Risk Factors for DVT Reconsidered in the Light of the VCHH

The major known 'risk factors' for DVT were listed in Chapter 1 and were evaluated e.g. by O'Shaughnessy et al. (2005, 2007). We noted (Chapter 3) that an aetiological hypothesis should explain why these factors increase the likelihood of DVT. However, a caveat must be entered: it would be both scientifically and philosophically erroneous to confuse factors that predispose towards a condition with causes of that condition. Combinations of the known 'DVT risk factors' certainly increase the likelihood of thromboembolism, but ad hoc circumstantial incidences are not a priori causes. DVT is not 'multifactorial'. 'Risk factors', jointly or severally, figure because they exacerbate one or more stages in this aetiological process.

Traumatic hypovolaemia and possibly high haematocrit may result in impaired perfusion and oxygenation of VVP (Chapter 9), and some autoimmune conditions lead to thrombophilias (Chapter 3). Oral contraceptives decrease antithrombin III levels by up to 60% (cf. Chapter 3), and may thus potentiate the risk of thrombus propagation.10 Some ethnic differences in susceptibility were considered earlier in this chapter (Section 11.4.1.2).

All circumstances vitiating the ability of muscles to 'oppose' and overcome the adverse force of gravity are thrombogenic, as already argued in detail. Clearly, muscle weakness and absence of expulsive pressure on the soles of the feet will lead to sustained non-pulsatile venous blood flow, and if such periods are interrupted by short pulses of weak or recovering muscle activity, or external pressure/handling by nursing staff, then DVT may be encouraged. Cardiac failure is classically -notoriously - complicated by notable rates of DVT and embolism (Belt 1934;

10 It seems implausible that contraceptives would prolong venous valve evacuation. Perhaps hormone courses could change the living habits of the patients taking them, though this also seems unlikely. On the face of it, oral contraceptives seem far more likely to promote thrombus propagation than the inception of DVT, but the seemingly increased incidence is unexplained.

Hadfield 195011). 'Long term' decubitus in the horizontal position, and any profound organic leg weakness, is prone to similar complications. In principle, this is comparable to the pathogenesis of ischaemia-reperfusion injury in arterial vessels. Cardiac failure of a certain degree necessarily reduces muscle blood flow and over a longer period may impair normal VVP perfusion.

Ageing is generically associated with impaired bodily fitness. Increased inefficiency of valve cusp function and therefore an imperfect valve cycle (Chapter 9), as well as the expected onset of degenerative diseases, impaired mobility, pain and general deterioration of health after the age of 50, make hypoxaemic injury to the parietalis correspondingly more likely. A personal history of thromboembolic episodes increases the probability of progressive functional impairment in venous valves. Sustained periods of non-pulsatile flow may have injured valves in whatever segments of vein are involved and thrombi may have developed in some of these, destroying them in the process; others will have become functionally impaired because of the overlayering of blood cells on the parietalis. IV lines are considered to cause local injury to the endothelium and to lead to a 'traumatic' DVT. Speculatively: a catheter in a leg or arm vein could conceivably force/keep open a parietal valve through which it passes, and the commonly applied external splinting perhaps alters the balance of pulsatile and non-pulsatile blood flow.

Smoking, which is often (O'Shaughnessy et al. 2005) though not universally considered a significant DVT risk factor, may aggravate VVP hypoxaemia, swaying the probabilities in otherwise less severe circulatory circumstances. Were the oxygen content of blood to be lowered further by cigarette CO, then the duration of non-pulsatile fow required to cause hypoxic injury to the endothelium could be shortened (cf. discussion of traveller's thrombosis in Chapter 10). In the presence of other 'risk factors' such as a defined thrombophilia, the likelihood of DVT might increase significantly. In addition, there is evidence that smoking can reduce levels of factor V and activated protein C under certain conditions, notably late pregnancy (Kafkas et al. 2007).

The relationship between other risk factors (cancers, infectious disorders and hormonal disturbances) and the VCHH will be discussed in Chapter 12, when the molecular biological aspects of DVT aetiology have been considered.

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