| disease | Primary Lower Extremity Venous Valve Insufficiency |
Insufficiency of the lower limb venous valve membrane is a common condition, frequently occurring in individuals engaged in prolonged physical labor or standing work, with higher incidence rates among farmers, barbers, athletes, and surgeons. This condition primarily causes heaviness, soreness, and lack of strength in the affected limb, along with superficial varicose veins, pigmentation, dermatitis, swelling, and persistent ulcers. It not only causes significant discomfort for patients but also impairs their ability to work.
bubble_chart Etiology
Congenital weakness and dilation of the venous wall, defects in the venous valve membrane, persistent elevation of venous pressure, and degenerative changes in the venous wall and valve membrane in the elderly are the main causes of venous valve insufficiency in the lower limbs.
Heavy manual labor and prolonged standing are prone to cause venous valve insufficiency in the lower limbs. During weight-bearing, intra-abdominal pressure increases, hindering venous return in the lower limbs, while prolonged standing with minimal muscle contraction in the lower limbs also impairs venous return. In individuals with congenital weakness of the venous wall and valve membrane, the addition of these factors can lead to venous valve insufficiency in the lower limbs.
bubble_chart Pathological Changes
Due to congenital weakness of the venous wall, combined with long-term blood stasis and increased venous pressure, the muscle fibers and elastic fibers undergo compensatory thickening in the early stage. In the late stage [third stage], the muscle fibers and elastic fibers atrophy and disappear, being replaced by connective tissue. The venous wall often becomes thinner due to dilation, and the elastic fibers of the venous valve membrane also degenerate. Although the valve membrane appears thin and membranous, without the thickening signs seen after deep vein inflammation, the valve becomes incompetent. The two valve leaflets cannot close tightly, leading to valve incompetence, allowing blood to reflux downward between the two sagging leaflets.
Incompetence of the deep venous valve causes blood to reflux into the distal deep veins, increasing venous pressure. The venous lumen dilates, and the vessel wall thins, leading to capillary congestion. The limb remains in a state of prolonged edema, and lymphatic vessels may become secondarily obstructed. Fibrosis of the edematous tissue worsens limb swelling. Persistent deep venous hypertension and incompetence of perforating veins allow deep venous blood to reflux into superficial veins, resulting in secondary varicose veins of the great saphenous vein.Slowed blood return and counterflow in the lower limbs lead to blood stasis, reduced oxygen levels, and increased permeability of capillary walls. Red blood cells leak out of the vessels, and hemosiderin, a metabolic product of hemoglobin, deposits subcutaneously, often causing brownish-black patchy pigmentation in the gaiter area. Local tissues become malnourished due to hypoxia, weakening resistance and making them prone to complications such as eczematous dermatitis, lymphangitis, and ulcers.
bubble_chart Clinical Manifestations
Patients often experience heaviness, soreness, and easy fatigue in the lower limbs when walking. Some may also have fleshy rigidity and spasms in the calf muscles. A portion of patients may not exhibit obvious discomfort.
In the affected limb, particularly the anteromedial part of the calf, superficial veins become raised, dilated, tortuous, and even coiled into clusters resembling varicose veins, which are more pronounced when standing. In cases with a longer disease course, the skin of the calf, especially around the ankle, often shows trophic changes such as pigmentation, desquamation, and even eczema formation.
Varicose veins are prone to complications such as thrombophlebitis, presenting as painful, red, swollen, and hardened cords with tenderness. Due to tissue hypoxia, subcutaneous fibrosis, and the leakage of blood metabolic byproducts, local resistance is significantly reduced. As a result, even minor injuries or infections can lead to stubborn, non-healing ulcers. According to Hoave's statistics from 800 cases of varicose veins he treated, 10% were complicated by venous stasis ulcers. Ulcers most commonly occur above the medial malleolus, as this area has the lowest position and highest venous pressure when standing. The soft tissue here is sparse, and nearby incompetent perforating veins often exacerbate the trophic disturbances. Ulcers are usually solitary, though multiple ulcers may occur in rare cases. The ulcer base consists of dark red, unhealthy granulation tissue, with a surface that may exude thin, foul-smelling fluid. Surrounding tissues show pigmentation, edema, or hardening, or may exhibit eczematous dermatitis. If an ulcer persists with raised edges, a crater-like or cauliflower appearance, a hard and uneven base, easy bleeding, and bloody, foul-smelling secretions mixed with mucus, it may suggest malignant transformation, though this is extremely rare.
