Haemoptoic Infarctus bears the greatest similarity to red hepatization of the pulmonary tissue; none but very inexperienced persons can, however, mistake one for the other, for each of the above properties of infarctus presents a distinguishing sign from hepatization. These, briefly summed up, are the well-defined limitation of the infarctus, the homogeneity of its consistence and color throughout its whole extent, the coarse and' irregularly granular appearance and the dry fragility of its cut or torn surface, and the nature of the product obtained on pressing or cutting its surface.

The pulmonary tissue in contact with the infarctus is either in a perfectly healthy condition or else in a state of some other pre-existing or consecutive disease; in every case it is clearly separated from the infarctus. Amongst the pre-existing diseases we must especially mention tuberculosis and pneumonia, whilst the most common consecutive affections are emphysema and oedema of the lungs.

It occasionally happens that this limitation of the haemoptoic infarctus cannot be detected without a somewhat close examination. This is the case when the parenchyma surrounding it to a certain distance, is the seat of an effusion of fluid blood, whose limitation is by no means sharply defined, since it changes towards its periphery into a palish, sanguineo-scrous infiltration, and thus gradually loses itself in the normal tissue. Still, by a careful investigation, we may discover the infarctus seated within the fluid effusion, and plainly separated from it by its consistence and darker color.

The size of the haemoptoic engorgement is seldom very great, for while, as Laennec observes, it scarcely ever exceeds four cubic inches, it is frequently less than one. We often find only one infarctus; sometimes, however, several are simultaneously present in one or both lungs.

They are deeply seated in the parenchyma of the lungs, near their roots, or in the posterior portion of the lower lobes; they are, however, occasionally found near the surface, and may be recognized through the pleura by external inspection. It sometimes happens that when they have existed for a considerable period, the pleura above them becomes inflamed.

They are often, but by no means always, accompanied by considerable haemoptysis; their size stands in no relation to its amount, indeed there may have been very considerable haemoptysis, without a trace of haemoptoic infarctus being perceptible after death; thus, when the effused blood has coagulated rapidly and completely in the pulmonary cells, notwithstanding the haemoptoic infarctus, there will be no haemoptysis; in another case the blood does not coagulate at all, but is coughed up in a fluid state, and then, notwithstanding the haemoptysis, there is no haemoptoic infarctus; or, again, the primary effusion may coagulate and form an infarctus, while hemorrhage in the surrounding parenchyma may be the source of haemoptysis (see above).

This form of apoplexy is very frequently found to be associated with active dilatation of the right side of the heart, and it seems to bear the same pathogenetic relation to this cardiac affection as cerebral apoplexy bears to active dilatation of the left side of the heart.

In recent times some doubts have been suggested regarding the true connection between haemoptoic infarctus and pulmonary hemorrhage, and it has been regarded as the result of hemorrhage of the finer bronchial ramifications, that is to say, as depending on the coagulation of the blood which has escaped from the bronchi into the pulmonary vesicles. Although we fully believe that this may sometimes be the case, yet in the absence of any positive proof we prefer adopting Laennec's view, in relation to the assumed bronchial hemorrhage, for the following reasons: (1), because haemoptoic infarctus very often occurs without haemoptysis, while a bronchial hemorrhage could hardly take place without any sanguineous expectoration; and (2), because if, as is reasonable, we recognize the influence of hypertrophy of the right side of the heart, we shall see that this influence, notwithstanding the anastomoses of the two systems of vessels, is especially exerted on the pulmonary arteries, and that it will thus serve to elucidate true pulmonary hemorrhage.

When this form of apoplexy is very much developed it is accompanied with laceration of the pulmonary tissue; we find a cavity in the lung similar to those which are met with in cerebral apoplexy, and containing a certain quantity of more or less coagulated blood. The surrounding pulmonary texture is torn, suffused with blood, and presents, to a certain degree of thickness, an appearance of haemoptoic infarctus.

The position of these cavities coincides with that of the haemoptoic infarctus; it has, in rare cases, happened that when situated in the peripheral portion of the lungs, they have opened by a rent into the pleural sac, thus giving rise to the free effusion of blood into that cavity, and to pneumothorax.

The size of these cavities varies, but it scarcely ever exceeds that of the haemoptoic infarctus. Gangrene of the lungs sometimes, however, gives rise to very considerable accumulation of blood.

Simple hyperaemia and stasis are easily reduced to the normal state, especially under proper and judicious treatment; but they leave a great predisposition to relapses, and hence they usually require a prolonged prophylaxis.

The following questions suggest themselves: - what alterations do haemoptoic infarctus and apoplexy with laceration undergo in the progress of time? and in what way is the tendency to cure and its successful accomplishment evinced?

It is only very rarely that experience presents us with pure indisputable facts bearing on the various stages of the healing process, necessary for the solution of these questions; still from the scanty materials in our possession, and by a comparison with analogous processes in other organs, we arrive at the following conclusions:

The effusion in haemoptoic infarctus either (1) quickly becomes fluid, assumes a blackish-brown, rusty, and wine-lees tint, and in this state is partly absorbed and partly excreted through the bronchi (thus, doubtless, causing the peculiar expectoration sometimes observed to follow haemoptysis), the parenchyma remaining for a time moist, soft, lacerable, and of a rusty or wine-lees color, and gradually returning to its normal state; or (2) the effusion is only partly removed in this manner, and there remains a tough fibrinous coagulum, which gradually becomes perfectly decolorized, or a loose glutinous coagulum, saturated with black pigment, the surrounding parenchyma becoming shrivelled up, and degenerating into a cellulo-fibrous tissue of either a white or a blackish tint.

Apoplexy with laceration heals, after the absorption of the effusion, either by a direct agglutination of the walls of the sac, or by the contraction of the parenchyma round a fibrinous coagulum, which finally becomes cretified, or by the conversion of the parenchyma into a cellulo-fibrous capsule, enclosing a glutinous coagulum, consisting for the most part of pigment.