Deep vein thrombosis (DVT) is defined as a blood clot, or thrombus, which forms within the deep veins of the body causing an interruption in blood flow. The coagulation cascade is the process responsible for thrombus formation, involving a complex set of reactions by which fibrinogen, a soluble plasma protein, is converted into insoluble fibrin (Chung et al. 2011; Freedman & Loscalzo, 2012).
DVT is considered to be a major acute complication that occurs after SCI. Importantly, managing this condition in terms of prevention is crucial as it may lead to fatal pulmonary embolism (PE). PE occurs when a portion of the thrombus travels through the bloodstream to the lung, blocking blood flow; together DVT and PE are collectively considered venous thromboembolism (VTE). Individuals with SCI, in particular, are at an increased risk of having a thromboembolic event occur during the acute phase following injury (Aito et al. 2002; Chen & Wang, 2013; Chung et al. 2011; Lo et al. 2013; Merli et al. 1993).
The etiology for DVT after SCI is related to immobilization, secondary to stabilization or functional impairment following injury, which contributes to venous stasis. This insufficiency, together with endothelial damage and hypercoagulability, are the three main etiological factors that simultaneously lead to the development of venous thrombosis and are known as the Virchow Triad (Aito et al. 2002; Anaya & Nathens, 2005; Merli et al. 1993; Tai et al. 2013). Characteristics of individuals with acute SCI that may be important for predicting the occurrence of fatal PE have been identified, which include injury level (specifically cervical injury), obesity and absence of spasticity (Green et al. 1994). Additionally, PE is more common in individuals with tetraplegia compared to those with paraplegia, and in complete rather than incomplete injuries (DeVivo et al. 1993).