Varicose veins can lead to acute bleeding due to trauma or other causes. This often occurs in the gaiter area, where atrophic skin becomes thin as paper, revealing high-pressure, engorged small veins beneath. Minor trauma can easily cause bleeding. Additionally, perforating veins at the base of ulcers are also prone to bleeding when injured.
Based on clinical manifestations, some physical examinations and special laboratory tests are still required, particularly lower extremity venography.
(I) Physical Examination
1. Measurement of Lower Limb Circumference Extend or slightly flex both lower limbs, and measure the circumference 15 cm above and below the knee. Generally, the lower edge of the patella (for the calf) and the upper edge of the patella (for the thigh) are used as reference points. Compare the measurements between the healthy and affected sides, as well as pre- and post-operation.
2. Deep Vein Patency Test (Perthes Test) Used to assess the patency of deep venous reflux. The method involves applying a tourniquet to the thigh to block the great saphenous vein trunk and instructing the patient to vigorously kick their legs or perform rapid squatting movements repeatedly. Due to muscle contraction, superficial venous blood should reflux into the deep veins, causing varicose veins to collapse and empty. If the deep veins are not patent or if venous pressure is elevated, the degree of varicose veins does not decrease and may even worsen.
Currently, there is no physical examination (referring to manual tests without instruments) that can detect incompetence of the deep venous valve membrane.
3. Great Saphenous Vein and Perforating Vein Valve Test (Trendelenburg Test) Used to determine the location of incompetent valves in the great saphenous vein and communicating veins. The patient lies down with the lower limb elevated, and the affected limb is massaged upward from the ankle to empty the veins. The examiner applies a tourniquet to the proximal thigh, then asks the patient to stand. If the great saphenous vein rapidly fills upon releasing the tourniquet, it indicates incompetence of the great saphenous vein valve. If the great saphenous vein in the calf rapidly fills within 30 seconds without releasing the tourniquet, it suggests incompetence of the perforating vein valve.
(II) Non-Invasive Laboratory Tests In recent years, Doppler ultrasound flowmetry, electrical impedance plethysmography, and photoelectric blood flowmetry have been beneficial in assessing deep venous patency and valve function in the lower limbs. However, ascending and descending venography remain the gold standard for visualizing and confirming deep venous patency and valve function.
(III) Lower Extremity Venography When limb swelling or persistent ulcers are present, lower extremity venography is recommended. This helps differentiate from post-thrombophlebitic syndrome and clarifies the degree of incompetence in deep and superficial venous valves, providing a basis for surgical planning.
Generally, ascending venography is performed first. If the deep veins are patent, descending venography is then conducted to determine whether venous valve pathology exists.
1. Ascending Venography Primarily used to assess deep venous patency and perforating vein valve function. Method: The patient lies supine in a semi-upright position at 45º. A rubber tourniquet is applied to the ankle to prevent superficial venous blood flow. A needle is percutaneously inserted into the dorsal foot superficial vein, and 80–120 ml of 60% or 40% meglumine diatrizoate is rapidly injected. Under fluoroscopic guidance, X-rays of the calf are taken first while the patient bears weight on the toes. The optimal contrast concentration is 40% meglumine diatrizoate, as higher concentrations may cause superficial phlebitis. After the procedure, saline can be injected to flush the vessels.
2. Descending Venography Mainly used to evaluate deep venous valve function. This test must be performed only after confirming the absence of deep venous obstruction, or it may fail. Method: The patient is placed in a 60º semi-upright position. A needle is directly inserted into the femoral vein at the groin, and 40 ml of 60% meglumine diatrizoate is injected. Under fluoroscopic guidance, X-rays of the hip are taken. If reflux is observed, X-rays of the calf are also taken.
Taheri reported a method involving catheter insertion via the upper limb superficial vein, passing through the cephalic vein, subclavian vein, and into the vena cava bifurcation, then advancing to the common iliac vein before injecting contrast. This method is more complex and less commonly used.
According to the level of retrograde flow shown by descending venography, the function of the venous valve membrane is classified into the following 5 grades:
Grade I: The valve membrane functions well. There is no significant reflux of contrast agent.
Grade II: The valve membrane shows mild (Grade I) insufficiency. The contrast agent refluxes to the proximal thigh.
