lung form islands between which the tuberculous deposit is wanting. Between these islands the lung not infrequently becomes emphysematous. This vicarious emphysema explains the existence of a vesiculo-tympanitic resonance in some cases notwithstanding the solidification. Exclusive of that sign, as thus accounted for, the solidification causes a dulness on percussion proportional in degree and extent to the solidified portion of lung. The auscultatory signs of solidification are generally present—namely, either bronchial or broncho-vesicular respiration, and bronchophony or increased vocal resonance, according to the degree of solidification. The existence of bronchitis over a larger extent is represented by more abundant and coarser moist bronchial or bubbling râles. These râles do not, as has been supposed, necessarily denote that softening of the tuberculous deposit has taken place. Dry circumscribed pleurisies occurring from time to time, even from the very commencement of the phthisical affection, may give rise to a pleuritic friction murmur. The escape of the liquefied tuberculous deposit into the bronchial tubes by ulceration, added to the products of the bronchial inflammation, occasions an increase of the bubbling râles. Moreover, the liquefied tuberculous deposit is better suited for the production of bubbling sounds than the products of bronchial inflammation. Hence the abundance of the bubbling râles, taken in connection with the characters of the matter of expectoration, is evidence of the escape of liquefied tuberculous deposit.

If phthisis be progressive, the physical conditions already enumerated—namely, solidification, liquid in the bronchial tubes, pleuritic exudation—continue. They are present in both lungs. Associated with these conditions are cavities. The cavities formed in different cases differ greatly in size and number. They differ also as regards the number and the size of the openings by which they communicate with the bronchial tubes. The latter conditions are of importance with reference to the free discharge of the contents of cavities and the production of certain physical signs. Enumerating here the cavernous signs, they are—tympanitic resonance within a circumscribed space, frequently with amphoric or cracked-metal intonation, cavernous and sometimes amphoric respiration, increased vocal resonance, cavernous whisper, pectoriloquy in some instances, and, as a rare sign, metallic tinkling. An accumulation of liquid within a cavity which has free communication with the bronchial tubes gives rise to the cavernous sign called gurgling. I have met with an instance in which a loud splashing sound was produced within a cavity synchronous with the impulse of the heart, and due to the agitation of the cavity by the cardiac movements. Owing to the association of cavities with solidified portions of lung, the latter varying greatly in different cases in the extent and the degree of solidification, with the cavernous signs are combined those which represent varying degrees of solidification—namely, either dulness or flatness on percussion, either bronchial or broncho-vesicular respiration, and either bronchophony or increased vocal resonance.

In the physical conditions incident to pulmonary complications of phthisis—namely, pleurisy with effusion, perforation of lung with pneumo-hydrothorax—the reader is referred to the article on DISEASES OF THE PLEURÆ.

With reference to the general pathology of phthisis, points relating to the morbid anatomy are to be considered. There are two distinct varieties of morbid product in cases of phthisis—namely, the miliary granulations and the infiltrated deposit formerly distinguished as crude tubercle. Laennec taught that these are only varieties of essentially the same morbid product, the former being preliminary in their occurrence to the latter. Following Virchow, some late writers have restricted the application of the term tubercle to the miliary granulations, regarding the infiltrated deposit as a non-tuberculous inflammatory product. Histological investigations have failed to establish an essential distinction between the two varieties. The fact that they are so constantly associated shows some close pathological connection. Both varieties undergo the same degenerative changes. Each is found by inoculation to produce tuberculous disease in certain animals. Moreover, according to the late researches of Koch and others, each contains the characteristic parasite, the bacillus tuberculosis. In view of these considerations, the doctrine of Virchow, advocated by Niemeyer and others, is not tenable, and, as already stated under the head of the Definition and Classification of pulmonary phthisis, the term tuberculous is properly applied to both varieties. There is no such affection as a non-tuberculous pulmonary phthisis. The terms pulmonary phthisis and pulmonary tuberculosis are now, as heretofore, to be regarded as synonymous.

