Patterns of short saphenous vein incompetence

Introduction

Chronic venous disease (CVD) is the most prevalent vascular disorder, and can result in a spectrum of disorders ranging from mild pain and oedema through to frank ulceration. ¹ The advent of duplex ultrasonography has permitted direct and accurate visualization of incompetent venous segments relating to reported symptomatology and clinical findings. The most commonly documented site of reflux is the great saphenous vein (GSV). ² While the association between small saphenous vein (SSV) incompetence and venous disease was established as early as 1959, ³ the significance of SSV reflux is an under-explored territory in CVD. ⁴

Tributaries from the dorsal aspect of the foot combine with those from the dorsal venous arch to form the SSV, which drains the heel and subcutaneous tissues of the posterior aspect of the leg. ⁵ Also termed the lesser or short saphenous vein, the SSV runs posterior to the lateral malleolus, within the saphenous fascia, and ascends to drain into the popliteal vein via the saphenopopliteal junction (SPJ). The latter is an entity of varying anatomical position, with both ultrasound and cadaveric studies showing little predictability in its localization.^6,7 This anatomical variation, together with the proximity of the SPJ to important neurovascular structures such as the common peroneal nerve, may complicate the invasive management of SSV disease.

Origin of SSV reflux

There remains no clear consensus on how superficial primary CVD commences and progresses, thus its natural history remains uncertain.^8,9 Traditionally, superficial venous incompetence was attributed to a primary valvular insufficiency that commenced at the saphenous junction and progressed distally ¹⁰ – the ‘descending theory’. This posed a significant problem for SSV reflux, as without deep venous incompetence or an incompetent Giacomini vein, there could not be a continuous blood column.

More recently, the advent of duplex ultrasonography has rendered support to an alternative ‘ascending theory’, that hypothesizes the proximal progression of distal venous incompetence.^2,11–14 This is supported by the observation that superficial venous incompetence often occurs with a competent saphenous junction. ¹⁵ Moreover, varicose veins can occur with no evidence of truncal incompetence (particularly in young patients), suggesting that varicose disease can extend in an antegrade manner, from saphenous tributaries to saphenous veins. ¹¹

Duplex imaging has also shown vein dilation occurring distal to an incompetent valve, as opposed to proximal dilation that would be expected as a consequence of descending incompetence. Studies have demonstrated that tributary incompetence predominates in younger patients suggesting that saphenous trunk or junction reflux may be a secondary occurrence. ¹¹

In fact, primary venous reflux can occur in any superficial or deep vein of the lower limb. The below-knee veins may well be affected in asymptomatic individuals and in those who have prominent or varicose veins. These data suggest that reflux appears to be a local or multifocal process in addition to or separate from a retrograde process. ¹²

Prevalence of SSV incompetence

The Edinburgh Vein Study assessed subjects with both clinical and duplex ultrasonographic examination, leading to a true estimate of the prevalence of CVD among the population. Of the 1092 subjects with complete scans, 43 had duplex evidence of SSV incompetence (3.9%). The prevalence of SSV reflux increased with progression of chronic venous insufficiency (P < 0.001). ¹⁶ The Bonn Vein Study echoed these findings with a prevalence of 3.5% and furthermore showed that SSV reflux (as well as GSV and deep venous incompetence) increased with age, obesity and CEAP (clinical, aetiological, anatomical and pathological elements) classification of disease. ¹⁷

SSV incompetence in primary CVD

Duplex ultrasonography studies have shown marked variation in the prevalence of SSV reflux in patients with symptoms and/or signs of primary CVD.^4,7,18–21

In a small study of 32 patients with symptomatic venous disease, only 2% of limbs were shown to have SSV incompetence. ¹⁸ Kurt et al. ⁴ found that 5.8% limbs from 178 patients with symptoms/signs of primary CVD had evidence of isolated SSV reflux; of note, there was no significant difference between the age, BMI, and gender of those with and without SSV disease. Labropoulos et al. ⁵ found a similar prevalence of isolated SSV incompetence at 6.6% in their large duplex ultrasonographic study of 2254 limbs. The most common pattern of reflux in the short saphenous system extended throughout the length of SSV (57%) without involvement of Giacomini or gastrocnemial veins. These patients were most likely to present at stage C2–C4. Nuehardt et al. ²² found a SSV reflux prevalence of 13% in a study of 410 symptomatic legs.

