This section is from the book "A Manual Of Pathological Anatomy", by Carl Rokitansky, William Edward Swaine. Also available from Amazon: A Manual of Pathological Anatomy.
The fibrin-crasis occurs in several most important forms and varieties, which the term hyperinosis - as designating a frequent but by no means necessary and invariable excess in the quantity of fibrin - does not sufficiently characterize. It overlooks the far more important, and, for the most part, very marked feature of quality. However certain may be the excess of fibrin, its qualitative deviation becomes more and more distinctly pronounced in proportion as in the series of fibrin-crasis the forms recede from the characters of true fibrin. This, with the exception of a few hints thrown out by Andral, has been hitherto ignored. In this qualitative anomaly, however, the varieties of the fibrin-crases are founded. Each may be, and very often is, a hyperinosis, at the same time. Still the qualitative anomaly is the essential point; and it may, in a hypinotic crasis - that is, in poverty of fibrin - cling to a minimum of fibrin, and with it manifest at once that peculiar tendency of fibrin-erases to localization, and a marked peculiarity in the product.
These different fibrin-erases are, as in the sequel their special delineation will show, manifested by certain anomalies of appearance and structure. They are distinguished in common by the proneness of their fibrin to coagulate, and by its deposition, more or less pure, within the vascular system, from the heart to the capillaries downwards. They are, moreover, marked by their localization in inflammations which are wont to affect very vascular organs, such as the lungs, mucous and serous membranes, and areolar tissue.
The fibrin-erases, including pyaemia, tend more particularly to prove that all those changes which the plasma undergoes in local dyscrasial inflammation, and its products or exudates, take place within the general circulation and by virtue of its own intrinsic relations, not through any local reciprocation between the blood and the textures-inflamed.
The fibrin-erases constitute, generally, the so-called phlogistic blood-admixture, against which, conformably with the view of a quantitative exaltation of the vital process, the lancet has ever been opposed. Yet amongst the processes in question, far-sighted pathologists have always discriminated some in which much bleeding appeared not only needless but even mischievous; we refer more particularly to the croupous processes. That in these, a qualitative deviation in the constitution of the fibrin plays the part chiefly deserving of attention, is proved not only by the more obvious anomalies of aspect and of structure before alluded to, but also by -
1. The proneness of these erases to become localized, even where the amount of anomalously constituted fibrin in the blood is very inconsiderable; as, for instance, in the secondary croupous erases emerging out of the typhus-crasis; in the tuberculous crasis, in which the last particle of fibrin is expended in the deposition (localization) of tubercle.
2. The reaction of many congenerous exudates upon their parent textures, - this reaction consisting in softening and corrosion.
3. The wasting attendant upon hyperinosis, or the predominance of fibrin, that element of the blood commonly held in an especial manner to preside over general nutrition. Here the alienation of functional activity can only be interpreted as qualitative.
We have already adverted to the localization of the fibrin-erases. In relation to this, it is a question equally interesting and opportune, whether the crases regarded as hyperinoses, in inflammations, be determined by the latter, or constitute the primary and fundamental disease? The view received in France, tends to demonstrate the dependence of the crasis upon the local inflammation; in other words, the symptomatic character of the crasis. With the setting in of the inflammation and its increase, the amount of the fibrin is supposed to become augmented.
We are fully convinced that an inflammation obviously called forth by external causes may, by the abduction of endogenous, and the resorption of exuded products, give rise to a corresponding crasis, which will become augmented in proportion as the inflammation increases in intensity and extent. On the other hand, we believe that spontaneous stases are localizations of a crasis, and stand to it in a dependent - a conditional - relation. This opinion is based upon the following facts:
Every Crasis [by no means the fibrinous crases alone, to which, as the so-called phlogistic, we might be disposed to concede this prerogative] is capable of localizing itself in the shape of inflammation; take for example, the typhous and the exanthematous erases. The objection that inflammations, and especially pneumoniae, arise during the progress of typhus, is met by the fact that those inflammations with the character of a fibrin-crasis are based upon a fibrino-croupous crasis - in other words, that they are the localization of a fibrino-croupous crasis into which the typhus has become converted. Genuine typhous pneumonia (pneumo-typhus) does not develope a fibrin-crasis, any more than does typhous inflammation of the intestinal follicles or of the mesenteric glands.
An objection of considerable weight against the opinion promulgated by Andral, is furnished by pneumonia, the very process commonly concurrent with the most marked hyperinosis. We believe that ordinary pneumonia [with fibrinous product] is, for the most part, the localization of a pre-existent, that is, precursorily developed crasis, a crasis characterized by an incontestable relation to the lungs, and to the mucous membrane of the air-passages. Such a view does away with the paradox that inflammation of the lungs, a disease which, in its intense form, attacks and disables large sections of the lung, should uphold so enormous a development of fibrin, whilst other lung diseases lead to erases of the very opposite kind - in a word, to venosity [Hypinosis, Albuminosis, Cyanosis].
2. Lastly, the argument derives force from the general disturbance which always precedes a localization, seeming to bear witness to an alteration in the crasis. And to this may be added, the nature of the causal influences, which appear to be rather general than local. We may instance epidemics, climate, weather, etc.
 
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