A hypothesis concerning the aetiology of venous thrombosis.

The historical background against which a new hypothesis must be discussed is presented, and the main threads of thinking about thrombosis are isolated so far as they can be. The interplay between such ideas as pus, white thrombus, white blood corpuscles, platelets, fibrin, and red blood cells, is traced: the origins of our concepts of blood circulation, stasis and slow blood flow, and vessel wall damage, are likewise dug up. The new hypothesis rearranges concepts which are not themselves actually or entirely new: instead of postulating that reduced blood flow results in 'silting' of presumably lifeless blood cells, it proposes that slow flow is more likely to injure venous endothelium by metabolic deprivation: and, in place of 'passive' silting, it postulates attachment of white blood cells and platelets to the damaged endothelium by virtue of their phagocytic or reparative function/s. This implies that thrombi are likely to form wherever living blood cells pass through veins whose endothelium is dying or dead from impaired nutrition (or other cause). The death of endothelium may be widespread, as in the agonal state, or, very limited, as in venous valve pockets when stasis is prolonged. The hypothesis is novel in that it seeks to explain thrombogenesis in functional or physiological terms, rather than in terms of purely biochemical pathogenesis.