Implications for Compression Prophylaxis

Irrespective of aetiological mechanism, the greatly increased risk and incidence of DVT attendant on sustained non-pulsatile venous blood flow affords a rational basis for prophylaxis by intermittent compression. This approach to prophylaxis, explored during the 1950s, was considered by Roberts and Cotton (1975) and its cost-effectiveness was assessed by Salzman and Davies (1980). Holford (1976), Scurr et al. (1977), Barnes et al. (1978), Hull et al. (1979, 1990), Nicolaides et al. (1980, 1983) and Dai et al. (1999) are among the many workers during the past three decades who have assessed its clinical efficacy. It seems especially effective for post-operative patients requiring prolonged bed rest. Most of these authors emphasised sequential compression to accelerate flow velocity; however, we maintain that maintenance of pulsatile flow is clinically far more important than boosting the linear blood velocity per se. Salzman et al. (1987) found that different types of compressor were similar in efficacy. Lurie et al. (2003a) showed that intermittent pneumatic compression significantly increases the venous flow volume and velocity, irrespective of whether the limbs are elevated, horizontal or dependent. The changes in segmental flow varied with the type of compression garment used and where it was applied (calf or foot), and there was individual variation among patients. Calf compression provided the maximal increases in volume flow and flow velocity through the deep veins. The efficacy and safety of mechanical prophylaxis for DVT after total hip replacement has been demonstrated by Pitto et al. (2004). We shall re-examine this topic in Chapter 11.

This correspondence between clinical success on the one hand and aetiological theory on the other seems to confirm that local cessation of pulsatile blood flow is instrumental in DVT. Bizarrely, however, some workers in the field have interpreted the clinical success of sequential compression treatment in terms of

'inhibition of thrombogenesis and promotion of fibrinolysis' (e.g. Salzman et al. 1987). The consensus belief that 'thrombosis is excessive or aberrant coagulation' persists throughout much of the biomedical world, and seems to have become a conceptual straitjacket into which data meriting quite different interpretations are forced.

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