. The elements of pathological histology with special reference to practical methods . or become partiallychanged into pigment. This detritus may then be absorbed, whilst atthe same time, through growth of the connective tissue in the vicinity, 212 THE BLOOD-VESSELS or of the still surviving connective-tissue cells of the infarction, agranulation tissue is formed which gradually replaces the latter, andis changed by subsequent contraction into a scar, which in the caseof ht^emorrhagic infarctions may still for a long time contain changes are otherwise, however, if the thrombus or e
. The elements of pathological histology with special reference to practical methods . or become partiallychanged into pigment. This detritus may then be absorbed, whilst atthe same time, through growth of the connective tissue in the vicinity, 212 THE BLOOD-VESSELS or of the still surviving connective-tissue cells of the infarction, agranulation tissue is formed which gradually replaces the latter, andis changed by subsequent contraction into a scar, which in the caseof ht^emorrhagic infarctions may still for a long time contain changes are otherwise, however, if the thrombus or emboluscontains pathogenic bacteria, especially pyococci. There will thenoccur, first, a purulent softening of the thrombus or embolus, withconsecutive vasculitis, and the bacteria will either soon grow throughthe wall of the vessel and penetrate into the tissue of the infarction,or their growth will first advance along the interior of the vessels ofthe latter, plugging them to a variable extent, and causing a necrosisof the vessel-wall (Fig. Ill, a). Owing to the penetration of the. Fig. 111.—Metastatic Infarction of the Spleen in Ulcerative 240. (Weigerts modification of Grams method.) a, Branched artery with necroticwalls ; b, Embolus of cocci; c, Embolus of cocci growing into the tissue of the in-farction ; d. Red corpuscles; e, Necrotic cells of the infarction, no longer capable ofbeing stained. bacteria into the tissue of the infarction, there results a formationin it of small suppurative foci (Fig. 110, l), which by their subse-quent coalescence finally change the infarction into an abscess {inetas-tatic abscess). Should the particles loosened from thrombi containing bacterialodge in the capillaries or in any of the smaller-sized blood-vesselswhich are not terminal arteries, they will cause no infarctions, butwill give rise in the neighbourhood of the occluded vessels to smallrounded foci of inflammation not uncommonly bordered by a ha:?mor-rhagic area, i
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Keywords: ., bookcentury1800, bookdecade1890, booksubjectpatholo, bookyear1895
