This crasis again represents a local pus-production, and also a spontaneous primitive pyaemia of the entire blood-mass.

In pyaemia it is necessary to distinguish two different grades or stages, in order to bring the various facts into mutual concord, and to avoid contradiction in the characteristic given of this blood disease. Those facts are, on the one side, the coagulation and deposition; on the other side, destruction, of the fibrin. The latter may become developed, as a higher grade, - as a consecutive stage, out of the former. The higher grade may, however, set in at once, as a protopathic crasis, without being preceded by the first or lesser grade.

In the lesser grade the blood-crasis is characterized by quantitative excess in the production of fibrin [hyperinosis], which is at the same time qualitatively impaired. It is marked by a high degree of coagulability and of proneness to separation from the blood-mass, - manifesting itself as croupous, liquefying fibrin. These main features of the crasis illustrate the following appearances.

The fibrin-coagula endogenous to the vascular system, are remarkable for their opacity, for their varying hues of dull white, of yellowish-green, of reddish-gray [from enclosed blood]. They are soft, and yet tough - their contained serum being of a whey-like turbidness. A closer inspection shows them to consist of a glebous basement, with the rudiments of fibrils, and about these a vast quantity of fine point-molecule. There are, besides these, nuclei, and nucleated cells the nuclei of which appear to resemble in various degrees, up to complete dissilience, pus-nuclei. Sometimes they exhibit little tubercle-like congeries, which consist of collected elements of pus. Having originated during life, they soften, with liquefaction of the said basement, to a fluid which assimilates to pus proportionately to the amount of pus-cells included in the clot.

This crasis, in its most developed grade, possesses the peculiarity of localizing itself in many areae in rapid succession. Along with highly acute inflammation with purulent effusion upon mucous membranes, upon serous membranes, and in areolar tissue, these areae appear in every variety of organ and of texture, and are generally distinguished for their small circumference and their sharp definition. They form suddenly in the textures as red obstructions, which almost as speedily deliquesce with sloughing and ulcerous fusion of the involved textures to a yellow or greenish-yellow pus. Wherefore, - as also owing to the lack of evidence of antecedent inflammation, - they have received the name of pus deposits or depots; of pus metastases. We have already described the attendant anatomical process, and seen that these acts [like others brought about under the fibrin-crases] consist essentially in a spontaneous coagulation of the blood-fibrin in the capillaries, and its immediate liquefaction, with ulcerous corrosion of the bloodvessel membranes and of the contiguous textures; to which process, inflammation with similar products, as the encompassing inflammatory areola, supervenes. Coagula of the same nature form in the great vessels, and, in the shape of purulent vegetations, also in the heart.

The blood appears, along with the endogenous fibrin-coagula described, as a tenacious fluid of a russet hue. It is seen spread out in a thin layer, and mingled with little soft particles, which turn out to be aggregates of pus-nuclei and pus-cells, along with blood-corpuscles, in a transparent clot.

The dead body, owing to the voluminous separation of coagula, presents extensive livid patches verging upon russet coloration; hypostases: tex-tural redness of imbibition; lack of rigor; flabby muscles; friable, doughy, collapsed parenchymata.

The higher grades of the pus-crasis consist in destruction of the fibrin; attenuation and discoloration of the blood; septic decomposition of the circulating fluid, of a nature corresponding to the rapid ulcerous and gangrenous up-breaking of textures in the local processes.

The more intense is the aggravation of the crasis, the less do we encounter the aforesaid depots. It is only in the transition to the higher grades that we meet with them, obviously breaking up, along with the involved textures, to a dingy brown, coffee-ground, or olive-colored, collapsing, fetid pulp. The same metamorphosis affects both the exudates and their parent strata. In the highest grade extensive passive stases affect the decomposed blood, producing necrosis with dark and hemorrhagic imbibition of the textures.

The dead bodies of persons who have died of pyaemia at this stage, manifest, apart from the external and internal local processes - due, it may be, to an earlier phase - long retention of animal warmth, little and evanescent rigor, flabby and pale muscle, more especially discoloration and lacerability of the heart, and rapid decomposition with extensive, brownish death-patches. The parenchymata are lax, easily torn, serum-drenched, pale, or of a spurious redness in various shades, owing to hyperaemia and imbibition of dissolved blood-pigment. The lungs are the especial seat of hypostatic congestion, with a dark coloration verging upon cherry-red or upon brown. The blood in the heart and vascular trunks contains scanty, colloid-like, cruor-holding, red, and sometimes greenish-red, coagula, and is itself of a cherry red, adhesive, or else attenuate, brownish; having stained the bloodvessel membranes and the endocardium with its coloring matter. Pyaemia is not unfre-quently primitive [protopathic - or deuteropathic, that is arising out of other anomalous crases - for example, the typhous, the exanthematous]. More commonly, however, it is consecutive to the reception of pus into the blood, or else to infection, brought about in the various ways, fully detailed at page 274 of the present volume.

This applies to both grades of pyaemia of which it has been stated that the second also occurs independently, determined through infection of the blood by a foul pus decomposed through stagnation. To this category belongs, amongst others, the infection proceeding from the poisoning of wounds with pus out of the dead body. Darcet brought forth the disease by injecting corrupt pus-plasma, a disease into which, as a purulent sepsis or necrosis of the blood, the minor grades of pyaemia with hyperinosis become spontaneously exalted, probably owing to the pus in the blood becoming oxidized in the respiratory process.

The circumstance that pus secreted bodily into the canal of a bloodvessel, commonly produces a more intense infection than pus-plasma probably received into the blood by resorption, might lead one to conclude that it is to the pus-cell that pyaemia is attributable. Nevertheless, apart from the incomparably larger proportion of pus received into the blood in the former case than in the latter, the occurrence of primitive pyaemia precludes our adjudicating in favor of either the pus-cell or pus-plasma as the causal agent. Far more depends, without any doubt, upon the quality of the pus; and it is certain that a large proportion of bland pus taken up into the circulation proves far less mischievous than an incomparably smaller quantity of purulent ichor. That the pus-cell taken up into the blood, or even that other cell formations of larger size - certain cancer-cells, for example - should, by obstructing the capillaries, give rise mechanically to so-called depots [metastases] will scarcely be credited at the present day.

Pyaemia generally proves fatal, as purulent poisoning: inconsiderable grades of it, however, are susceptible of cure. This occurs, without doubt, partly through a conversion of the pus, analogous to the metamorphosis of fibrin - partly through elimination of the pus in exudatory processes, especially upon extensive mucous membranes, like that of the intestinal tract. The elimination of pus through processes of secretion, for instance, its passage through the kidneys, with the concurrent disappearance of pus-deposits, is a phenomenon much talked of. The pus-cell both in the urine and in exudates is incapable of becoming reabsorbed, and equally so of passing out of the bloodvessels, either into the uriniferous tubules or at any other part. It follows, therefore, that pus-cells, either in the urine or in an exudate, must be a new creation out of effused plasma.