cular tone is reduced to a low ebb, so that both causes conspire to retain the blood in the pulmonary tissues. Hence, in estimating the pathological changes in the lungs connected with the actual disease, to which death has been attributed, we must be very careful in distinguishing between the effects of the dying and death itself, the secondary products of debility and dissolution, from the changes attributable to active disease. Both, however, often pass imperceptibly into one another, with gradations, which only confirm the view that disease is, in itself, incipient death. And though we may lay down rigid classifications of the modes of dissolution, and we may occasionally meet with types corresponding to our scientific arrangement, still, as Dr. Williams observes, in his admirable Principles of Medicine: "In the slower dissolution by which diseases generally prove fatal, all functions and structures are more or less involved, and life in all is dwindled down to so slight a thread, that, when it breaks in one, others scarcely retain it long enough to enable us to say that death begins distinctly in any part." Still, whether we can trace the death to asthenia or apnoea, coma or paralysis, the prevailing effect is to induce those symptoms to which we have above alluded in the lesser circulation.

It is not within our scope to dwell upon the treatment of disease, but we may be allowed to urge these facts as of the utmost importance in connection with that department of medicine, inasmuch as they demonstrate the necessity of, under all circumstances, attending to the state of the pulmonary circulation, and removing all avoidable sources of local embarrassment, while we stimulate the general forces to carry the patient through the valley of danger to the pleasant heights of recovery and health. The congestion which belongs chiefly to the causes first alluded to, is most liable to affect the posterior and inferior portions of lungs; after death, as in the debility resulting from disease, the blood follows the physical law of gravitation, and sinks to the lowest point it can gain. If there be no concomitant inflammatory changes, the congested portion presents a dark red color, and, though firmer than the more bloodless anterior part, still crepitates under the finger, and floats in water. The color is almost uniform, and the line of definition between the congested and the non-congested portion is tolerably defined. The pleural surface of the engorged portion presents a corresponding violet tint, which sometimes is more or less circumscribed at single points. The depth of the color varies somewhat in different diseases; and in very anæmic cases, especially in those associated with general dropsy, there is more or less serous effusion with the sanguineous congestion. In a medico-legal point of view, congestion of the lungs may become a question of life and death; thus, in the recent trial of Mr. Kirwan, in Dublin, the conclusion that his wife's death was due to violence, which has since been shown to be erroneous by the highest authority in medical jurisprudence in this country, Dr. Taylor, was based mainly upon the fact of the lungs being congested posteriorly. This was the main fact upon which the medical witness, Dr. Hatchett, relied, in proof of death having been brought about by drowning; we know that it may be the result

1

Dublin Quarterly Journal, Feb. 1853.

of post-mortem changes, and, as Dr. Taylor observes, "it is not of the least value as medical evidence of drowning, unless observed soon after death, and unless attended with other appearances, which, upon the assumption of death by drowning, or by some other form of asphyxia, ought always to accompany it."

But recently, a lad was examined at St. Mary's Hospital, who was brought in asphyxiated by drowning; he was, in fact, dead at the time, but still some efforts were made to restore him. The post-mortem examination showed none of the visible signs commonly attributed to drowning, and there was no congestion of any of the viscera.

It is doubtful whether there are any means of determining whether hypostatic congestion has occurred after death or within a few days of dissolution. We know that in full vigor the blood is not disobedient to the laws of gravitation, as we may easily ascertain by allowing our arm to hang down and then raise it into a vertical position, or by elevating our feet above our head; therefore, it is not surprising that, in the recumbent position, as the powers of life fail, the blood should gravitate to the posterior portion of the lungs. If the congestion is confined to one lung, or to the anterior parts of the lungs, we may safely attribute it to morbid processes; and if there are any other traces of inflammatory action, to which we shall advert further on, we may equally set down the congestion to a pathological cause.

Hypostatic congestion is closely allied to the disease which has been termed pneumonie des agonisans, by Laennec, and has been fully described by Mr. Erichsen as the congestive pneumonia, to which the majority of deaths following capital operations are due.

PULMONARY APOPLEXY.

The most formidable phenomenon to which congestion of the lungs gives rise, is the disease to which, from the earliest times, the term of pulmonary apoplexy has been applied. It is distinct from the hemorrhage that occurs from the bronchial mucous membranes, either owing to an adynamic state of the blood or to active congestion, both in the symptoms it produces during life, as well as in the post-mortem appearances. The seat of pulmonary apoplexy is the parenchyma of the lung, and, most probably, with few exceptions, only the intervesicular tissue, for it is rarely associated with hæmoptysis, which we should expect if the effusion took place into the air-vesicles themselves. The apoplectic spot may be felt before the lung is cut into as a globular mass, of greater density than the surrounding tissue, and, if near the surface, its darker color also attracts attention. On section, we find a dark red, almost black, homogeneous, circumscribed spot, varying in size from a pin's head to an orange, of the appearance and consistency of damson cheese, bounded by tissue, which is comparatively healthy both in color and consistency. The only interruption to the uniform color that is met with, is that caused by the dividend bronchules, which are less dark

1 Medico-Chirurgical Transact. vol. xxvi. p. 29.

than the surrounding parts. The more recent the hemorrhage, the more defined the outline; while, if the patient has survived the immediate shock, the margin of the spot fades away, owing to incipient absorption. Thus we have seen, as in the patient from whom the accompanying drawing was taken, several spots, evidently varying in their date. The breathing capacity of the part is entirely destroyed; it contains no air,

Pulmonary apoplexy, occurring in a man aged 53. There were several apoplectic masses, exhibiting a deep purple, almost black hue, and causing an homogeneous solid appearance of the part affected, as shown in the section.

and when scraped, only yields a dark, thick, bloody fluid, in which the microscope detects nothing but blood-corpuscles and some pulmonary debris. If the margins of the clot be scraped and examined, we may find exudation corpuscles, varying in size from 3 of an inch, showing that some irritative action and organic change are going on.

