No organ with the exception of the brain, is so frequently the seat of hyperoemia as the lung. It occurs in various degrees, and developes itself either gradually or with intense rapidity, and is the anatomical basis of most sudden deaths.

In a lesser degree, as simple hyperaemia, it is frequently an habitual, and not rarely a periodic affection of an active nature; it often ensues with great rapidity, and may prove speedily fatal by itself, or more frequently by the superaddition of acute oedema. We then find both lungs uniformly puffy, and of a dark-red color; their vessels, even to the capillaries, being filled with dark blood, and their tissue being succulent and softened, but still crepitating. In the bronchi we find a grayish, sometimes reddish mucus mixed with air-bubbles. The heart is usually somewhat dilated, and always contains a large quantity of thin liquid or slighty coagulated dark blood, especially in its right cavities. The veins of the membranes of the brain are usually full to distension, and serous effusion into the cerebral ventricles frequently occurs as a consecutive complication. The outer surface of the body is characterized by livor, and by the rapid occurrence of extensive and very dark-colored death-spots; the face in particular is very puffy, and of a more or less bluish tint; the eyes and mouth are generally more or less open, and the conjunctivae injected; the mucous membrane of the mouth is livid, and that of the throat is covered with tough mucus. Grayish or pale reddish, frothy mucus is found in the trachea.

In a higher degree hypersemia amounts to stasis. In this stage the parenchyma of the lung is of a purple or black-red tint, and, as it were, saturated with blood; and as it somewhat resembles the substance of the spleen, this condition has received the name of spleniza-tion. Several of the other characters of this condition are subject to various modifications, depending primarily on the degree and the duration of the hyperaemia, but to a lesser extent on the nature of the stasis and the composition of the blood. When it is recent and comparatively slight, the parenchyma is denser, but easily torn; it crepitates, although less clearly than in the normal state; on cutting it, a large quantity of fluid blood escapes; the diseased portion is puffy, and floats on water. In a higher degree, and when the stasis has continued for a longer period, the walls of the air-cells and the interstitial tissue become swollen, so that the former may become perfectly impermeable to air: the parenchyma consequently become denser, hard, and heavy, and ceases to crepitate; and on making an incision only a comparatively trifling quantity of thick fluid blood escapes. The blood appears, as it were, fused into the tissue of the lung, the whole affected portion having a somewhat shrunken appearance.

The blood contained in the splenified portion of the lung presents various shades of discoloration, viscidity, fluidity, or gaseity, according to the nature of its composition and the character of the stasis.

According to circumstances we occasionally find in the bronchial tubes either a sanguineo-mucous or sanguineo-serous fluid.

Stasis is the result of an active or passive, or of a mechanical hyperaemia; either of these may prove fatal by itself, especially when extensively developed; and either may sooner or later pass into inflammatory stasis and inflammation. It never attacks both lungs simultaneously and in an equal degree; it generally exhibits a preference for the lower lobes, and when it extends over a whole lung, usually commences inferiorly.

Stases of a passive nature in the most dependent posterior and inferior portions of the lungs, such as are developed in bedridden old persons, or in individuals confined to bed for a length of time in consequence of cerebral disease, typhus and typhoid affections, any adynamic diseases, and especially paralyzed conditions of the lungs, are important. They constitute the pulmonary hypostasis of Piorry.

Mechanical stasis is most commonly dependent on organic diseases of the heart, although excessive density of the lungs may give rise to it.

It is developed, according to circumstances, either in the arterial or the venous portion of the capillary system of the lungs.

It is of great importance to distinguish, as clearly as possible, between these conditions and the stasis which is developed in the body after death, - cadaveric hyperemia of the lungs, more especially as this is very frequent and is often combined with the former. The latter is always most marked at the posterior portion of the lungs, gradually diminishing in the superior and anterior directions. The lung is soft and crepitates, and apparently is not so much saturated with actual blood, as with a sanguineous, dark-red, frothy, discolored serosity, which is poured forth in abundance from the cut surface, and may be entirely removed by moderate pressure, after which there remains a pale, discolored parenchyma compressed in proportion to the pressure employed. In consequence of prolonged imbibition, the pleural sacs not only become discolored, but a certain quantity of sanguineous discolored serosity makes its way into their cavities.

Different views have been held, especially in recent times, since doubts have been entertained regarding Laennec's theory of haemoptoic infarctus, respecting the relation which these conditions bear to pulmonary hemorrhage and apoplexy of the lungs. For our own part, on the one hand, we regard them as representing hyperoemia of a lower or higher degree, which, under certain conditions, may give rise to haemoptysis, and, on the other hand, it appears clear to us that they also represent apoplexies, namely, in a less degree a vascular apoplexy, and in a higher degree an apoplexy with effusion of blood into the parenchyma of the lungs; but as the blood is not at all events originally effused into the cavities of the air-cells, apoplexies are not necessarily associated with haemoptysis, and hence must be distinguished from it.

The latter variety, namely, hemorrhage into the cavities of the air-cells, corresponds with Laennec's pulmonary apoplexy or hosmoptoic infarctus. Our own experience confirms the views of that great physician regarding the existence of this morbid change, and the manner in which it is produced. When highly developed, it is attended with laceration of the texture of the lungs.

The apoplexy of Laennec is characterized by the following signs: -

We find blackish-red patches in the substance of the lungs, which attract attention not only by their color and consistence, but also by their definite outline. On examining the cut, or, what is better, the torn surface of the diseased portion, we observe it to be more or less coarsely granular and dry, the granulation being often very irregularly distributed. The tissue itself is tough and yet easily torn, and presents throughout, both at the centre and at the periphery, the same consistence. The whole represents an effusion of blood into the cavities of the air-cells, which distends them to a certain extent and then coagulates within them, thus giving rise to the granular texture of the haemoptoic infarctus. The interstitial tissues are compressed, and infiltrated with blood, and hence the color of the diseased part is uniform throughout. The terminations of the bronchial tubes are also filled with the extrava-sated blood, their walls being reddened by imbibition, just as we observe in the case of bloodvessels. On scraping the infarctus with the back of a scalpel, there is poured forth a very slight quantity of thick blood intermixed with numerous, black, grumous flocculi.