That the pathology of pulmonary phthisis involves a predisposition or a tuberculous diathesis has been already shown by facts pertaining to the etiology. It does not in the least invalidate this logical conclusion that in the present state of our knowledge pathologists are unable to explain this diathetic condition; that is to say, in what it consists. Its recognition is not merely a matter of speculative or theoretical interest; it has an important bearing upon a rational prophylaxis and on the treatment of phthisis.

Up to a very recent date the opinion has generally been held by pathologists that the local phthisical affection may be determined entirely by a tuberculous cachexia—that the latter, in other words, may produce the affection exclusive of any local extrinsic cause; and the question has been much discussed whether or not at the outset the phthisical affection is an inflammation. But if the parasitic doctrine be accepted, a local causative agent derived from without—namely, the bacillus tuberculosis—is essential, the predisposition or the cachexia consisting of certain unknown conditions which are required for the development and the multiplication of the parasite. According to this doctrine, the extension of the local affection is due to invasions successively of different portions of the lungs, and the development of tuberculous disease in other situations is due to the migrations of this parasite. Without the presence of the bacillus, no matter in how great degree the required conditions may exist, phthisis will not occur.

Inflammatory processes, however, accompany and follow the development of the tuberculous affection. Bronchitis, peribronchitis, periarteritis, endoarteritis, interstitial pneumonia, and pleurisy are terms which denote inflammation. To these are to be added ulceration and suppuration within cavities. The infiltrated tuberculous deposit is to be regarded as an inflammatory exudation. There is an intrinsic propriety, therefore, in calling it a pneumonia. But the behavior of this deposit differs widely from that of the exudation in lobar pneumonia. In the latter affection it is readily absorbed and disappears, leaving the pulmonary structure intact, whereas in phthisis it is absorbed with difficulty, and in most cases leads to more or less destruction of the pulmonary structure. For these reasons, irrespective of histological points of difference, the term tuberculous should be used to distinguish the exudative pneumonia which is characteristic of phthisis. The term desquamative pneumonia was proposed by Buhl. The so-called cheesy degeneration of the tuberculous products—a necrotic, not an inflammatory, process—was considered by Laennec as a distinctive mark of the products. This doctrine has been disproved. Other morbid exudations and growths may undergo similar degenerative changes.

DIAGNOSIS.—It is evidently very desirable to recognize the existence of phthisis at as early a period as possible with reference to the adoption of measures with a view to prevent the further development and progress of the disease. It is also very desirable, if practicable, to determine that phthisis does not exist; that is, by the absence of diagnostic points to exclude it. Difficulty of diagnosis relates almost exclusively to an early period when the phthisical affection is small. The diagnostic points pertaining to the symptoms and the physical signs in the incipiency of the disease therefore especially claim attention.

A cough of more or less duration, which was at first slight and dry, gradually increasing and accompanied by the expectoration of mucus, should always excite a suspicion of phthisis, especially if the patient's age be between twenty and thirty years. This is not the history of a chronic primary bronchitis. A cough as just described should never be considered as nervous or sympathetic without due investigation. It should not be attributed to pharyngitis, although the latter affection is found to exist. Want of breath on exercise is a symptom pointing to something more than a bronchial or pharyngeal affection. The import of these symptoms is still greater if, after the commencement of the cough or from an earlier date, there has been decrease in weight and strength. Their significance is much increased by the occurrence of hæmoptysis. Hæmoptysis followed by a persistent cough, and still more if cough preceded its occurrence, is always presumptive evidence of a phthisical affection. Occurring without having been preceded by cough, and when cough does not immediately follow, it should suggest the probability of phthisis. In the larger proportion of cases under these circumstances it is a forerunner of the diagnostic symptoms and signs of the disease. In connection with the cough a persistent increase of the temperature of the body is an important diagnostic symptom. Chilly sensations and flashes of heat are symptoms of some importance. Especially significant are pleuritic stitch-pains referable to the upper part of the chest or beneath the scapula, these being symptomatic of the circumscribed dry pleurisies which may occur at an early period of the disease. Impaired appetite, pallor of the face, and a tendency to perspire during sleep have much significance taken in connection with the pulmonary and other symptoms.