Grade III: The valve membrane exhibits Grade I insufficiency. The contrast agent refluxes to the level above the knee.
Grade IV: The valve membrane shows Grade II insufficiency. The contrast agent refluxes below the knee.
Grade V: The valve membrane has severe insufficiency. The contrast agent refluxes to the lower leg, reaching the ankle level.
Postoperatively, the degree of improvement in valve membrane function can be assessed using descending venography.
Raju performed descending venography on 14 asymptomatic volunteers and found Grade I reflux in 2 cases. Therefore, analyzing venography results must be combined with clinical symptoms and signs to draw accurate conclusions.
From February 1983 to February 1988, the Vascular Surgery Department of Shanghai Zhongshan Hospital performed ascending and/or descending venography on 120 patients with lower limb venous insufficiency (including primary and secondary cases). It was confirmed that 66% of primary lower limb venous insufficiency patients without a history of deep vein thrombosis had severe deep vein valve membrane insufficiency, with blood refluxing below the knee.
The X-ray manifestations of primary deep vein valve membrane insufficiency mainly include the following points.
1. The valve membrane shadows in the deep veins are present but indistinct, and the contrast agent refluxes distally through these valves. The veins may sometimes appear bamboo-like, with the contrast agent becoming progressively lighter segment by segment, indicating that the valves still partially function—some blood is blocked by the valves, while some refluxes through the sagging, loose valve leaflets. The further distal, the less the refluxed contrast agent.
2. The venous lumen is significantly dilated.
3. No thrombotic lesions are observed in the entire venous system. Part of the contrast agent refluxes, while another part flows back toward the proximal end.
1. Mostly seen in individuals with prolonged standing or heavy physical labor, or those whose symptoms did not improve or recurred shortly after great saphenous vein stripping.
2. Swelling of the affected limb, with severe bursting pain upon prolonged standing. Symptoms and signs are consistent with simple lower extremity varicose veins.
3. Venous pressure measurement and directional Doppler ultrasound are helpful for diagnosis.
4. Venography: ① Antegrade venography. The main trunk of the deep vein shows tubular dilation, losing its bamboo-joint-like appearance, with blurred valve shadows, often accompanied by superficial vein dilation. ② Retrograde venography. Can determine valve function: Grade I—Normal valve function, no contrast reflux to the distal side during quiet breathing; Grade II—Mild valve insufficiency, slight contrast reflux not exceeding the proximal thigh; Grades III and IV—Moderate valve insufficiency, contrast reflux reaching the knee and below the knee, respectively, but still with significant contrast return; Grade V—Severe valve insufficiency, most or all contrast refluxes directly to the ankle. {|103|}
bubble_chart Treatment Measures
The principle of major surgical treatment for this disease is to reduce the venous cavity pressure caused by valve insufficiency, including elevating the affected limb, appropriate activity, and the use of elastic bandages. These can serve as adjuvant therapy both before and after surgery.
Different surgical methods can be employed for lower extremity venous valve insufficiency depending on the severity of the condition. The commonly used surgical techniques are introduced as follows:
(1) High Ligation and Stripping of the Great Saphenous Vein
Indications: Suitable for cases of great saphenous vein valve insufficiency and deep vein valve insufficiency of grades I–II.
Surgical Steps: Make a longitudinal incision about 2 cm medial to the femoral pulse, extending downward from the inguinal ligament, approximately 5–6 cm in length. A straight incision is preferable to a transverse one, as the latter provides poorer exposure and often severs the lymphatic vessels in the fossa ovalis. After incising the skin and subcutaneous tissue, locate the great saphenous vein and expose the fossa ovalis to identify the junction of the great saphenous vein and the femoral vein. Branches such as the superficial circumflex iliac, superficial epigastric, external pudendal, and lateral and medial femoral veins should be individually ligated and divided. Then, clamp and divide the great saphenous vein about 0.5 cm from its entrance, ligate the proximal end, and perform a transfixion suture. Insert a stripper into the distal end and advance it as far distally as possible. At the point where it can no longer be advanced, make a small incision to expose and divide the vein. Tie the proximal end tightly above the conical tip of the stripper and strip upward. During stripping, an assistant should apply pressure with gauze over the skin of the stripped area to facilitate the insertion of the stripper into larger branches, continuing until the medial malleolus is reached. If significant resistance is encountered during stripping, it often indicates the presence of a larger branch or perforating vein, which should be addressed with another small incision for ligation and division. Varicose veins that cannot accommodate the stripper and appear as clumps require an additional incision for direct visualization and stripping or excision.
