Alessandro Frullini
Studio medico Flebologico – Figline Valdarno Florence, Italy
E-mail: info@venevaricose.it
AbstractTo evaluate the chemical reaction of the venous wall to different sclerosing agents, the Authors studied the level of blood histamine concentration before and 8-10 min after sclerotherapy injection into large 3-6 mm subcutaneous varices. A total of 45 sessions were studied: a solution of iodine 2% was used in 15 (group A), liquid 2% polidocanol in 15 (group B), polidocanol 0.5% foam in 15 (group C). Histamine basal level was 4.49, 4.48 and 4.52 µg/100 mL, respectively, while after injection an increase was found of 4.50 (102%), 4.42 (99%) and 4.46 (100%) µg/100 mL, respectively. No significant relationship was found between agents and reactions. In C group, 2 cases had visual symptoms, both showing an 150% increase in histamine.
Migraine with aura seems to be associated with high hematic levels of histamine. High histamine levels caused by sclerotherapy may explain the visual symptoms frequently reported after treatments. In fact, histamine is a vessel vasoconstrictor (venous spasm) but also a small artery vasodilator (hypotension). It could, therefore, mediate these minor sclerotherapy complications. For this reason, an antihistaminic pre-medication could be justified. The recently suggested endotheline hypothesis could support this. |
This paper by Francesco Ferrara has clear merit in that it confirms that sclerotherapy is not simply the closure of a vein. Instead, it has to be considered as a complex phenomenon in which a particular reaction is elicited in the target vein. This includes release of mediators and probably other products from the vein or from the blood inside the vein itself. Furthermore, the venous spasm that sclerotherapy provokes introduces a strong variable in revealing side effects: a partial spasm means the presence of a flux in the irritated vein and this could be a key point when withdrawing mediators with consequent systemic side effects. The release of histamin after sclerotherapy is a well-known phenomenon for the experienced sclerotherapist. Indeed, after sclerotherapy for teleangectasias, wheal formation is a clear sign of histamin release. Dr Ferrara’s demonstration and measurement of this deserves recognition. In my opinion, there is a balance between vasodilator and vasospastic mediator release after sclerotherapy. This is made more complex by the presence of receptors that act as antagonists for the same mediators; endothelin has ET-A and ET-B receptors with different effects. In any case, it is now clear that to explain systemic side effects of foam sclerotherapy by the presence of gas bubbles is too simplistic if not completely wrong. The dramatic onset of a neurological or visual disturbance after sclerotherapy has to be considered the epiphenomenon of a truly complex reaction between an irritant and the vein wall. This includes mediator release and can be affected by many other conditions, such as vasospasm, concomitant drug treatments, width of the treated area, etc. Fully understanding this process will hopefully help us to prevent these rare but very annoying complications.
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