A positive diagnosis must rest on physical signs, together with more or less of the foregoing symptoms. The physical conditions which furnish the diagnostic signs are solidification of a small portion or of small portions of lung, usually at or near the apex, the presence of mucus in the small-sized bronchial tubes, and perhaps fibrinous exudation on the pleural surface within a circumscribed area corresponding to the solidified portion or portions of lung. The signs furnished by these conditions are slight dulness on percussion, a broncho-vesicular (formerly called rude or harsh) respiration, some increase of vocal resonance and of the whispered voice, subcrepitant râles, and perhaps a grazing friction murmur. It may be important to consider the physical signs of phthisis with some detail. Aside from their importance, a reason for this is that terms by which some signs are designated are not used in precisely the same sense by all medical writers.

A small phthisical affection gives rise to slight or moderate dulness on percussion. In order to appreciate this sign if the dulness be slight, attention should be paid to the pitch of the resonance as well as to the lessened intensity of resonance. The pitch is always raised. By attention to the latter character, in conjunction with the diminution of intensity, a degree of dulness may be sometimes appreciated which, without attention to the pitch, might not be determinable.¹³ In determining abnormal dulness in the infra-clavicular region on one side, the normal disparity between the two sides of the chest in this region must be taken into account. The resonance at the right summit, as compared with that of the left summit, is, normally, somewhat dull. Hence it is not as easy to make out an abnormal dulness at the right as at the left summit. If the relative abnormal dulness at the right summit be but slight, the question is whether there be more than a normal disparity. This question is rendered difficult by the fact that the degree of normal disparity varies somewhat in different healthy persons. In cases of doubt little reliance is to be placed on this sign alone, but it is to be taken in connection with auscultatory signs.

¹³ The author was the first to indicate the fact that dulness is always associated with elevation of pitch. Vide "Prize Essay on Variations of Pitch in the Sounds obtained by Percussion and Auscultation," Transactions of the American Medical Association, 1852.

With reference to the auscultatory signs in cases of phthisis, it is to be premised that often, owing to the importance of studying the sounds derived from a limited area and of localizing morbid conditions, the use of the stethoscope is indispensable. It is impossible to meet all the requirements of physical diagnosis by immediate auscultation. After an experience of more than a quarter of a century the writer would advise the binaural stethoscope in preference to any other. For the benefit of those who are not practically familiar with this instrument, it should be added that in order to appreciate its advantages, the instrument, in the first place, must be properly constructed, and, in the second place, some practice is necessary. A sound produced within the instrument is at first an obstacle, but it is speedily overcome by use.¹⁴

¹⁴ The dissatisfaction with the binaural stethoscope so often comes from defects in its construction that it seems proper to refer to Tiemann & Co., and to Ford & Co., of New York as reliable makers of this instrument.

