constant, and becomes less and less manifest in proportion as the disease advances. Now, though Hasse makes no allusion to the subject, we are disposed to think that much of the difference of character presented by the effused fluids in the earlier periods of pleurisy depends on the implication or non-implication of the external sub-serous tissues. The statement of Gross regarding the changes presented by the serous membrane in the early stages is meagre in the extreme, and in many respects incorrect. Hasse denies the existence of a dry stage of pleurisy, characterized, as it is believed, by a total suppression of secretion, and says, "I have never encountered this dry stage as described; having always, even at the very outset, found the serous fluid somewhat, however slightly, augmented in quantity, and marked by its deep yellow tinge and its increased consistency. There were likewise almost invariably present those grayish or yellowish points the initial and quickly expanding rudiments of membranaceous effusions." P. 184. Gross, however, adopts the more usual, and, we think, the more correct view, and states that, at first, there is "if not an entire suppression, at least a considerable diminution, of the natu ral secretion." The truth of the position maintained by Hasse, and many of the French pathologists, he thinks, is by no means established. One of the highest authorities in our own country, Dr. Hodgkin, coincides with Hasse, and states, in his 2d Lecture on the Serous Membranes, that, when turbidity of the serous effusion and false membranes "are not observed in persons who have died of suspected pleurisy, inflammation of the muscles or cellular membrane must, in most instances, have been mistaken for it," and further he says that, from his own experience, he cannot cite any case in which the inflammation, however remote, had not left some traces of its existence. If the inflammation have been "so rapid that no false membrane has been formed, we find an effusion of serum which, in the majority of cases, is sanguinolent or puriform." Analogy, however, is certainly in favour of a suppression of the ordinary secretions in the early stages of inflammation of a serous membrane.

Having portrayed the subsequent steps in the inflammatory process, Hasse enters on the consideration of the mode in which inflammatory products become organized. He justly observes, that as no one has yet been able to watch the movements of blood currents in inflammatory products during life, cadaveric phenomena are deserving of close investigation.

"With this intent, I have omitted no opportunity of removing false membranes of every description, either alone or together with the subjacent pleura; and, having first washed them carefully in cold water, proceeded at once to spread them on glass plates to dry. As the congested blood-canals in inflamed or newlyorganized textures, do not part with their contents to the larger veins, as in healthy parts, I have been able to furnish a series of preparations in which the course of at least the larger of the newly-formed branches is conspicuously shown by a surprisingly delicate distribution of blood-vessels.

"Wherever vessels had formed in the adventitious membranes, they proved to be continuations of the branches ramifying in the serous coat; they penetrated the false membrane at numerous points, and then branched out in a stellate manner, or formed into partly divergent, partly parallel, fascicular groups. Hodgkin describes them similarly. Such was the character of the vascular development, more particularly in the gelatinous form of exudation, which, in

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this respect, so nearly approaches the normal formative substance, as, after a short period, to display ramifications of vessels precisely similar to the parent ones, and, in all probability created in the manner witnessed by Döllinger in the embryo of fishes. I have repeatedly and very carefully taken up, upon pieces of glass, detached and floating fragments of the gelatinous product in question, and searched for independent vascular development, but in vain; and I feel convinced, that if such flakes should ever be found to contain blood-vessels, they must originally have clung to the pleura, and been severed subsequently." P. 195.

In less organizable false membranes, these processes do not take place so readily, and in these, Hasse considers the descriptions given by Laennec and Gendrin to be applicable. Where tubercular matter is effused with the more ordinary products, and does not prove rapidly fatal, it is occasionally met with as a residue of the aggregate morbid product in small scattered masses included between the pleuritic adhesions. These isolated masses are susceptible of farther transformations, which Hasse thus describes ::

"Most frequently, a deposition of phosphate of lime takes place little by little, until the whole is converted into a hard earthy concrement, constituting an irregular, rough plate, sometimes separable into two layers, which inclose an intermediate residue of the caseous, atheroma-like mass already alluded to. The plates in question are wont to adhere so firmly both to the parietes of the thorax and to the surface of the lungs as to prevent the two folds of pleura being distinctly recognized. These relations apply to most instances of so-termed ossifications of the pleura, which would seem, even where they form in the pleura itself, or in the cellular tissue external to it, to originate in inflammatory action (Hodgkin) The thin lamellæ occasionally found without any accompaniment of pleuritic adhesions, and the fibro-osseous tumours of the pleura, are obviously referable to a different source." P. 197.

We do not, however, see wherein lies the proof that these changes are referable to calcareous transformation of tubercular matter. Under the head of Empyema we have looked in vain for any corroboration of the important observations of McDonnell with reference to enlargement of the liver or the discharge of the purulent accumulations by the bronchial membrane, independent of any perforation.

The Chapter on Pneumonia, we are compelled to pass over, with the exception of the following passage, the practical importance of which our own experience has taught us :

"Drunkards are proportionately most prone to the disease, and, what is remarkable, it scarcely manifests itself in them by the usual vital symptoms, although spreading, and advancing to the last stage with astonishing rapidity." P. 216.

