Understanding Postthrombotic Venous Insufficiency

Many physicians fail to recognize the difference in the pathophysiology of primary versus postthrombotic venous insufficiency. As a result, the value of thrombus removal in preventing postthrombotic morbidity in patients with acute DVT is underestimated. The pathophysiology of chronic venous insufficiency is ambulatory venous hypertension, which is defined as an elevated venous pressure during exercise. In individuals with a normal deep venous system, ambulatory venous pressures in the lower leg and foot should drop to less than 50% of the standing venous pressure. In patients with postthrombotic syndrome, the ambulatory venous pressure drops very little, and in those with persistent proximal venous occlusion, the ambulatory pressures may actually rise above standing pressure. This degree of ambulatory venous hypertension often leads to the debilitating symptoms of venous claudication.

The anatomic components contributing to ambulatory venous hypertension are venous valvular incompetence and luminal obstruction. It has been consistently shown that the most severe postthrombotic sequelae and the highest ambulatory venous pressures occur in patients with valvular incompetence accompanied by luminal venous obstruction.4,5

Venous obstruction is not synonymous with occlusion. Occlusion is complete obliteration whereas obstruction (for the most part) is relative narrowing of the lumen. Although relative degrees of obstruction are reliably quantitated on the arterial side of the circulation, technology has not advanced to the point that allows this degree of accuracy on the venous side. Furthermore, physicians often cannot put venous obstruction into proper perspective pathophysiologically in

Iliofemoral Venous Segment

FIGURE 49.1 Chronic venous disease in a patient who had iliofemoral DVT 10 years earlier. The patient suffered with the postthrombotic syndrome leading to multiple hospitalizations due to venous ulcers. Ascending phlebography showed chronic venous disease with "no evidence of obstruction." An IPG was normal. A classic Linton procedure, which includes ligation of the femoral vein distal to its junction with the profunda, was performed, showing recanaliza-tion of the femoral vein with significant luminal obstruction.

FIGURE 49.1 Chronic venous disease in a patient who had iliofemoral DVT 10 years earlier. The patient suffered with the postthrombotic syndrome leading to multiple hospitalizations due to venous ulcers. Ascending phlebography showed chronic venous disease with "no evidence of obstruction." An IPG was normal. A classic Linton procedure, which includes ligation of the femoral vein distal to its junction with the profunda, was performed, showing recanaliza-tion of the femoral vein with significant luminal obstruction.

terms of its contribution to postthrombotic discomfort or distal leg soft tissue damage. Our ability to identify and quantitate venous obstruction is so poor that there is widespread underappreciation regarding the importance of the contribution of obstruction to postthrombotic morbidity.

Unfortunately, physiologic testing on the venous side of the circulation has not kept pace with similar advances on the arterial side of the vascular tree. Vascular laboratories have traditionally (and paradoxically) tested the hemody-namics of venous obstruction with patients in the resting, supine position with their legs elevated, which is the standard position for measuring maximum venous outflow, the commonly accepted test for venous obstruction. However, the pathophysiology of chronic venous disease is defined in the upright, exercising patient, with increased arterial inflow stressing venous return. Phlebograms of postthrombotic recanalized veins frequently document patency, and nonin-vasive studies may indeed show normal maximal venous outflow values, giving the mistaken impression that venous obstruction contributes little to postthrombotic morbidity.

This is clearly illustrated by the patient represented in Figure 49.1, who had iliofemoral DVT 10 years earlier and was suffering with severe postthrombotic syndrome and a venous ulcer. Noninvasive testing demonstrated that the patient had valvular incompetence but a normal three-second maximal venous outflow. An ascending phlebogram was interpreted as "the classic tree-barking appearance of chronic venous disease. There is no evidence of venous obstruction." The following day the patient underwent a classic Linton procedure, which included femoral vein ligation with division just below its junction with the profunda femoris vein. A cross-section of the divided femoral vein is shown in Figure 49.1, along with its corresponding level on the ascending phlebogram. The vein shows multiple recanaliza-tion channels and substantial luminal obstruction. This severity of luminal obstruction becomes hemodynamically important in the exercising limb, in which substantial increases in arterial flow occur as a result of exercise. With exercise, venous outflow becomes restricted by the luminal obstruction, significantly contributing to ambulatory venous hypertension. Of course, the valves within these diseased veins are destroyed, and patients also have valvular incompetence.

It makes intuitive sense that eliminating the acute thrombus leading to the persistent venous obstruction would benefit patients over the long term, and indeed it does. Furthermore, thrombus extraction not only eliminates venous obstruction but also preserves valvular function.

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