A small tuberculous solidification is represented by a broncho-vesicular respiration. This sign was named and described by me in 1856. The name takes the place of the terms rudeness, harshness, and hardness—terms which are not only inadequate, but convey an erroneous idea. Quoting from another work, the characters of the broncho-vesicular respiration and its comprehensive signification are as follows: "The sign represents the different degrees of solidification of lung between an amount so slight as to occasion only the smallest appreciable modification of the respiratory sounds, and an amount so great as to approximate closely to the degree giving rise to bronchial or tubular respiration. In other words, all the gradations of respiratory modifications caused by incomplete or an inconsiderable solidification are embraced under the name broncho-vesicular. The gradations correspond to the amount of solidification; that is, they show the solidification to be either very slight, moderate, or nearly sufficient to be regarded as considerable or complete. The sign is therefore important as evidence, first, of the existence of solidification, and, second, of the degree of solidification. Analyzing this sign, the most distinctive feature is the combination of the vesicular and the tubular quality in the inspiratory sound. These two qualities may be combined in variable proportions. The pitch of the sound is raised in proportion as the tubular predominates over the vesicular quality. The expiratory sound is more or less prolonged, tubular in quality, and the pitch raised. The prolongation of this sound, its tubular quality, and the raised pitch are proportionate to the predominance of the tubular over the vesicular quality in the inspiratory sound. If the solidification be slight, the characters of the normal vesicular respiration predominate; that is, the inspiratory sound has but a small proportion of the tubular quality, and is but little raised in pitch, the expiratory sound being not much prolonged, its tubularity not marked, the pitch not high. If, on the other hand, the solidification be almost enough to give a bronchial respiration, the inspiratory sound has only a little vesicular quality, the tubular quality predominating, the pitch proportionately raised, and the expiratory sound is prolonged, high, and tubular, nearly to the same extent as in bronchial respiration. The less the solidification the more the characters of the normal vesicular respiration predominate over those of the bronchial respiration; and, per contra, the greater the solidification the more the characters of the bronchial predominate over those of the normal vesicular respiration."¹⁵ By means of the broncho-vesicular respiration a slight morbid solidification may be recognized in one of the infra-clavicular regions or over the scapula. Here, however, as with regard to percussion, an allowance is to made on the right side for a normal disparity. The respiratory sounds on the right side at the summit, as compared with those at the left, have normally the characters more or less marked of a broncho-vesicular respiration. These characters are more marked as the stethoscope is brought toward the sternum. Hence a small solidification of lung is more easily ascertained by auscultation at the left than at the right summit.

¹⁵ Vide Manual of Auscultation and Percussion, by the author; also, paper contained in the Transactions of the International Medical Congress, London, 1882. The broncho-vesicular respiration was called by Skoda indeterminate (unbestimmt), and this term is still used by German writers. These sounds are not indeterminate if the characters derived from pitch and quality be analytically studied; they are sounds intermediate between the normal respiratory murmur and bronchial respiration.

Not infrequently in cases of incipient phthisis the respiratory sounds at the summit on the affected side are so weakened that their characters cannot be studied. Weakness of the respiratory murmur in these cases becomes a diagnostic sign taken in connection with other signs.

A small tuberculous deposit may increase the vocal resonance. But, again, a normal disparity between the two sides must be allowed for. The normal vocal resonance is always greater on the right side. If, therefore, it be a question as to the existence of a small tuberculous affection at the right summit, it is to be decided whether the disparity be greater than normal. A small tuberculous deposit at the apex of the left lung, on the other hand, may not increase the resonance to an equality with that at the right summit.

Attention should be paid to the whispered voice, and, still again, the two sides show a normal disparity. The sound heard with the whispered voice, which may be distinguished as the normal bronchial whisper, is louder on the right than on the left side, and somewhat higher in pitch on the left side, at the summit of the chest. If at the right summit it exceed the normal disparity, and the pitch be higher than at the left summit, the sign may be distinguished as increased bronchial whisper, and it denotes solidification. If, on the other hand, the sound at the left summit be louder than that of the right summit, there is increased bronchial whisper, representing the solidification at the apex of the left lung.¹⁶

¹⁶ The different abnormal modifications of sounds produced by the whispered voice were first named and described by the author. Vide Manual of Auscultation and Percussion.

The normal points of disparity at the summit of the chest render the diagnosis of incipient phthisis by means of alterations in the resonance on percussion, the respiratory sounds, the vocal resonance, and the whispered voice a problem in some cases of not a little difficulty. In these cases an examination of the sputa for the presence of the tuberculous parasite may furnish proof of the existence of the disease. This proof may in some instances be obtained when the physical signs, together with the symptoms, do not render the diagnosis positive, and it may be sought for in order to corroborate the evidence derived from other sources. The author can testify from considerable experience to the value of an examination of sputa for bacilli in cases in which the diagnosis is not rendered positive by other signs and by symptoms. It must, however, be borne in mind that the absence of bacilli in the sputa is not sufficient to exclude phthisis, especially if but a single examination be made. In doubtful cases, if an examination of the sputa be negative, the examination should be repeated. The weight of evidence against the existence of phthisis is, of course, greater in proportion to the number of examinations with negative results.¹⁷