When considering patients with primary superficial incompetence only (and competent deep and perforating veins), the presence of isolated SSV reflux rose to 33%, with 19% of limbs showing evidence of both GSV and SSV incompetence. ⁷ While the presence of ache or pain was not related to the extent of reflux, the presence of extensive reflux in both GSV and SSV was associated with a higher incidence of ulceration. This association is not clear-cut, as early duplex ultrasonography studies related ulceration to SPJ incompetence, as opposed to reflux of the SSV. ²³

The influence of SPJ reflux on lateral leg ulceration was emphasized in a study of 20 legs with isolated lateral malleolar ulceration. Ligation and division of the refluxing SPJ in association with conservative management resulted in all ulcers healing within 12 weeks. ²⁴ However, 15 of these limbs had been previously treated as a non-venous aetiology, and there was no control group. A larger study compared patterns of venous incompetence in 776 limbs with primary uncomplicated varicose veins with those in 166 limbs with the complications of lipodermatosclerosis or past venous ulceration (C4–C5). Limbs with complications more frequently showed SSV reflux (P < 0.05). ²⁵

Despite the suggested association between SSV incompetence and high CEAP classifications of disease,^21,24,25 short saphenous reflux has also been demonstrated in patients with primary varicose veins but no clinical suspicion of SSV incompetence. Jutley et al. ²⁶ reported 42 of 223 scanned limbs (19%) to demonstrate SSV reflux, of which 67% had not been clinically suspected. This highlights the importance of preoperative duplex assessment.

SSV incompetence in recurrent venous disease

The recurrence of venous reflux following treatment is highly variable and, like primary venous disease, often multifocal. ²⁷

Studies have highlighted the increased likelihood of recurrence in the presence of SSV reflux, following surgical treatment.^28,29 This may be due to anatomical variation in the position of the SPJ. ³⁰

Labropoulos et al. studied patterns of recurrent venous incompetence following surgical intervention in patients with CVD. One hundred and thirty-four limbs from 123 patients with recurrent varicose veins underwent duplex ultrasonography assessment of GSV and SSV systems to determine extent of reflux. Following SPJ ligation, the more common pattern of incompetence observed was SSV reflux (75%), whereas after SSV stripping was performed, SSV tributary reflux predominated (64%). ³¹

Treatment of SSV incompetence

The pattern of venous reflux is often unpredictable, and with specific regard to the short saphenous system, the position of the SPJ is inconsistent. Invasive management may be further complicated by the proximity of the SPJ with important neurovascular structures, such as the common peroneal nerve, and the added anaesthetic risk of intervention with the patient placed in the prone position. Traditional open surgery – ligation of the PSJ with or without vein stripping is effective, but has a high recurrence rate, likely due to anatomical complexity. ³²

However, with the advent of endovenous techniques using ultrasound guidance, standardized treatment of the SPJ and SSV is now far easier to replicate with few side-effects. ³³

The degree of heterogeneity of patterns of SSV incompetence and their clinical sequelae imply that individualized treatment is necessary to achieve the optimum outcome.^18,19 Few studies have investigated the effect of SSV treatment in the context of deep venous incompetence, though previous work has shown improvement in haemodynamics with superficial vein ablation. ³⁴

Conclusion

SSV incompetence is a significant contributor to the global burden of CVD but due to anatomical variability it remains a complex variable. Endovenous treatments offer a reproducible answer to this variability. Further work is needed to delineate the impact of SSV disease in secondary venous disease and in deep venous incompetence.