The next Chapter, entitled "Diseases of the Lung not necessarily dependent upon or allied to Inflammation," comprises gangrene, oedema, hæmoptysis, apoplexy, and the atelectasis of Jörg. Of hæmoptysis considered as a primary affection, Hasse admits four varieties, simple bronchial hæmorrhage, (or genuine hæmoptysis,) effusion of blood into the pulmonary vesicles, (apoplexy in a restricted sense,) hæmorrhage from rupture of the pulmonary texture, (pneumorrhagia,) and the most fatal form arising from rupture of the large blood-vessels. There can be no doubt that much unnecessary alarm is often occasioned by confounding simple bronchial

hæmorrhage with that which is symptomatic of incipient tubercular disease, and we fully agree with the following remarks:

"This kind of hæmoptysis is seldom fatal, unless when complicated with other morbid processes. It presents itself in its simplest and least hazardous form, in very plethoric individuals, during the years of puberty, generally ceasing spontaneously when the thoracic organs have become fully developed. There is more ground for alarm, when it occurs as a forerunner of menstruation, or as the reflex of hemorrhoidal ailment, in which cases the attacks often recur to an exhausting amount. Even here, however, it hardly by itself endangers life, however serious its immediate and remote consequences, (dropsy, &c.) Examples are indeed known of these bronchial hemorrhages acting vicariously for the menstrual or the regular hemorrhoidal flux, with greater or less violence, periodically, during a space of thirty or forty years, the patients at last succumbing under some other disease. Under these circumstances there is no real local disease, the lung being merely in a state of congestion, or, more correctly speaking of hyperæmia." P. 242.

The propriety of the term pulmonary apoplexy has been disputed, but Hasse very properly says that, in true apoplexy of the lungs, the effusion of blood into the air-cells, or into the general pulmonary texture, is attended with the loss of consciousness through sudden suspension of the main springs of vital action. In this sense, since the time of Hippocrates, the term apoplexy has been as applicable to the lungs as to the brain. Indeed, the prostration of the vital powers, from the first, forms the most striking characteristic of these cases, which are seldom accompanied by hæmoptysis.

The anatomical division of pulmonary apoplexy into that in which the effusion is thrown out into the air-cells, and that in which it is produced by rupture of the pulmonary texture, Hasse thinks is borne out by the etiological relations and by the vital symptoms. In true apoplectic effusions the blood, he believes, is thrown out from the twigs of the pulmonary artery directly into the air-cells of the smaller bronchial ramifications, and then becomes consolidated without any further change. The defined limits of the apoplectic centre are owing to the absence of rupture, the effusion being limited to a set of pulmonary cells, supplied by particular ramifications of vessels; in short, to a single lobule, whose covering separates the diseased from the healthy parts. The well-known connexion of pulmonary apoplexy with hypertrophy of the right ventricle, is certainly corroborative of this view, and against the notion which Hasse, and we believe Rokitansky also, controverted, viz., that the apoplectic clot is formed by the reflux of blood from the bronchia. Moreover, by the theory of Hasse, the dark black colour of the clot is accounted for by the complete exclusion of the air.

Under the head of Atelectasis of the Lungs will be found a very good account of that peculiar pulmonary affection of children, the inflammatory character of which Hasse very successfully controverts. We think, how. ever, that we are as yet scarcely in a condition to affirm with confidence that it is nothing more than imperfectly expanded lung. We cannot find that Gross has more than a passing allusion to this interesting morbid condition. Diseases of the Air passages are next considered. Under the head of Catarrh, acute or chronic; we have not found anything specially deserving of notice. The following remarks, however, are of practical value :

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"It is remarkable that senile catarrh, by determining a continued irritation to the respiratory organs, causes morbid predisposition to unfold itself there,or disease, elsewhere existing, to throw itself upon the lungs. Thus in the very individuals, who in their youth had been scrofulous, but then escaped,—perhaps even recovered from tubercular disease by means of repeated catarrh and its sequelæ, bronchial dilatation and pulmonary emphysema, we find, in the decline of life, catarrh productive of tubercular development, and even of phthisis. We have already seen what an ascendency gout exercises over catarrh. In like manner hemorrhoidal disease,-which at the age of manhood is prone to manifest its periodical exacerbations by hemorrhage from the rectum,-sometimes gives rise, under the influence of catarrhal irritation, to repeated bronchial hemorrhage. In females, at the period of menstrual decline, catarrh probably leads to similar accidents." P. 269.

After pointing out the various causes inducing those very serious and fatal forms of angina termed oedematosa, Hasse observes that it was probably in consequence of Bayle having noticed only the latent forms depending on mechanical obstruction to the circulation, from long-standing disease in the contiguous parts, and where the oedema is the result of exhaustion, diminished vascular and nervous energy, rather than of inflammation, that this pathologist characterised œdema of the glottis as essentially uninflammatory. The disease is comparatively rare, and our readers may therefore be glad to have Hasse's account of the post-mortem ap

pearances.

"The whole of the mucous membrane between the root of the tongue and the glottis, is uniformly tumefied, so that the outlines of the epiglottis and arytenoid cartilages, together with the numerous folds and recesses in the vicinity of those parts, have become effaced.

