The high risk of DVT in acute individuals with SCI is due to the simultaneous presence of three factors of Virchow’s triad: hypercoagulability, stasis, and intimal (inner vessel layer) injury (Aito et al. 2002). VTE usually begins with a calf DVT (Cogo et al. 1998; Nicolaides et al. 1971; Philbrick & Becker, 1988). Other contributing factors include partial or total limb paralysis and absence of spasticity which is a significant independent risk factor for DVT (Do et al. 2013). VTE affects blood flow, reduces the capacity of the vessels and increases the venous resistance. These as a result promote a cascade of metabolic derangements resulting in activation of the coagulation cascade and venous thrombosis (de Campos Guerra et al. 2014).
Approximately 20% of DVTs extend into the proximal veins (Brandstater et al. 1992; Kakkar et al. 1969; Lagerstedt et al. 1985); over 80% of symptomatic DVTs involve the popliteal or more proximal veins. Non-extending distal (i.e., calf) DVTs rarely cause PEs and as such are rarely worrisome (Kakkar et al. 1969), although they may account for over 80% of the incidence of DVT (Germing et al. 2010). Proximal (i.e., knee or above) DVTs often lead to PEs and are a cause for concern (Kakkar et al. 1969). Selassie et al., (2011) noted that individuals who developed a PE had a twofold increase in the risk of in-hospital death compared to those who did not develop a DVT. Distal DVT, which is more common, is associated with post-thrombotic phlebitis and venous valvular insufficiency (Do et al. 2013).
Post SCI pulmonary emboli incidence is 4.6-14% and is mostly asymptomatic or unrecognized. However, in 1.7-4.7% of the cases, it is large and fatal (de Campos Guerra et al. 2014).
Deep venous thrombosis is common among individuals with SCI who are receiving or not receiving prophylactic treatment.