Chylous Reflux

mucusor chondrin-containing tissues, and in which the cells can progress to puriform structure. To this is added the fact that blood-vessels incorporate themselves into the thickened places, that simultaneously with the thickening there is a hyperaemia of the underlying membranes which can consolidate themselves ; it thus becomes clear that one cannot overlook either the irritative nature of the process or the nutritional disturbance. The whole series of events that makes up the well-known inflammatory process is therefore present. Once the thickening of the inner wall has progressed to a certain degree, fatty metamorphosis usually sets in. But even this does not necessarily always lead to formation of atheroma, and the fatty change itself cannot once and for all be described as atherematous. The true arterial atheroma arises only from the second kind of patch, namely the real sclerotic (half-cartilaginous) type and in a way often described-namely, not at the surface but under the surface-so that an initially closed and fatty mash-filled focus of softening is formed. In contrast to this it is much commoner in the jelly-like patches to have the fatty softening from within the surface itself in an exactly similar way that the degeneration occurring in joint cartilages in malum senile articulorum leads to superficial destruction. These two processes differ from each other as ulceration differs from abscess formation, except that, instead of pus, a finely granular fatty mass develops and that the process carries with it not a productive but a destructive character. The atheroma, like the abscess, forms enclosed foci which open and likewise show ulcerous surfaces, but these latter retain almost always a greater depth and sharper outline than the primarily superficial festering and fatty suppuration. So little as one calls a superficial ulcer an abscess, so little does the expression atheroma apply to the superficial suppuration of the arteries and for the fatty ulcer. The atheroma as well as the fatty ulcer begins with a fatty metamorphosis of the connective-tissue particles in the thickened segments of the endothelium-that is, in the same way. Within these particles and in the hard patches apparently in the gaps and cavities of the girder and meshnet, very small fatty particles are deposited, and these gradually accumulate so that eventually one finds thick and large granular cells, often of stellate structure and complete with anastomosing processes. Even here a further difference becomes evident in that in true atheroma the granular cells become larger and more numerous, and eventually, as the ground-substance between them softens, consolidate to one communal form in which the granular spheres quickly change to a granular mash in which larger fat droplets and cholesterol crystals precipitate out. Upon the surface and particularly in the more jelly-like patches in contrast, this formation of the granular cells is often incomplete; the individual cells themselves develop only small amounts of fat and the fat particles therefore lie more scattered within the soft groundsubstance. After destruction of the cells the ground-substance is unable to hold them together in an orderly fashion and then begins, as already described for the ordinary fat-metamorphosis of the intima, at its surface a probably very fine, but not exactly molecular, detachment of the softened products which then lands up in the blood stream. In this way the superficial ulcer is formed and one can detect these macroscopically as being somewhat raw, dull and muddy; microscopically long vertical sections no longer reveal a smooth boundary like on the intima, but one sees liberal prominent fragments, soft girder and fibre tracts, matter protuberances and uneven hollows, indeed everything of minor height and depth. One can see these conditions most easily in the pulmonary artery with prolonged dilatation, while the atheroma formation commonly occurs to a most marked extent in the aorta.