Incidence of DVT has been examined in-depth in the literature with the incidence in patients with acute SCI to be very high, more than 50% in early prospective studies (Joffe 1975; Todd et al. 1976; Brach et al. 1977; Rossi et al. 1980; Becker et al. 1987). More widespread reports, according to Aito et al. (2000), Li et al. (2012), and Sasa et al. (2012) place the incidence of DVTs at between 10% and 30%. This incidence has increased in the last years, ranging between 18 and 100% (De Campos Guerra et al. 2014), 5.4% and 90% (Chung et al. 2014). That is probably due to the utilization of more advanced diagnostic tools. Among multi-trauma patients, SCI patients have the highest rates of venous thromboembolism (9.07%) with a higher risk among cervical and thoracic SCI. The risk is highest in the first few days after the injury up to three months then falls at 6 months onward. At one year after SCI, the risk ranges from 0% to 0.31% (Godat et al. 2014; Hagen et al. 2012; Lo et al. 2013; Thumbikat et al. 2002).
Incidence rates have been shown to depend on the nature of the SCI. Verschueren et al. (2011) noted that 9.8% of non-traumatic SCI patients and 22.8% of traumatic SCI patients had DVTs. No significant difference has been noted in the incidence of DVT based on AIS scores (p=0.58; Sugimoto et al. 2009).
In an analysis by Cao et al. (2013) examining risk factors for mortality, the authors did not find that DVT was significantly associated with future mortality. The study was based on evidence from 22 studies and provides insight into the methodological issues noted by studies when reporting incidence rates. Current findings suggest that early recognition of DVT and successful treatment are necessary in reducing the likelihood of mortality.
The high risk of DVT in acute SCI patients is due to the simultaneous presence of three factors of Virchow’s triad: hypercoagulability, stasis, and intimal (inner vessel layer) injury (Aito et al. 2000). Venous thromboembolism usually begins with a calf DVT (Nicolaides et al. 1971; Philbrick et al. 1988; Cogo et al. 1998). 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). Venous thromboembolism 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 (Kakkar et al. 1969; Lagestedt et al. 1985; Brandstater et al. 1992); over 80% of symptomatic DVTs involve the popliteal or more proximal veins (Kearon et al. 1998). 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. (2013) noted that patients who developed a pulmonary embolism 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 in SCI patients not receiving prophylactic treatment.
Deep venous thrombosis is common in spinal cord injured patients not receiving prophylaxis.