¹⁷ The following method of staining the bacilli tuberculosis in the sputum is essentially that recommended by Ehrlich in the Deutsche medicinische Wochenschrift, Mai 6, 1882:

It is important that the sputum to be examined should be derived from the lungs, and should not be solely that from the upper air-passages. A small opaque particle from the sputum is to be pressed between two cover-glasses, so that when these are drawn apart a thin film will remain upon each. Each cover-glass, as soon as the film is dry, is to be passed, with the preparation upward, rather rapidly three times through the flame of a Bunsen's burner or of an alcohol lamp. The preparation is now ready for staining.

A small quantity of water in a test-tube or flask is now shaken with an excess of aniline oil (which need be only in small amount), and after a few moments is filtered through moistened filter-paper. To the clear filtrate thus obtained is to be added, drop by drop, a saturated alcoholic solution of fuchsin (gentian-violet, methyl-violet, and several other aniline colors may be substituted) until the fluid begins to be opalescent, showing that it is saturated with the coloring agent. In this manner an alkaline-aniline staining solution is prepared.

Into this staining solution the cover-glasses, having the dried films of sputum prepared as above described, are dropped, preferably so that they will float with the preparation downward. Here they remain from a half hour to twenty-four hours. If taken out in a short time, the fluid, at least for a time during the staining process, should be heated moderately over a water-bath, and in any case the process of staining is accelerated and rendered more certain by heating.

After removal from the staining fluid the cover-glass is washed for a few moments in water, and is then dipped into a mixture of one part of pure nitric acid (it should contain no nitrous acid) to about three or four parts of water. Here it remains only a few moments, when it will be found that the preparation has lost its color, although a part will be restored by the subsequent washing in water, which should be done at once. If the preparation has not been sufficiently decolorized, it may be placed again in nitric acid, but it is not necessary or desirable that it should remain there many minutes. The object of the nitric acid is to extract the color from all but the tubercle bacilli.

The preparation may now be at once examined either in glycerin or (after drying or after treatment with alcohol and oil of cloves) in balsam. Ehrlich recommends, previous to this, a staining of the background with some color other than that of the bacilli; thus, with methyline blue if the organisms are stained red with fuchsin. This staining of the background, however, is not necessary. While the ideal method of studying the stained bacilli is by means of Leis's oil-immersion lenses and Abbé's illuminating apparatus, they can usually be seen readily enough with the high powers in ordinary use, such as the one-fifth or one-sixth inch objectives of our American microscope. After staining with fuchsin the bacilli appear as short rods of a red color, frequently curved or bent.

The adventitious sounds which have been mentioned—namely, the subcrepitant râle and the pleural friction murmur—sometimes afford valuable aid in the diagnosis. Taken in connection with the direct signs obtained by auscultation and percussion, these accessory signs when present make the diagnosis positive: they are by no means uniformly present, and therefore their absence is not proof against the existence of a phthisical affection. To these accessory signs another sign may be added—namely, an abnormal transmission of the heart-sounds within one of the infra-clavicular regions. In the middle of this region there is nearly an equal transmission of these sounds normally. Comparing the two sides as regards the two sounds respectively, the first sound is a little louder on the left, and the second sound a little louder on the right side. Now, with a little solidification the sounds may be better transmitted, so that they are abnormally loud on the affected side.

A decision that there is no physical proof of phthisis must rest on the absence of all the foregoing signs after repeated examinations of the chest.

It is not to be concluded that for a positive diagnosis of incipient phthisis all or most of the foregoing diagnostic signs must be recognized. They are not all present in all cases. Two or three of these signs, and even a single one if well marked and associated with diagnostic points pertaining to the symptoms and history, may suffice for a positive diagnosis.