Close the skin in layers, cover the incision with a dressing, and wrap the leg with an elastic bandage from the foot to the groin.
Postoperative Management: Encourage the patient to ambulate early, typically attempting to walk on the second postoperative day, but avoid prolonged sitting or standing. Elevate the affected limb while in bed and encourage active ankle movement to prevent deep vein thrombosis. Sutures are removed around 10 days postoperatively, and long-term use of medical compression stockings is recommended.
(2) Subfascial Ligation of Perforating Veins
Indications: Patients with a positive Trendelenburg test or venography showing perforating vein valve insufficiency and deep vein valve insufficiency of grade II or higher but without lower limb swelling or ulcers may undergo great saphenous vein stripping combined with subfascial perforating vein ligation.
Surgical Steps: Make a long longitudinal incision along the course of the great saphenous vein from below the knee to the medial malleolus. Incise the deep fascia longitudinally slightly anterior to the great saphenous vein. Dissect beneath the deep fascia anteriorly to the tibial margin and posteriorly to the midline of the calf. Ligate and divide all perforating veins penetrating the deep fascia. The perforating veins are notably larger near the knee joint and 4 cm above the ankle joint. After ligating the perforating veins, suture the deep fascia and skin. Postoperative management is the same as for great saphenous vein stripping.
In 1985, Johnson reported the clinical outcomes of 47 cases of recurrent venous ulcers treated with subfascial perforating vein ligation, with an average follow-up of 3.5 years. The ulcer recurrence rates at 1, 3, and 5 years were 22%, 41%, and 51%, respectively.
(3) Deep vein valve membrane reconstructive surgery. In the 1950s, the understanding of lower extremity vein valve membrane insufficiency was vague, but Linton pioneered the use of ligation of the superficial femoral vein combined with great saphenous vein stripping to treat venous stasis ulcers, reportedly with some efficacy. Kistner reported 5 cases of superficial femoral vein ligation and transection, with follow-up of 2 to 8 years, showing symptom relief in 4 cases. When performing superficial femoral vein ligation, care should be taken to ligate precisely at the point where the superficial femoral vein enters the common femoral vein, avoiding leaving a residual stump of the superficial femoral vein, as this could otherwise lead to thrombus formation in the blind segment postoperatively.
In the 1960s, Psathakis introduced a new attempt to improve the reconstruction of incompetent deep venous valves. He transversely pulled the gracilis tendon between the popliteal vein and the popliteal pulse and sutured it to the biceps femoris tendon to act as a contractile valve, correcting popliteal vein valve incompetence and preventing blood reflux. A total of 124 cases were performed, with good results after a follow-up of one and a half years.
Additionally, Hallberg reported the use of a "sleeve-type" polyester fabric placed outside the incompetent vein valve to serve as an external valve.
In the 1980s, Kistner summarized clinical experience since the 1960s and proposed a new diagnosis of "primary deep venous valve incompetence." He treated valve incompetence with deep venous valve repair, ushering in a new era of precise repair for deep venous and perforator vein valve dysfunction. This marked a shift from destructive procedures (such as ligation of the superficial femoral vein) to indirect valve surgery (external valve surgery) and then to direct valve repair (valvuloplasty and valve transplantation), revolutionizing the understanding and management of lower extremity venous insufficiency.
1. Venous Valve Repair
Indications: Lower extremity swelling or ulcer with descending venography showing grade III–IV femoral vein valve incompetence and no signs of chronic venous inflammation.
Surgical steps: If the great saphenous vein is diseased, first perform routine great saphenous vein ligation and stripping, along with subfascial perforator vein interruption. One week later, proceed with valve repair.
Make a longitudinal incision along the femoral vein and dissect the common femoral, deep femoral, and superficial femoral veins. Valve cusps can be palpated through the venous wall. First, test valve function by clamping the distal vein and milking blood toward the proximal valve, then forcibly pushing blood back toward the valve. A competent valve will prevent reflux, while an incompetent valve will allow reflux even without manual compression. After assessing valve function, decide which valve to repair. The highest superficial femoral vein valve is the preferred choice, as it prevents reflux from the deep femoral vein into the superficial femoral vein. If the second valve of the superficial femoral vein is more suitable for repair, it may also be selected.
