Post-thrombotic syndrome is the development of symptoms and signs of chronic venous insufficiency following deep vein thrombosis (DVT) and is an all too common, burdensome, and costly complication . The term “post-thrombotic” replaces the prior terminology "postphlebitic” syndrome . A combination of reflux due to valvular incompetence, and venous hypertension due to thrombotic obstruction, is thought to contribute to post-thrombotic syndrome [3,4]. Symptoms and signs of chronic venous insufficiency may include pain, vein dilation, edema, skin pigmentation, and venous ulcers.
Prevention of DVT through prophylaxis, timely recognition and treatment of DVT, and prevention of recurrent DVT will continue to have the greatest impact on reducing the overall burden of post-thrombotic syndrome . The treatment of lower extremity DVT is discussed separately. (See "Treatment of lower extremity deep vein thrombosis".)
Post-thrombotic syndrome develops as a consequence of long-standing venous hypertension . A combination of reflux due to valvular incompetence, and venous hypertension due to thrombotic obstruction, is thought to contribute to post-thrombotic syndrome [3,4]. One study identified a high peak reflux velocity in the deep proximal veins as an independent predictor of post-thrombotic syndrome . Increased venous pressures are transmitted to the capillary beds, promoting transudation of fluid and large molecules, resulting in tissue edema, subcutaneous fibrosis, and, finally, tissue hypoxia and ulceration [7-9]. (See "Pathophysiology of chronic venous disease".)
Acute DVT causes obstruction of venous outflow, which can be partial or complete. Increased levels of inflammatory cytokines or adhesion molecules, such as interleukin-6 and intercellular adhesion molecule-1 have also been linked with the development of post-thrombotic syndrome, suggesting that inflammation may play a role in the pathophysiology of post-thrombotic syndrome [10-12]. The inflammatory response to acute thrombosis and the process of recanalization directly damages venous valves.
Reflux occurs early, progressively increasing from 17 percent of patients at one week to 69 percent of patients at one year following the diagnosis of DVT . The degree of initial vein occlusion correlates with the likelihood of developing reflux . Reflux in the more proximal lower extremity veins may be particularly important to the development of post-thrombotic syndrome. However, popliteal valve incompetence has also been found to increase the risk of post-thrombotic syndrome, particularly when combined with residual vein thrombosis [14,15]. (See 'Risk factors' below.)