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.
Fibrin, albumen, blood-globules, are here all diminished in quantity; the amount of ivater increased. The blood is attenuate, watery, pale in various degrees to the point of water in which flesh has been steeped, wanting in tenacity. It contains very inconsiderable, loose, soft, curdlike coagula holding much serum, which, by pressure is reducible to a few drops.
The water transudes through the parietes of the vessels in dependent parts, or in such as, owing to mechanical influences, are particularly obnoxious to hyperaemia, drenches the textures in the form of oedema, especially the areolar tissue, even to the medullary system of the bones, and forms, in serous cavities, dropsical effusion. It may transude pure, or may contain a certain proportion of albumen and even of fibrin, which latter [as so called spurious fibrin] determines in the textures a soft curdlike coagulation of the dropsical fluid; and in the cavities separates in the shape of soft curd-like flakes. Inflammatory products are marked by the large amount of their serous contents, and by their poverty in plastic materials.
The dropsical crasis occasions defective nutrition, with pallor of the textures, relaxation of the contractile fibre; in the dead body, the development of pale death-patches.
It becomes mortal through insufficiency of nutritive matter in the blood; but for the most part proves fatal at an earlier stage through local oedema of the textures, and dropsy of the great serous cavities.
Not every dropsy is, however, the result of hydraemia. We allude to those local and general dropsies brought about by mechanical impediments to the circulation in the veins, in the heart and great vascular trunks, and in the lungs.
The serous crasis is sometimes idiopathic, produced by climatic relations, by peculiar alimentation, by anomalies in the chylopoietic system, by repeated, exhausting hemorrhages, etc. Nay, it may be even congenital and constitutional. The condition of the blood in haemorrhophilis, seems to be essentially that of hydraemia. In most instances, however, it is secondary, developed as a sequela to some other crasis, for example, as a consequence of the habitual outpouring of albumen, the separation of fibrin in large aneurisms, the deposition of fibrin and albumen in inflammation-products, in tubercle, in cancer, in albuminuria. Or else it ensues upon a specific, chronic or acute blood-consuming dyscrasis, upon metallic poisoning, typhus, and the like.
Deficiency of blood, in various degrees, by no means offers any distinctive crasial characters, if we except the hydraemia - the excess of water - into which every persistent anaemia eventually resolves itself. The anaemia or oligaemia, is brought about in various ways; for, whatever be the crasial constitution of the blood, it is liable to an accidental reduction of its mass.
It is, most frequently of all, a consequence of loss of blood through the various kinds of hemorrhage; next to that, of insufficient alimentation, of excessive bodily and mental labor, and of the continuous loss of fluids; of the inordinate production and increase of new growths, even of redundant fat formation, especially in children; of disease of the nerve-centres, especially of the brain, such as hypertrophy, heterologous growths, concussion. Or it is the sequel and issue of intense typhus-crasis; of chronic metallic poisoning, etc. It accompanies all general atrophy, both in old age and in earlier life.
Moreover, oligemia is not unfrequently a congenital, constitutional state, and affects by preference the female sex. It involves a corresponding defective development of the calibre of the arteries, with smallness of the heart, and with a generally stunted growth of the animal frame. The female sexual organs seem more especially crippled in their development. It was stated that blood of every admixture may suffer an accidental reduction of its mass through hemorrhage, without becoming alienated from its original crasis. In like manner, anaemia is probably never purely such; that is to say, never brought about by the equable reduction of each of its constituent parts, but at the same time invariably a dyscrasial condition. How inextinguishably the dyscrasis clings to croupous blood, even after the most copious bloodlettings; how, in the highest grades of blood-deficiency, thetuberculous constitution attaches to the smallest remnant of fibrin, we have already seen.
The most striking picture of angemia is furnished in the dead bodies of persons who have died of hemorrhage. Collapse and pallor are the outward signs reflected from within. The deathmarks, if there be any, are very pale. There is considerable rigidity of muscle, firmly contracted heart, presenting the aspect of concentrical hypertrophy, bloodlessness, both of the endocardial cavities and of the vascular trunks, especially the arteries. In corpulent individuals with a white skin, the common integument is of a waxy paleness. In profound dyscrasial angemise [the consequence of typhous or metallic poison] the dead subject retains, together with the pallor, the characteristic cachectic hue.
 
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