Make a longitudinal incision in the vein anterior to the valve, ensuring the incision passes through the commissure of the two valve cusps. Make another incision 3 cm below the prolapsed valve, gently lift the venous wall with forceps, and carefully cut toward the valve commissure with fine scissors, then extend the incision 3 cm toward the common femoral vein. This step must be precise, as damage to the valve cusps will hinder the repair.
After opening the vein, inspect the valve. Prolapse of one or both valve cusps due to elongation causes reflux. The valve must remain intact. Shorten the elongated cusps by suturing them to the venous wall with interrupted stitches, passing the suture from outside to inside the vein, through the free edge of the elongated cusp 2 mm from the commissure, and back outside to tie the knot. Sutures may be placed on both sides of the cusp, and the commissure in the middle of the opened vein should also be tightened. Typically, 4–6 sutures are needed for adequate tightening. If small injuries or holes occur during repair, use 9-0 sutures for patching. Determining the degree of valve shortening is crucial. When suturing the valve edge to the vein wall, avoid excessive looseness or tightness. At the end of the procedure, the valve cusps should lightly tension the venous wall.
After valve repair, close the venous incision carefully to avoid tearing the valve cusps. Use fine interrupted sutures near the valve tip, and close the remaining incision with a continuous suture. After closing the vein, recheck valve function with squeezing and pressing manipulation. If significant reflux persists, consider re-repair or ligation of the superficial femoral vein.
Efficacy: Kistner reported 22 cases of superficial femoral vein valve insufficiency treated with valve repair and plasty. After a follow-up of 5 to 10 years, 15 cases showed ulcer healing, with complete disappearance of pain and swelling, and no need for elastic bandages; 3 cases had symptoms nearly completely relieved but required intermittent use of elastic bandages; 4 cases showed no improvement in swelling or ulcers. The excellent efficacy rate was 82%, while the poor efficacy rate was 18%.
In 1982, Jones proposed a new and simple venous valve membrane plasty, called the triangular resection of the venous wall for valve membrane plasty. The procedure is as follows: First, the proximal ends of the common femoral vein, deep femoral vein, and superficial femoral vein are dissected. Jones chose to repair the valve membrane of the common femoral vein, believing that the valve membranes of the superficial and deep femoral veins often exhibit concurrent insufficiency. Utilizing the valve membrane above the tributaries of the femoral vein can prevent blood reflux into the superficial or deep femoral veins. Before blocking the vein, the patient is fully heparinized. A small incision is made in the venous wall above the attachment point of the valve leaflet at the commissure of the selected valve membrane. This location is difficult to identify externally on the venous wall, but once the small incision is made, it can be extended distally. Care must be taken not to separate the valve leaflet from the venous wall. The valve membrane can then be directly observed. If the leaflets appear soft and delicate, with only lip-like elongation, they are suitable for this procedure. First, fine 6-0 monofilament sutures are used to perform triangular interrupted sutures on the unopened half of the leaflet wall, tapering and tightening the venous wall to achieve maximum narrowing at the level of the commissure of the two leaflets. Three to five sutures are placed to close the incision in a triangular fashion, maximizing the tightening of the venous wall at the commissure level, after which the vascular clamp is removed.
Jones believed this method could serve as an alternative to Kistner's intravenous valve membrane repair. He performed this procedure on five cases of valve membrane plasty, with follow-ups ranging from 6 to 12 months, and none exhibited lower limb swelling or ulcer recurrence. This method is relatively simple, taking only about an hour to complete and requiring only local anesthesia. Although the follow-up period was short, the ulcers healed, swelling significantly subsided, and the short-term results were undoubtedly satisfactory. Long-term efficacy remains to be observed.
2. Venous Valve Membrane Transplantation (or Valve Membrane-Bearing Venous Segment Transplantation)
Indications: Descending venography shows primary deep venous valve membrane insufficiency of grades III–IV, where valve membrane plasty is not feasible due to the absence of the valve membrane or excessive laxity.
(1) Post-thrombotic Syndrome of Lower Extremity Deep Veins Both this condition and post-thrombotic syndrome of deep veins involve venous stasis in the lower limbs, with highly similar symptoms and signs. This is especially true for patients with a long history of deep vein thrombosis, where the initial onset may be unclear in memory and the deep veins have already recanalized, making differentiation even more challenging. However, there are still many aspects that can aid in distinguishing the two, as shown in Table 49-1.
