**3.1.1 Precedents and mutations of 'Virchow's triad'**

In its original form - the statement that DVT is caused by some combination of disturbed blood flow, altered blood composition and vessel wall abnormality - 'Virchow's triad' was unexceptionable though misconceived. It afforded a general view of causation, and it is hard to imagine any contribution to the aetiology other than the three named facets. Moreover, it was one of a line of general points of view about DVT dating from the late 19th and early 20th centuries and thus belonged to an institutionalised tradition. For example, Aschoff (1924) proposed a 'tetrad': that DVT is caused by some combination of changes in the coagulability of the blood, changes in the formed elements of the blood, changes in the circulatory blood flow and changes in the vessel walls. But Virchow did not contribute to that tradition.

However, 'Virchow's triad' underwent mutations early in its history (late 1950s). 'Disturbed blood flow' came to be equated with 'venous stasis' (and to mean slow-flow rather than literally no-flow), just as 'altered blood composition' came to be interpreted as 'hypercoagulability'. It must be emphasised that Virchow never mentioned 'hypercoagulability' and furthermore explicitly rejected the 'doctrine' (*die Lehre*) that stasis has any causal role in thrombosis or embolism. 'Virchow's triad' would have bewildered him. The mutations continued and some authors, contrary to the superb studies by Welch (1887, 1899), have doubted whether vessel injury is causally significant in venous thrombosis (Comerota *et al*., 1985; Kyrle & Eichinger, 2009); however, others such as López & Chen (2009) have recognised that events at the vessel wall precede coagulation. Moreover, retarded blood flow or 'stasis' is sometimes viewed as only a 'potentiating influence' because – so it is conjectured - it allows coagulation factors to accumulate locally (Thomas, 1988; Mammen, 1992; Hamby, 2005). Thus, increasing emphasis has been placed on the presumption of abnormally rapid blood coagulation (Thiangarajan, 2002; Bulger *et al*., 2004), i.e. on thrombophilias, fostering the misleading impression that the aetiology of DVT is to be understood within the domain of haematology rather than that of circulatory anatomy and physiology.

Interestingly, the invention of 'Virchow's triad' in the late 1950s - and the concomitant assumption that DVT is a haematological disorder - followed in the wake of the FDA's acceptance of anticoagulant therapy and prophylaxis (Cundiff *et al*., 2010). Some connection might be suspected, and was indeed suspected at the time. We have quoted the barbed comments of Pulvertaft (1947) elsewhere (Malone & Agutter, 2008). Robb-Smith (1955) wrote: "*In recent years haematologists have been forced to take an interest in the practical if not the theoretical aspects of thrombosis by the introduction of anticoagulant therapy*." Later in the same article, he observed: "… *the coagulationist, tilting his tubes with stop-watch in hand, appears to have inherited the mantle of druidical haematomancy, like the medieval physician who based his prognosis on the appearance of the buffy coat in the bleeding bowl… one has the feeling that the stockin-trade of reagents and reactions to produce a fibrin clot is remote from a thrombus*". Robb-Smith understood the spirit of Virchow's work. (Of course, he did not use the phrase 'Virchow's triad', which would not be coined for another two years.)
