Open Surgical, Endoscopic, and Endovascular Treatment of Perforating Veins

Treatment of incompetent perforating veins (ICPVs) has evolved through numerous approaches, each holding the promise of being less invasive and as a result associated with reduced morbidity. The goal of ablating ICPVs, however, has not changed. The interruption of ICPVs has been based on the theory that the transmission of deleterious high pressure from the deep venous system through incompetent calf perforating veins contributes significantly to marked superficial venous hypertension, particularly in the subdermal venous plexus of patients with advanced chronic venous insufficiency. The rationale for treating ICPVs has been based on numerous clinical series, whose study design has been observational and, in many instances, subject to multiple sources of design bias.

Anatomy and Function of Perforators

Perforating veins are distributed throughout the lower extremity. The most clinically relevant ones are found in the calf and the foot. Perforating veins in the calf contain a bicuspid valve, usually located at the subfascial level, that allows blood to flow in one direction from the superficial veins to the deep veins. Pathologic flow in the calf perforating veins is considered outward flow.

An important anatomic consideration in calf perforating veins is that below the fascia they usually form one trunk, but above the fascia they arborize into a variable number of branches. In the upper part of the calf, perforating veins pass through the intramuscular septum located between the flexor digitorum longus and soleus and in addition traverse the lamina profunda of the deep fascia of the deep posterior compartment of the leg. Perforating veins have been classified as direct, which connect superficial to deep axial veins, and indirect, which connect superficial veins to muscular veins. The nomenclature of the medial perforating veins had been based on Cockett’s original descriptions.

New Nomenclature

Under the auspices of the 14th World Congress of the International Union of Phlebology (IUP), Caggiati headed a committee to meet the “need for revision and extension of the official terminologia anatomica with regard to the veins of the lower limb.” The relevant perforators were classified topographically and divided into foot, ankle, and leg perforators. The leg (calf) perforators, which were customarily described by the eponym Cockett perforators, become the medial perforators. These are subdivided into the paratibial perforators, which connect the main trunk of the greater saphenous vein (GSV) or its tributaries with the posterior tibial veins, and posterior tibial perforators, which connect the posterior accessory GSV with the posterior tibial veins. The posterior tibial perforators are defined further topographically as the upper, middle, and lower perforating veins, similar to Cockett’s original description.

Common Sites of Perforating Veins

Several studies, including those by the author's group, examined the location ICPVs as observed directly at surgery. ICPVs were located 45% of the time in an area 10 to 15 cm above the medial malleolus, the typical Cockett ⅔ area.

Pathophysiology

Before the availability of duplex ultrasound, ambulatory venous pressure was the major method for detailing the pathophysiologic changes in advanced chronic venous insufficiency. In his early articles, Linton clearly showed outflow through dilated ICPVs on the inner side of the lower leg. He theorized that the deleterious high ambulatory deep venous pressure was transmitted through these ICPVs to the superficial venous system.

With colleagues at St. Thomas’ Hospital, the author carried out a series of clinical studies on 109 legs in 77 patients and 30 healthy volunteers. This clinical investigation detailed how pathology of the great saphenous vein (GSV) or ICPVs in combination or alone affect ambulatory venous pressure patterns and the pathophysiology of chronic venous insufficiency.

The percentage drop in superficial venous pressure with exercise (% VP DEC) was used as a method for assessing hemodynamic function. We observed the following in patients after treatment. Ligation and stripping of the GSV alone improved %VP DEC to near normal. Combining subfascial ligation of ICPVs with ligation and stripping in the group with both GSV and ICPV incompetence did not improve the % VP DEC under that observed in the ligation and stripping alone group. Ablation of ICPVs alone in a limb with a normal deep system had minimal improvement in % VP DEC. Ablation of ICPVs in a limb with deep venous reflux resulted in no significant improvement in % VP DEC.

These findings were similar to findings in several other hemodynamic studies, which showed little hemodynamic improvement when ICPVs alone were treated. The greatest hemodynamic improvement was observed with GSV ablation. Although these hemodynamic studies employed surrogate endpoints, they question the role of perforator ablation as a form of treatment when GSV or deep venous reflux is present.

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