Table 49-1 Differential Diagnosis Between Primary Deep Venous Valve Insufficiency of the Lower Extremity and Post-thrombotic Syndrome of Deep Veins
| Primary Deep Venous Valve Insufficiency of the Lower Extremity | Post-thrombotic Syndrome of Deep Veins | |
| Onset | Insidious and gradual | Sudden, sometimes with fever and groin pain |
| Precipitating Factors | Prolonged standing, heavy physical labor | Postpartum, major surgery, trauma, cold exposure, tumors, prolonged bed rest |
| Varicose Veins | Often localized to the calf, clustered and protruding, less common in the thigh | More extensive, often involving the lateral hip, thigh, and lower abdominal wall; collateral veins may be found in the perineum; varicose veins in the calf are milder and less protruding due to tissue edema |
| Degree of Swelling | Mild, mainly in the calf, rarely in the thigh; calf circumference typically 1–3 cm larger than the unaffected side | Moderate, affecting both calf and thigh; calf circumference often 3–6 cm larger than the unaffected side, thigh circumference 3–9 cm larger |
| Pigmentation | Limited area, may be absent in some cases | Extensive area, present in almost all cases |
| Ulcer | Less common | More common |
| Femoral Vein Tenderness | Absent | Marked tenderness in early cases |
| Cord-like Structure in the Groin | Absent | Often palpable |
| Ascending Venography | Shows patent femoral vein with dilated lumen | Shows thrombus formation in the femoral vein |
| Descending Venography | Shows femoral vein reflux, but valves are still visible | In some advanced cases, femoral vein reflux may also be observed, but valves are often destroyed by inflammation and not visible |
(2) Lower limb stirred pulse venous fistula. Lower extremity arteriovenous fistulas also present with varicose veins, pigmentation, dermatitis, and ulcers, thus requiring differentiation from this condition. If caused by trauma, there is a history of injury, often including knife wounds, bullet penetrations, sharp object punctures, etc. A persistent vascular tremor can be palpated locally, and continuous vascular murmurs are heard during auscultation. If congenital, it is detected from childhood, with possible limb lengthening and thickening, significantly elevated skin temperature, as well as palpable tremors and audible vascular murmurs. Differential diagnosis is generally not difficult. If necessary, a lower limb stirred pulse angiography can be performed to further clarify the diagnosis.
(3) Lymphedema In some obese individuals with lower limb deep venous valve insufficiency, superficial varicose veins may not be obvious. These patients still need to be differentiated from lymphedema. Lymphedema presents with lower limb swelling but no pigmentation or ulceration. The skin is often thickened, with the most pronounced swelling in the calf, ankle, and dorsum of the foot. In contrast, venous valve insufficiency primarily causes swelling in the calf, with rare swelling in the ankle and dorsum of the foot. Venous stasis in venous valve insufficiency is mainly observed in the calf and is not prominent. Lymphedema primarily occurs in the subcutaneous tissue, where the ankle and dorsum of the foot have less soft tissue, making the swelling more noticeable. Descending venography may be performed when necessary. Patients with lymphedema do not exhibit venous reflux.
(4) Klippel-Trenaunay Syndrome This condition may also present with superficial varicose veins and limb swelling, necessitating differentiation. Klippel-Trenaunay syndrome is a congenital vascular malformation characterized by a triad of superficial varicose veins, limb hypertrophy, and cutaneous hemangiomas. It often involves increased skin temperature, and the lesions may affect not only the calf and thigh but also the buttocks. Ascending venography can reveal venous malformations, with most cases involving congenital atresia of the popliteal or femoral veins. Differential diagnosis is not difficult.
(5) Isolated Great Saphenous Vein Valve Insufficiency Descending venography can differentiate isolated great saphenous vein valve insufficiency from deep venous valve insufficiency. Deep venous valve insufficiency is often accompanied by great saphenous vein valve insufficiency and perforator vein valve insufficiency. Clinically, the symptoms and signs of the two conditions are very similar and difficult to distinguish. Some cases of deep venous valve insufficiency may not exhibit lower limb swelling due to compensatory mechanisms of the calf muscle pump, which aids venous return. Extensive venographic studies have revealed that approximately 66% of patients previously diagnosed with isolated great saphenous varicose veins also had concurrent deep venous valve insufficiency. Therefore, we consider these two conditions to be part of the same disease spectrum, differing only in the stage or severity of the pathology.
