Comment to: Pulmonary gas exchange after foam sclerotherapy (Research letter) by Moro L, Rossi Bartoli I, Cesari M, Scarlata S, Serino F-M, Antonelli Incalzi R. JAMA Dermatol 2014;150:207-9.

Lorenzo Tessari

Abstract

A venous gas microembolization should lead to some loss of gas exchange surface, with consequent gas exchange abnormalities and reduction in the transfer factor of the lung for carbon monoxide (TLCO). Aim of this proof-of-concept study was to verify whether TLCO worsens after foam sclerotherapy (FS) treatment.
Eleven consecutive voluntary patients [7 women and 4 men, mean age of 64 (SD=12) years], scheduled to undergo FS for varicose veins, were enrolled in the study. The patients (7 women and 4 men) had mean age of 64 (SD=12) years. Respiratory function tests (RFT) were performed after an overnight fasting and 24 h smoke-free using a Baires computerized system. The following parameter were obtained and adjusted for hemoglobin concentration: TLCO, CO diffusion index (through alveolus-capillary barrier), and kCO (i.e., TLCO adjusted for alveolar volume). FS was performed mixing 1% polidocanol with physiological gas (70% CO2, 30% O2). The mean volume of injected foam was 6 cc (standard deviation, SD=2.82) in SSV (2 cases) and 6.25 cc (SD=1.67) in GSV (9 cases).
The timetable of the study was: General clinical assessment; After 10 min, RFT (time 0, T0); After 10 min, sclerotherapy; After 20 min, RFT (time 1, T1); After 7 days, RFT (time 2, T2). None of the patients reported adverse events of the FS. No statistically significant difference across study time-points was reported for RFT (all P values >0.05). Lung bubble microembolism seems unlikely to complicate FS, at least if a CO2/O2-based mixture (less emboligen than an air-based mixture) is used. It is possible that gas exchange modifications may occur in case of major respiratory alterations. However, the TLCO parameter we adopted, is highly sensitive even to clinically silent modifications. In conclusion, bubble microembolism either is not a typical effect of FS or only minimally impact on gas exchanges. Other mechanisms may be accounted for FS-related respiratory adverse effects.


Comment by Lorenzo Tessari

All my congrats to the Authors for the excellent work and for the objectives they gained. It was time that someone pointed out the difference among sclerotherapy adverse events that are linked to the drug and those linked to the carrier (the gas bubble) or to the release of endothelial cathabolites deriving from the drug itself (endothelin1, histamin, serotonin, etc.).
In the paper the Authors demonstrate that there is no link with the biocompatible soluble (CO2, O2) gas for some adverse events that, even if rarely, can happen (bronchospasm, stroke, etc.) after foam sclerotherapy.
Nevertheless, it would have been useful to compare biocompatible gases with air.
Concerning the drug, Australian, English and Italian Authors (Parsi,Watkins, Tessari, Izzo ) (1,2,3) have already demonstrated the drug inactivation as soon as it is bound by the blood proteins, a binding that occurs as soon as the sclerosing agent gets into the blood stream.
Surely, the sclerotherapy adverse effects can derive from the endothelial cathabolites release, as suggested by the Authors, in an amount that is proportional to the endothelial treated area, as derived from the major frequency of complications following spider veins rather than saphenous trunk treatments.

References

1. Watkins MR. Deactivation of sodium tetradecyl sulphate injection by blood proteins. Eur J Vasc Endovasc Surg 2011;41:521-5.[Abstract][PubMed]
2. Parsi K, Exner T, Low J, et al. In vitro effects of detergent sclerosants on antithrombotic mechanism. Eur J Vasc Endovasc Surg 2009;38:220-8.[Abstract][PubMed]
3. Tessari L, Cavezzi A, Izzo M, et al. In vivo demonstration of sodiumtetradecysulphate sclerosant foam binding with blood proteins. (Abstract - 13th Annual meeting of the European Venous Forum, Thursday 28 June–Saturday 30 June 2012, Florence, Italy). Phlebology 2012;27:307-26.[Abstract]

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