Deep Venous Thrombosis: Prophylaxis and Treatment in the Critically Ill and Injured Patient

The complications of acute deep venous thrombosis (DVT), pulmonary embolism and the post-thrombotic syndrome, are important not only as the most common preventable cause of hospital death, but also as a source of substantial long term morbidity. Although Rudolph Virchow’s description of the pathophysiologic factors responsible for deep venous thrombosis- stasis, venous injury, and abnormalities of blood — was remarkably accurate, an improved understanding of coagulation and vascular biology has led to refinements of his initial model. Some component of hypercoagulability is now understood to underlie most episodes of deep venous thrombosis, with stasis serving largely as a permissive factor, localizing activated coagulation to sites prone to thrombosis. Furthermore, it is now recognized that biologic injury to the normally anti-thrombogenic endothelium may be more important than overt mechanical injury in most circumstances. Most of the components of Virchow’s triad are present in the critically ill and injured patient and not surprisingly, a high incidence of venous thromboembolism (VTE) has been documented in these patients. Immobilization by skeletal fixation and critical illness, direct mechanical venous injury from trauma or venous catheters, endothelial injury due to shock or sepsis, and activated coagulation with concurrent depletion of inhibitors and components of the fibrinolytic system may all be present in this patient population.