n(iViiorrliai:;ic, CJangrenons IiiHaimiutlioiis. 283 



bands running across the space, perhaps as thick as a lead pencil, 

 their walls not destroyed by the suppurative process but hardened 

 by cicatricial proliferation and resisting destruction. 



The vascular connective tissue which develops upon exposed 

 suppurating surfaces (ulcers, surfaces of wounds) presents a red- 

 dish-gray color and a granular or finely nodular, uneven appearance 

 {gramilatioii tissue) ; purulent exudate arises from this also so long 

 as the microorganismal cause of inflammation continues active. This 

 tissue serves to restore the tissue loss, filling out the cavity into scar 

 tissue (cf. Regeneration). 



With multiplication of the pyogenic organisms in the affected 

 tissue not only does the local suppurative inflammation become cor- 

 respondingly prolonged, but there arises the probability of its exten- 

 sion. The bacteria advancing along the lymph spaces give rise 

 to fresh inflammatory reaction in a constantly expanding area. The 

 fact that the leucocytes have wandered into the suppurating area, 

 may take up some of the bacteria and carry them some distance 

 away, until stopped by the occurrence of paralysis and death 

 and their transporting function thus ended, gives an excellent 

 opportunity for the entrance of pus-producing germs into the lymph 

 channels, lymph nodes and even tlie blood. Malignant and activelv 

 multiplying organisms, over which the bactericidal forces of the 

 blood have no influence and the phagocytic cells no power, 

 are thus likely to set up new foci of suppuration, so-called metas- 

 tatic suppuration, in the lymph glands and_ any other places into 

 which they have been carried as emboli. 



We speak of iKTinorrhagie iiiflammatioii, where the exudate 

 contains a notable admixture of red blood cells, and is consequently 

 of a reddish, grayish-red to dark red, chocolate or cafe-au-lait ap- 

 pearance. Serous as well as fibrinous and purulent exudates mav 

 assume this character, which may be regarded as indicative of 

 some especially severe disturbance of the vessel walls, which in 

 turn has occasioned marked slowing of the blood current in the 

 inflamed part, diapedesis of the erytlirocytes or actual rupture of 

 the vessels, and is therefore accompanied by stasis and haemorrhage. 



Putrefaction of the exudate and of the inflamed tissue {ichorous, 

 gangrenous or putrid inflammation) is necessarily the result of the 

 invasion of putrefying bacteria into the necrotic tissue and the 

 masses of blood and exudate, dead material like the tissue itself. This 

 combination of inflammation and moist gangrene, or, rather, the 

 secondary changes produced by gangrene, breaks down the tissue 

 or exudate into a dirty, grayish-green or dark green, malodorous 