It is an interesting question how small a portion of solidification may furnish signs sufficient for a diagnosis. I have the records of two cases bearing on this question. A patient came under my observation at Bellevue Hospital in 1867. In the right infra-clavicular region the respiration was abnormally broncho-vesicular, the vocal resonance was increased, and there was increase of the bronchial whisper within a small circumscribed space. On these signs was based the diagnosis of a small tuberculous deposit. The case served to illustrate the signs just named to classes for practical instruction in auscultation and percussion. The patient, who was employed as a helper in the apothecary's shop, died suddenly from taking by mistake an overdose of the fluid extract of aconite. The autopsy showed at the apex of the right lung a nodule of the size of a filbert, no tuberculous deposit being elsewhere found.

A recent medical graduate, twenty-two years of age, had cough and two attacks of hæmoptysis. His father and a sister had died with phthisis. There was slight dulness on percussion on the summit of the chest on the left side, with crepitation at both summits. These were the only signs noted. This case was included among the cases of recovery reported in my work on phthisis published in 1875. He enjoyed excellent health and was notably vigorous for twenty-eight years. Death took place in 1880 from disease of the heart and kidneys. The autopsy showed at the apex of each lung a small indurated portion somewhat larger on the left than on the right side. Elsewhere there was no appearance denoting present or past pulmonary disease.

It is in only a small proportion of cases that, when patients first come under medical observation, the phthisical affection is so small as to render the diagnosis difficult. The tuberculous solidification is generally sufficient to give rise to well-marked signs. The shrinkage of the lung at the apex from interstitial growth and diminished capability of expansion may have caused a small infra-clavicular depression and restricted respiratory movements in this region. The dulness on percussion is readily recognized. The characters of the broncho-vesicular respiration are easily determined. The increase of vocal resonance and increased bronchial whisper admit of no doubt. With these signs, oftener than at an earlier period, are associated accessory signs—namely, subcrepitant râles and bubbling in larger tubes, pleuritic friction murmur, and undue transmission of the heart-sounds.

At a somewhat later period, and sometimes even when cases are first observed, the physical signs denote a still greater degree of solidification. Infra-clavicular depression and restricted movements on one side are marked. The respiration is bronchial and the voice bronchophonic. There may be pectoriloquy with the bronchophonic characters, showing that the speech is transmitted through solidified lung.¹⁸

¹⁸ Bronchophony is to be understood as a sign distinct from increased vocal resonance. In bronchophony the resonance may or may not be increased. Intensity is not a character of this sign. Its distinctive characters are concentration of the voice sound, nearness to the ear, and elevation of pitch. The terms concentration and nearness to the ear properly express what was intended by Laennec in the words "la transmission évidente de la voix à travers le stethoscope." Pectoriloquy is to be distinguished from bronchophony. These two terms are sometimes confounded. Bronchophony is transmission of the voice, pectoriloquy the transmission of speech—that is, articulate words.

Exceptional cases are to be referred to in which over lung containing solidified portions from tuberculous deposit dulness on percussion is wanting. Not only is dulness wanting, but the resonance is greater than normal. The resonance is altered in character. With an increase of intensity the quality is in part tympanitic and the pitch is raised. This is the sign described by me many years ago under the name vesiculo-tympanitic resonance. The distinctive characters are those just mentioned—namely, increase of intensity, the quality a combination of the vesicular and the tympanitic, and more or less elevation of pitch. The name vesiculo-tympanitic expresses these characters. It is the sign of pulmonary emphysema. It denotes that portions of lung situated between islands of solidification have become emphysematous. The emphysema is vicarious; that is, supplementary to the shrinkage of the portions solidified, and, added thereto, probably collapsed lobules. Were one to be governed by percussion alone in the physical diagnosis, this sign would in some cases mislead. The liability to error is avoided by taking due cognizance of the associated signs furnished by auscultation.