5000

The base of the lungs is the part most commonly affected, and there may be one, two, or three isolated apoplectic spots. Laennec, who viewed pulmonary apoplexy and hæmoptoic engorgement as modifications of the same disease, considered hæmoptysis as a symptom equally of both, and was of opinion that the former not unfrequently terminated in resolution and recovery. Without disputing the possibility of the absorption of an apoplectic clot, it certainly appears that there is an essential distinction between bronchial and parenchymatous hemorrhage, which we must explain by a preliminary alteration, as yet not sufficiently understood, in the proper lung tissue. This is the more probable when we consider that the hæmoptysis which is the harbinger and concomitant of tubercular disease, rarely, if ever, presents the lesion denominated pulmonary apoplexy, and that the latter is frequently met with in the dead body without its presence having been manifested by hemorrhage during life. Louis' states that, during the epidemic yellow fever, which occurred in Gibraltar, in 1828, pulmonary apoplexy was very frequently found in the victims to the disease, in none of whom hæmoptysis had taken place; on the other hand, he had never, in phthisical patients who had died during, or shortly after, attacks of hæmoptysis, met with ap

1 Researches on Phthisis, Syd. Soc. Ed. p. 168.

pearances resembling those of pulmonary apoplexy. We are, therefore, in every way justified in looking upon the two affections as essentially

distinct from one another.

Pulmonary apoplexy occasionally gives rise to hemorrhage into the pleural sac, from a laceration occurring in the pleura; this will probably be owing to the same process of disintegration, which permitted the apoplectic effusion in the first instance.

The interstitial form of pulmonary hemorrhage may be due to various predisposing causes, that affect the constitution of the blood, or of the tissues, or both together; while the exciting cause is most commonly to be found in a morbid condition of the heart and great vessels, and more particularly in hypertrophy of the right ventricle. About two-thirds of the cases on record have exhibited some lesion of this kind; still, as Hasse very justly remarks, a preternatural condition of the pulmonary texture appears always to precede, while a chemical analysis of the blood would probably exhibit a scorbutic diathesis or an hydræmic character. It has been observed that drunkards are prone to be affected with pulmonary apoplexy.

The secondary processes to which apoplectic spots of the lungs are subject are, a gradual absorption of the blood effused, suppuration and abscess, or isolation by the formation of a cyst; none of these processes, however, extend far, and with regard to the last, no satisfactory proof is extant of its occurring at all, beyond an imperfect observation by Bouillaud.'

1 Archives Générales de Médecine, vol. xii. p. 399.

CHAPTER XXIX.

PNEUMONIA.

INFLAMMATION of the pulmonary tissue is commonly assumed to present three stages, which we may trace in regular succession in the patient, or which we find coexisting at various portions of the lungs in the same dead subject. The first stage, that of congestion, we have already considered; its situation, its effect upon the cohesion of the tissues, the coexistence of other inflammatory changes, and the history of the case must assist us in determining its character, though it is often difficult to be certain of its nature. The general effect of acute inflammation, in altering the cohesion of the tissues, is a point of considerable importance; it particularly affects, as Sir Robert Carswell has pointed out, the uniting cellular element, and may thus demonstrate the previous existence of inflammation, though the redness and vascularity have disappeared, or but faintly mark the degree of alteration which the disease has effected in the process of nutrition. This general law is compatible with the observation that the second stage of pneumonia, or hepatization, is accompanied by a state of solidification; for, as the first-named author remarks, though the tissues feel harder than natural when compressed, the diminution of cohesion which has taken place between their anatomical elements is rendered conspicuous by the facility with which they are penetrated, broken down, or crushed.

In doubtful cases the microscope would aid us, by determining the presence or absence, in the congested portion, of exudation-corpuscles, which we find where the naked eye fails in distinguishing the existence of inflammation, and which, at all events, show that some organic metamorphosis of the vital fluids is taking place, not consistent with the ordinary physiological changes. The confines of the first and second stages merge into one another, and are often difficult to define. In the second, the stasis of the blood becomes more marked, the specific gravity of the pulmonary tissue increases, the overcharged vessels relieve themselves by fibrinous exudation into the interstitial tissue, and by slight hemorrhage into the air-vessels, which, mingling with the bronchial secretions, gives rise to the pathognomonic rust-colored expectoration of pneumonia. This stage has received the name of hepatization, owing to the increased density of the parenchyma causing the affected portion of the lungs to resemble a piece of liver. M. Andral, who considers the softening process to predominate, prefers the term ramollissement rouge, as applied to this condition. It is well to remember that both designations are used indiscriminately for the same morbid condition.