Servier – Phlebolymphology

II. Anatomy

Alessandro Pieri, Italy


An anterior accessory saphenous vein (AASV) is found in only 44%-52% of individuals, but it is incompetent in approximately 50% of cases, and is a very important source of reflux when the terminal or pre-terminal valves are not competent.

The other differential characteristic of the AASV is that it is the only saphenous junction tributary that joins the saphenofemoral junction against gravity. Its length ranges from 3 to 30 cm (mean 10 cm), and it is located over the muscular fascia in alignment with the femoral artery.

The lymph nodes of the groin drain into the AASV, and these lymphoganglionar relationships have special importance in inguinal varicose recurrence.

To avoid recurrences when the AASV is insufficient, endovascular treatment of the greater saphenous vein should be performed with associated crossectomy.

Jean-François Uhl, France


The author’s research group produces realistic 3D vectorial models of human embryo lower limbs. The technique used is computer-assisted anatomical dissection with immune markers and manual segmentation. The results appear to confirm Gillot’s theory regarding “angioguiding” nerves. In fact, it is possible to observe a close relationship between the main venous axis and the nerves.

Focusing on the anatomy of the small saphenous vein (SSV), the author underlined the complexity of the popliteal fossa, which can be better understood by a thorough knowledge of embryology. According to the author, the clinician needs to be aware of potentially hazardous areas in the treatment of the SSV, either by sclerotherapy, surgery, or endovenous procedures. Due to the possible existence of a “short saphenous artery,” it is advisable to perform sclerotherapy under echoguidance because of the highly variable location of this artery.

The superficial veins are in close proximity to associated nerves at the ankle level, apex of the calf, and in the popliteal fossa, and clinicians should be aware of these anatomical pitfalls in order to avoid nerve injury.

The foot pump is not located at the level of the “sole of Lejars,” but appears instead to be situated in the lateral plantar veins. These veins make a deep plexus positioned between the muscles of the sole. Their blood content is about 25 ml and is injected with each step into the posterior tibial veins. This explains the relevance of static foot disorders in chronic venous disease (CVD), as impairment of the foot pump will worsen venous return. Indeed, the frequency of static foot disorders is roughly 18% in the normal population, compared with 37% in CVD patients.¹ As a result, the author recommends a thorough examination of the foot in these patients and a correction of the foot disorders when they are observed.

The discussant, Alberto Caggiati (Italy), stated that the introduction of techniques for vein imaging in living subjects has transformed classic anatomic knowledge based on cadaver studies. In fact, it is now possible to define the “dynamic anatomy” of the inferior limb veins.

The author described the presence of three different pumps located in the calf: the distal leg pump, which empties during dorsiflexion of the ankle (in contradiction to what is currently considered); the anterior leg pump, which mostly empties the anterior tibial veins during dorsiflexion of the ankle; and the proximal posterior pump, which empties the posterior tibial, peroneal, and sural veins during the plantar pump. The author also described the popliteal pump, whose associated vein is completely compressed during knee extension,2 and the anterior thigh or femoral pump; the femoral vein is compressed by muscles in Hunter’s canal, where it is squeezed by the Sartorius during flexion of the hip. Finally, he described the posterior thigh pump, which works during flexion of the knee, and the inferior vena cava pump, which drives the blood when intra-abdominal pressure increases.3

References
1. Uhl JF, Chahim M, Allaert FA. Static foot disorders: a major risk factor for chronic venous disease? Phlebology. 2012;27:13-18.
2. Dijkstra ML, Khin NY, Thomas SD, Lane RJ. Popliteal vein compression syndrome pathophysiology and correlation with popliteal compartment pressures. J Vasc Surg: Venous Lymphat Disord. 2013;1:181-186.
3. Miller JD, Pegelow DF, Jacques AJ, Dempsey JA. Skeletal muscle pump versus respiratory muscle pump: modulation of venous return from the locomotor limb in humans. J Physiol. 2005;563:925-943.

Andre van Rij, New Zealand


Until relatively recently, it was assumed and published that veins <2 mm in diameter do not have valves. However, contemporary studies have provided robust evidence for the existence of valves in veins <2 mm diameter in the skin. Accordingly, the author presented his work on the role of the microvenous valves of the superficial venous system in the development and progression of chronic venous disease. The author’s group examined several amputated limbs (some without any clinical venous disease, and others with varicose veins and ulcers) with retrograde venography corrosion casting. They were able to demonstrate that valvular incompetence can occur independently in small superficial veins in the absence of reflux within the great saphenous vein (GSV). Microvalves were identified down to the sixth generation of tributaries from the GSV. They were also able to show that once the third generation microvalves are incompetent, reflux can extend into the entire microvenous networks in the skin, despite the presence of subsequent competent valves, bypassed in the network. In limbs with varicose veins and venous ulcers, reflux into the microvenous networks and capillary loops was more extensive with more dense networks and greater tortuosity. The presence of microvalves in the very small veins in the skin and their dysfunction may be decisive for the development of skin changes in venous insufficiency. This may also explain why some patients with longstanding varicose veins do not develop venous ulcers. Additionally, degenerative changes in the microvenous network in the skin may be related to the appearance of reticular veins, corona phlebectatica, and venous flares.¹

Reference
1. Vincent JR, Jones GT, Hill GB, van Rij AM. Failure of microvenous valves in small superficial veins is a key to the skin changes of venous insufficiency. J Vasc Surg. 2011;54:62S-69S.