"This is the result of inflammatory effusion into the interspaces of the loose cellular texture, subjacent to the mucous membrane. In proportion to the intensity and duration of the inflammatory process, this exudation is sometimes of a purely serous and liquid nature, so as to flow away upon incision; sometimes blended with coagulable materials, and jelly-like; sometimes again mingled in various proportions with pus; sometimes wholly purulent. Hence the tumour, which is always soft, lax, and tremulous, like jelly, varies greatly in colour, being of a pale or of a reddish yellow,—sometimes of a dingy yellow or grayish white, and more or less opaque,-but for the most part superficially dotted with red. The swelling being dependent upon infiltration of the sub-mucous cellular texture, cannot extend to the inferior surface of the epiglottis, because, there, no layer of cellular tissue exists; hence the epiglottis has the aspect of having both its lateral edges bent over towards its nether surface, so as to form a narrow perpendicular groove, which is sometimes almost covered by the overhanging tumour. Neither does the swelling extend to the vocal ligaments (so that the term adema glottidis is not strictly correct ;) but the tumour, hanging down on each side and in size often exceeding a pigeon's egg, overlays the glottis in such wise as to leave but a narrow opening towards the posterior part, which allows the column of air to pass out during expiration, but is closed up by any attempt at inspiration. In no example recorded did the cedematous infiltration beneath the mucous membrane show itself in any marked degree beyond the glottis. The inner surface of the larynx was reddened, puffy, and covered with a puriform mucous layer. Galen's (Morgagni's) ventricles were always more or less implicated in the sub-mucous tumefaction. The mucous membrane of the affected parts is always variously changed. Its surface is rough, its epithelium partly thrown off in single scales and tufts, or raised by serous fluid; it exhibits here and there blood-specks, or scattered bright-red vascular streaks; it is moreover No. 105.

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easily separable, and, when separated, friable. The neighbouring muscles, especially the arytenoid, are sometimes unaltered, at other times saturated in like manner with the effused fluid, in which case they have become blanched, or undergone yellowish or grayish softening. Where the disease is of catarrhal origin, the fauces and the palatine region are generally found simultaneously inflamed, and the tonsils destroyed by suppuration. The inflammation commonly ends where the pharynx passes into the œsophagus, and again at the glottis; yet there have been instances (see Bouillaud's first case) of its pervading the whole of the air-passages and attacking portions of the lungs.

"Edema of the glottis, when at all violent, commonly proves fatal. Inflammation of the epiglottis alone is perhaps more susceptible of cure, in which case the organ appears to undergo hardening, and to shrivel and diminish in size.” P. 273.

In the chapter on Exudative Inflammation of the Air-passages there is one passage having reference to croup which deserves notice. It is observed that, where the false membrane cannot be entirely expelled, the whole mass sometimes liquefies into a grayish or puriform mucus; or else it becomes attenuated and perforated with little holes, without separating, so as occasionally to remain long fastened like a network to the surface of the mucous membrane. In such cases, suffocation may ensue (as it is known to do) some days after apparent amelioration, owing to remnants of the false membrane becoming detached, and clogging up the aperture of the glottis.

The catarrhal pneumonia of Hasse is the peripneumonia notha of the ancients. The condition of the lung in this form of pneumonia is thus described:

"In many instances this variety differs from ordinary pneumonia in nothing else than in the peculiar mode in which it is developed and diffused. In other cases, on the contrary, there is a wide difference in the condition of the pulmonary texture, in the quality of the inflammatory product, and in the phases which the latter undergoes. When near the surface of the lung, the diseased portions rather sink in than bulge out, and are, if recent, somewhat incompressible, but of progressively increasing flabbiness where the disease has been protracted. They are, at the outset, of a dingy, blue reddish hue, which, however, becomes paler by degrees, changing first to a brown-red, and eventually to a yellowbrown. The texture thus altered is altogether impermeable, and soft, though less friable than in hepatization. At the beginning, it is saturated with a turbid reddish fluid, which contains numerous blood-globules; by-and-bye it becomes more and more opaque, gradually passing into grayish,—as though it were mixed with purulent mucus, and ultimately assuming altogether the aspect of a pale, yellowish-brown, puriform fluid. This, when examined by the microscope, is seldom found to be amorpho-granular; it usually contains granule-cells in predominant numbers, but often intermingled with exudation-cells, and sometimes with a proportion of pus-globules. When a large portion of a pulmonary lobe becomes thus disorganized, which is, however, rare, it is found shrivelled, lax, moist, of a yellow-brown hue, and wholly devoid of air,-resembling a wet rag. This kind of catarrhal pneumonia appears peculiarly calculated to produce obliteration of the pulmonary texture, with permanent exclusion of air therefrom, and consequent general dilatation of the several branchlets of the bronchia engaged." P. 285.

Catarrhal pneumonia invariably originates in a catarrhal affection of the air-passages, is a frequent result of pertussis, and almost invariably pre sent, to a greater or less extent, in fatal cases of bronchitis, more particu