High production of endothelin after foam sclerotherapy: a new pathogenetic hypothesis for neurological and visual disturbances after sclerotherapy

Abstract

Background Visual and neurological disturbances have always been reported following liquid sclerotherapy (LS) for venous insufficiency. In 1993 Cabrera introduced foam sclerotherapy (FS) using a detergent sclerosant as Lauromacrogol 400 or sodium tetradecyl sulphate. Several authors have reported with FS an increased incidence of such transient visual disturbances and neurological complications. This has been associated with gas or air used to generate the sclerosing foam. The frequent association of the presence of a patent foramen ovale, a common condition in normal population, and such complications has led several authors to consider neurological and visual disturbances as paradoxical gas embolism. Objective We are introducing a new pathogenetic hypothesis for sclerotherapy complications. Medical literature shows evidence of a clear relationship among cerebral and retinal vasospasm, migraine and intimal irritation. We think that the irritating sclerosant agent may stimulate a significant release of vasoactive substances from the venous wall, specifically endothelin 1 (ET-1), the most powerful vasoconstricting agent. Method We have studied systemic ET-1 levels after LS and FS with Lauromacrogol 400 in a group of 13 rats at one and five minutes after injection. Results While ET-1 levels did not change significantly in control and in the LS group, a significant increase was detected after FS at one and five minutes. Conclusion We conclude that should the same results be found in patients treated using sclerosing foam (SF), ET-1 levels may closely correlate to the onset of visual or cerebral complications. Due to the bronchoconstrictor activity of ET-1, a relationship with post-treatment cough can be also postulated.