454 OP NUTRITION. 



newly-formed materials appearing either iu a state iu which they may pass 

 into a low form of organized tissue, or in such a degraded condition that 

 they are altogether uoorgauizable, and are fit only to be cast out from the 

 body. Each of these phenomena requires a separate examination, both as 

 to its causes and its consequences. 



371. Although it has been customary to speak of Inflammation as a state 

 of "increased action" in the part affected, of which increased action, the 

 augmentation in the bulk and weight of an inflamed part, and in the quan- 

 tity of blood which passes through it, together with its higher temperature 

 and more acute sensibility, would seem to furnish sufficient evidence, yet 

 all these signs are found to be deceptive when they are more closely exam- 

 ined ; and the conclusion is forced' upon us, that the vital power of the part 

 is really depressed rather than exalted. For the increase in bulk and weight 

 is not due to such an augmentation of its proper tissue, as would truly con- 

 stitute Hypertrophy ; on the contrary, even in the slightest forms of Inflam- 

 mation there is such a diminution in the rate of its nutrition as really con- 

 stitutes Atrophy; and such augmentation of the solid mass as may take 

 place, is produced by the passage of the fluid which should properly have 

 been applied to the nutrition of the part, into an organized tissue of the 

 lowest kind, and this in virtue rather of its own plasticity than of the vital 

 force which it derives from the tissues which it infiltrates. That there has 

 been an atrophy rather than a hypertroply of the proper fabric of the part, 

 becomes evident enough when the inflammation has passed away, and this 

 newly-formed tissue undergoes degeneration and absorption. The only tis- 

 sues in which there is any appearance of increased formation during the in- 

 flammatory state, are those which correspond in their low type of organiza- 

 tion with the new tissue thus generated, namely, the areolar and other simple 

 fibrous tissues, and also the osseous, in all of which, as Virchow has shown, 

 the cells undergo a remarkable increase, constituting what he has termed 

 Hyperplasia, or a formation of new elements, in opposition to Hypertrophy, 

 or an increase in the nutrition of existing parts. 1 When the Inflammation 

 is more severe, the tendency to degeneration in the proper tissues of the part 

 becomes very obvious; for it is by their interstitial decay and removal, that 

 the cavity of an abscess is formed ; it is by their superficial death and absorp- 

 tion or solution that ulceration takes places ; and it is in the death of a 

 whole mass at once that gangrene consists. 



372. That a diminution in the formative activity of the Tissues is an 

 essential characteristic of the Inflammatory state, further appears from the 

 study of its Etiology ; for whether the causes to which the inflammatory 

 attack may be traced are local or general, acting primarily upon the tissues 

 of the part, or first affecting the blood, their operation is essentially the 

 same. Thus the local causes are all obviously such as tend either directly 

 to depress the vital powers, or to elevate them at first, and then to depress 

 them by exhaustion. Of the former kind are cold and mechanical injury; 

 also many chemical agents, whose operation tends to bring back the living 

 tissues to the condition of inorganic compounds. Under the latter category 

 are to be ranked all those agencies which produce overexert ion of the func- 

 tional power of the part; amongst which may be named heat, when not so 

 excessive as to produce a directly destructive effect. Now cold, heat, chemi- 

 cal agents, and mechanical injury, when operating in sufficient intensity, at 

 once //// the part, by entirely destroying, instead of merely depressing, its 

 vital powers ; and it is on the borders of the dead part, where the cause has 

 acted with less potency, that we find the inflammatory state subsequently pre- 



1 Cellular Pathology, 1860, p. 403. 



