Fibrin-Erases become, for the most part, primitively developed under the conditions of a free respiratory function. Of this fact, striking examples offer in the tuberculoses, and the setting in of croupous and of tuberculous processes after childbirth, that is to say, after the release of the thoracic spaces and of the lungs, resulting from deliverance of the womb.

Certain fibrin-erases are primary, and distinguished by their localization upon the mucous membrane of the air-passages [laryngeal, tracheal, bronchial, pulmonary croup], upon serous and synovial membranes, and in large accumulations of areolar tissue. Others are secondary, that is, the consequence or the conversion of other crases, for example, of the typhus-, of the exanthema-, of the cholera-crasis. In these, a qualitative anomaly of the fibrin predominates, as shown by this, that, even where but an inconsiderable amount of fibrin becomes developed, localization takes place, and this of an unwonted kind, as, for instance, upon the mucous membrane of the intestinal tract, of the urinary passages, of the gall-ducts, etc. Others, again, are primitive, spontaneous, or even consecutive affections of the blood determined by infection with analogous substances. They are often epidemical.

Above all other crases, the fibrin-erases, like the fibrin-exudates, are never thoroughly pure. Every portion of morbid fibrin has, associated with it, another portion of less diseased, or even of normal fibrin.

The products of the localized fibrin-erases [endogenous coagulations, and especially exudates engendered by inflammatory stasis] are partly organizable [designed for regeneration, or expended in hypertrophy], partly unorganizable, liquefying, corrosive, purulent, or ichorous. These exudates correspond so completely with the nature of the coexistent fibrin-coagula within the vascular system, that the character of the one may with safety be inferred from an acquaintance with the other.

It is interesting that coagulations in the left heart, that is out of arterial blood, are not alone more decidedly compact, but also more frequent than those out of venous blood. As evidence of this we may cite the incomparably more frequent globular vegetations in the arterial chambers of the heart.

As yet, chemical analysis has contented itself with demonstrating the quantitative excess of fibrin in the blood. According to our own researches, however, investigations are urgently requisite which have for their principal aim to determine the qualitative impairment of the fibrin. An augmentation of the fibrin is always coupled with a diminution in the amount of blood-globules, and, as chemists maintain, at the same time with an increase in the proportion of fat present in the blood. This certainly, however, does not apply to every fibrin-crasis.

Fibrin-erases attended with great exudation, frequently bequeath, as consequent upon the exhaustion of fibrin, a condition of hypinosis [defibrination], and of hydraemia. They eventually prove fatal from this source, if the patient have escaped the deadly influence of paralysis of the organ of localization, or of spontaneous coagulation in important sections of the vascular system; for instance, in the ramifications of the pulmonary artery. The highest grades of dyscrasial fibrin-constitution, finally degenerate into sepsis of the fibrin, and, indirectly, of the entire blood-mass.

The crasis may also terminate in restoration of the normal crasis, through conversion of the morbid excess of fibrin into nitrogenous substances, eliminated with the urine and perspiration. The fibrin thus becomes largely converted into excrementitious matter.

(A.) Simple [Organizable Fibrin-Yielding] Fibrin-Crasis

It is the attendant upon inflammations with an organizable exudate, - that is, an exudate susceptible of textural conversion. It comprises the inflammations of wounds healing by the first intention; many inflammations of glandular organs, and of serous and synovial membranes which terminate, not in purulent liquefaction of their products, but in gradual resorption or in textural conversion of the latter, - or in the case of pneumonia, in obliteration of the pulmonary texture.

The product of these processes - that is, the exudate-fibrin determined by these processes - answers to the character of fibrin 2. [See "Fibrin."]

The crasis consists in this: namely, that the fibrin, besides increase in quantity, usually manifests, within the bloodvessels, the character of the exudate-fibrin just adverted to; in other words, those qualities which fibrin acquires in certain processes of inflammation. The tendency of fibrin to coagulate is sometimes aggravated into spontaneous coagulation within the vascular system.

The coagula are white, or yellowish-white, compact, frequently holding enclosed a notable quantity of serum. Under a closer inspection they appear as a glebous, fibro-glebous blastema, here and there delicately fibrillated in wavy curls. Through this are interspersed numerous black-contoured, spherical or fibre-drawn nuclei, along with scattered, dull-granular nuclei, and nucleated cells. All the nucleus-formations are rendered more sharply defined by the influence of acetic acid, the blastema itself becoming turgescent and transparent. [See "Fibrin 2".

To this category belong not a few of the so-called vegetations or fibrin-coagula within the heart's cavities, not a few coagula in bloodvessels of every calibre down to the capillaries, perhaps also the intraarterial stratiform coagula, and those endogenous depositions which are the primitive source of phlebolites.

Unless these coagula - produced during life - be, in a state of minute subdivision, taken up again into the blood, they enter into a textural conversion.

The crasis is either a spontaneous, primitive, or else a consecutive one engendered by infection of the blood with a product of a corresponding kind.

The dead subject is marked by great cadaveric rigidity, by firm, deep-red muscles, by tense, dry areolar tissue, and by retarded lividity and decomposition.

(B.) The Croupous Crasis [Piorry's Haemitis.]

The croupous crasis occurs under several forms, which at the same time represent various gradations of disease of the fibrin. Amongst them we find, on the one side, the most marked hyperinoses; on the other, a scanty proportion of fibrin, but that deeply affected in quality. This is manifested first by its augmented coagulability, by a greatly increased tendency to deposition in the shape of intra-vascular coagulation [in the capillaries, as capillary phlebitis], and, lastly, by acute processes of exudation.

Both the intra-vascular coagula and the exudates are distinguished by their indisposition to become organized, by their early liquefaction, and very often by their corroding, solvent effect upon the textures. Both are opaque, yellow, or of a greenish-yellow, and contain fat. The adhesive property gradually diminishes.

To the latter, namely, the exudates, must be reckoned some, exhausting by their volume and abundance, others inferior in quantity, but indicating, by their tendency to liquefy and by their reaction upon the textures, the deep impairment of the fibrin.

They are often idiopathic, but more frequently consecutive Crases, emerging out of others, - the typhous, the exanthematous, etc. In the former case they are marked hyperinoses; in the latter case they are determined by inflammation, and the infection of the blood with congenial products. They constitute the so-called haemites of Piorry.

In their processes of exudation, they evince a preference for the mucous membranes, especially of the respiratory and of the digestive tracts, as also for the serous and synovial membranes.