Histopathologic differences in the endovenous laser ablation between jacketed and radial fibers, in an ex vivo dominant extrafascial tributary of the great saphenous vein in an in vitro model, using histology and immunohistochemistry.

OBJECTIVE: The study aimed to investigate the biologic effects of the 1470-nm endovenous laser (EVL), with a jacketed fiber and a radial fiber, during EVL ablation of an ex vivo dominant extrafascial tributary of the great saphenous vein in our in vitro model by histology and immunohistochemistry. METHODS: Ten segments of the dominant extrafascial tributary of the great saphenous vein were harvested by a consultant vascular surgeon from patients during routine varicose vein surgery. Six segments were treated using an ex vivo model of our design by a 1470-nm EVL with a jacketed fiber. The other four segments were also treated by a 1470-nm EVL but with a radial-firing fiber. Each segment was split into five sections and treated at five different linear endovenous energy densities (LEEDs) at 10 W: 0, 20, 40, 60, and 80 J/cm. The veins were incubated and subsections collected at 6 and 24 hours after treatment. Subsections were immersed in buffered formalin and taken for histologic and immunohistochemical analysis. Histopathologic analysis was then performed. RESULTS: Treatment with the radial fiber led to a pattern of damage that was more homogeneous than with the jacketed fiber, with no carbonization of tissue present. Significant transmural damage and necrosis were observed at LEEDs of 60 and 80 J/cm in both treatment groups. At the same LEEDs, p53 and caspase 3 analysis showed that transmural cell wall vein death (necrosis or apoptosis) occurred by 6 hours after treatment with both fibers. CONCLUSIONS: There was a significant difference in the effects of treatment with a jacketed fiber and a radial fiber in EVL ablation in vitro. Although both fibers caused transmural vein wall cell death at similar LEEDs, the pattern of damage with the radial fiber was more homogeneous. There was no overtreatment of tissue in terms of carbonization after treatment with the radial fiber. Treatment with the jacketed fiber showed carbonization of tissue at the same LEEDs.

Implication of foam sclerosant inactivation by human whole blood in a laboratory setting.

Background During sclerotherapy, it has been recommended to confirm intravenous placement of the needle by aspirating blood into the sclerosant syringe. This may inactivate some, or all of the sclerosant. Aims To quantify the volume of human blood needed to completely inactivate 1 ml of sodium tetradecyl sulphate, and comparing fresh blood and blood that has been stored in an ethylenediaminetetraacetic acid tube. Methods A series of manual titrations were carried out following a procedure developed at STD Pharmaceutical Products Ltd (Hereford, UK) and listed in the British Pharmacopeia. Three percent of sodium tetradecyl sulphate stock solutions were made with increasing volumes of blood and titrated against benzethonium chloride to determine the active concentration (% w/v) of sodium tetradecyl sulphate remaining in the solution. Results A calculated approximation showed 0.3 ml of blood is required to fully inactivate 1 ml of 3% sodium tetradecyl sulphate when made into a foam. A comparison was made between the use of fresh blood and blood stored in ethylenediaminetetraacetic acid tubes. Blood stored in ethylenediaminetetraacetic acid tubes showed more inactivation of sodium tetradecyl sulphate, but this was not significant at the P ≤ 0.05 level. Conclusion The data from our study have shown that a minimum of 0.3 ml of fresh blood is required to inactivate 1 ml of 3% sodium tetradecyl sulphate as a foam and it is not significantly affected by storing blood in an ethylenediaminetetraacetic acid tube. Our methodology suggests that during foam sclerotherapy treatment, blood should not be aspirated into the syringe to confirm position, and that ultrasound guidance is more appropriate for needle placement.

Suprapubic varicose vein formation during pregnancy following pre-pregnancy pelvic vein embolisation with coils, without any residual pelvic venous reflux or obstruction.

Suprapubic varicose veins are usually indicative of unilateral iliac vein occlusion and venous collateralisation. We report two cases of suprapubic varicose veins following pelvic vein embolisation and subsequent pregnancy; both presented without residual pelvic venous reflux or pelvic venous obstruction. In both cases, there was no significant flow in the suprapubic veins indicating that they were not acting as a collateral post-pregnancy. One patient had this venous abnormality treated successfully with TRansluminal Occlusion of Perforators, followed by foam sclerotherapy to the main part of the suprapubic vein. This patient has since completed the reminder of her lower limb varicose vein treatment. We suggest that pregnancy may have caused prolonged intermittent compression of the left common iliac vein, and that this, together with the physiological impact of previous embolisation procedures, obstructed venous drainage from the left leg resulting in collateral vein formation within the 9-month gestation period.