In cases of advanced phthisis cavities are added to tuberculous solidification. It is desirable to recognize the existence of these. In most instances the signs which may be distinguished as cavernous suffice for the recognition of cavities. The cavernous signs are furnished by percussion and by auscultation of the respiration and of the voice.

A purely tympanitic resonance within a circumscribed space points to a cavity, but a tympanitic resonance with either an amphoric or a cracked-metal intonation is more especially a cavernous sign. An amphoric or a cracked-metal resonance over a cavity may often be obtained by observing certain rules in percussion—namely, percussing with a single and rather forcible blow, the mouth of the patient being open and brought close to the ear. These signs may be rendered still more distinct by means of the binaural stethoscope, the pectoral extremity being close to the patient's opened mouth, an assistant making the percussion. These cavernous signs are not present when cavities contain much liquid or when communication with the bronchial tubes is temporarily obstructed; hence the signs are sometimes present and sometimes absent.

There is a distinctive cavernous respiratory sign. This assertion is called for by the fact that the existence of the sign is not as yet recognized by all medical writers. According to Laennec, the respiratory sounds derived from cavities resemble the bronchial respiration. From his description it would be impossible to distinguish the former from the latter. Skoda considered the cavernous and the bronchial respiration as absolutely identical; and this view is held by German writers at the present time. Walshe indicated an essential differential point pertaining to the inspiratory sound in cavernous respiration—namely, its low pitch. The fact that in purely cavernous respiration the pitch of the expiratory is lower than that of the inspiratory sound was stated by me in 1852.¹⁹ The distinctive characters of the cavernous respiratory sign as then indicated were as follows: An inspiratory sound low in pitch and non-tubular in quality, followed by an expiratory sound still lower in pitch and non-tubular. The quality of the sound in inspiration and in expiration may be said to be blowing, after the term soufflante used by Laennec, but applied by him to a sound either bronchial or from a cavity, when the air seems to be drawn from the ear of the auscultator.

¹⁹ Vide "Prize Essay."

Appreciating clearly the characters which are distinctive of cavernous respiration, it is impossible to confound this sign with bronchial respiration, both the inspiratory and the expiratory sound in the latter sign being high in pitch and tubular in quality. This cavernous sign approaches much nearer to the normal vesicular respiration. The only distinction between these two signs is the presence of the vesicular quality in the latter and its absence in the former. Hence, the only liability to error is in confounding the two. This error can only be committed when the respiratory murmur is so feeble that the vesicular quality is not readily appreciable. In order to avoid the error, the respiration should not be pronounced cavernous when the sounds are quite weak, except there be present other correlative cavernous signs.

Cavities are often situated in close proximity to lung solidified by tuberculous deposit or interstitial pneumonia: cavernous respiration and bronchial respiration are then in juxtaposition, and their differential characters are rendered very distinct by contrast. Under these circumstances, however, the cavernous respiration is sometimes modified by combination with the characters of the bronchial respiration. Not infrequently a cavernous inspiration is joined to a bronchial expiration, the more intense expiratory sound representing adjacent solidification extending over the site of the cavity and drowning the weaker cavernous expiration. In another mode of combination the inspiratory sound is bronchial at the beginning and cavernous at the end. Here the cavernous sound occurs a little later than the bronchial, and the latter is supplanted by the former. This variety of broncho-cavernous respiration has been recently described by Seitz under the name metamorphosing respiratory murmur (metamorphosirendes athmungs geräusch). In like manner, the characters of the cavernous and of the normal vesicular respiration may be combined. This combination may be expressed by the term vesiculo-cavernous respiration.

The effect of a cavity upon vocal resonance is to increase its intensity without giving rise to the characters distinctive of bronchophony—namely, nearness to the ear, concentration, and elevation of pitch. Increased vocal resonance, and not bronchophony, is therefore a cavernous sign. If bronchophony be present over a cavity, it denotes adjacent solidification of lung. With the vocal resonance more or less increased the vocal fremitus appreciable on auscultation is often intensified.