What is the role of hemodynamic venous insufficiency in the pathogenesis of thrombosis (DVT)?

Updated: Jul 05, 2017
  • Author: Kaushal (Kevin) Patel, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
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Answer

The acute effect of an occluded outflow vein may be minimal if adequate collateral pathways exist. As an alternative, it may produce marked pain and swelling if flow is forced retrograde. In the presence of deep vein outflow obstruction, contraction of the calf muscle produces dilation of the feeding perforating veins, it renders the valves nonfunctional (because the leaflets no longer coapt), and it forces the blood retrograde through the perforator branches and into the superficial system. This high-pressure flow may cause dilation of the superficial (usually low-pressure) system and produce superficial venous incompetence. In clinical terms, the increased incidence of reflux in the ipsilateral greater saphenous vein increases 8.7-fold on follow-up of DVT. [30] This chain of events (ie, obstruction to antegrade flow producing dilation, stasis, further valve dysfunction, with upstream increased pressure, dilation, and other processes) may produce hemodynamic findings of venous insufficiency.

Another mechanism that contributes to venous incompetence is the natural healing process of the thrombotic vein. The thrombotic mass is broken down over weeks to months by inflammatory reaction and fibrinolysis, and the valves and venous wall are altered by organization and ingrowth of smooth muscle cells and production of neointima. This process leaves damaged, incompetent, underlying valves, predisposing them to venous reflux. The mural inflammatory reaction breaks down collagen and elastin, leaving a noncompliant venous wall. [30, 31, 32, 33, 34, 35]

Persistent obstructive thrombus, coupled with valvular damage, ensures continuation of this cycle. Over time, the venous damage may become irreversible. Hemodynamic venous insufficiency is the underlying pathology of postthrombotic syndrome (PTS), also referred to as postphlebitic syndrome. If numerous valves are affected, flow does not occur centrally unless the leg is elevated. Inadequate expulsion of venous blood results in stasis and a persistently elevated venous pressure or venous hypertension. As fibrin extravasates and inflammation occurs, the superficial tissues become edematous and hyperpigmented. With progression, fibrosis compromises tissue oxygenation, and ulceration may result. After venous insufficiency occurs, no treatment is ideal; elevation and use of compression stockings may compensate, or surgical thrombectomy or venous bypass may be attempted. [37, 38, 39, 40]


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