RHEOLOGY AND VENOUS THROMBOEMBOLISM
Authors: Lowe O DG 
Published: August 2018

Changes in the composition of the blood, venous stasis, and interaction of the blood with the vessel wall (Virchow's triad) all have rheological aspects which may promote venous thrombogenesis.

Blood composition and rheology. Increasing levels of venous haematocrit and fibrinogen increase bulk blood viscosity, especially at low shear rates such as are encountered in veins, when red cell aggregation occurs. Static blood requires a minimum shear stress for flow (yield stress), which is also strongly dependent on haematocrit and fibrinogen levels. Increases in haematocrit and fibrinogen also promote platelet adhesion and aggregation. Polycythaemia carries an increased risk of venous thromboembolism, which can be reduced by lowering the haematocrit; conversely, anaemic patients (renal failure, pernicious anaemia) have a subnormal prevalence of pulmonary embolism at autopsy. Increased preoperative levels of haematocrit, fibrinogen and blood viscosity predicted postoperative deep vein thrombosis in some studies, but not in others: they have complex relationships to other risk factors and illnesses. Postoperative changes in haematocrit, fibrinogen and blood viscosity may also be relevant to thrombogenesis, as may haemoconcentration in leg veins.

Venous flow disturbance and rheology. The flow behaviour of particles and cells in venous valve pockets has been studied by Karino: particles and cells were observed to leave mainstream flow and circulate in paired vortices in low-shear areas within the valve pockets. A cell-poor hypoxic area at the apex of the valve pocket may favour thrombogenesis. Valve pockets might therefore act as in vivo aggregometers, with optimal conditions for activated cells or coagulation products to promote platelet and red cell aggregation, which might be facilitated by increases in haematocrit or fibrinogen. Sevitt has observed cellular aggregates in valve pockets at autopsy, which might act as a nidus for thrombus initiation. Successive layers of thrombus will disturb flow steamlines, as well as generating procoagulant activity: hence a series of "aggregometers" might result in successive bursts of thrombosis and the layered structure of venous thrombi observed by Sevitt. Variations in haematocrit, fibrinogen and red cell aggregation may influence stasis of blood following venous occlusion by thrombus, and hence affect thrombotic extension; they may also influence residual lung perfusion following pulmonary embolism.

Therapeutic aspects of rheology. Leg stockings and other physical methods of preventing deep vein thrombosis may improve flow disturbance in valve pockets, as well as in axial veins. The efficacy of perioperative dextran in prevention of venous thromboembolism may partly reflect haemodilution and its rheological consequences. Likewise, postoperative defibrination with ancrod reduced the incidence and extent of deep vein thrombosis after hip surgery, which may partly reflect reductions in plasma viscosity and red cell aggregation. Defibrination with ancrod reduced the haemodynamic disturbance, and the mortality, of experimental pulmonary embolism in dogs, possibly by increasing residual perfusion.. Similarly, improved perfusion after thrombolytic therapy of pulmonary embolism in man may reflect the rheological consequences of fibrinogen depletion, as well as thrombolysis.