Is the treatment of the small saphenous veins with foam sclerotherapy at risk of deep vein thrombosis?

OBJECTIVE: To assess the deep vein thrombosis risk of the treatment of the small saphenous veins depending on the anatomical pattern of the veins. METHOD: A multicenter, prospective and controlled study was carried out in which small saphenous vein trunks were treated with ultrasound-guided foam sclerotherapy. The anatomical pattern (saphenopopliteal junction, perforators) was assessed by Duplex ultrasound before the treatment. All patients were systematically checked by Duplex ultrasound 8 to 30 days after the procedure to identify a potential deep vein thrombosis. RESULTS: Three hundred and thirty-one small saphenous veins were treated in 22 phlebology clinics. No proximal deep vein thrombosis occurred. Two (0.6%) medial gastrocnemius veins thrombosis occurred in symptomatic patients. Five medial gastrocnemius veins thrombosis and four cases of extension of the small saphenous vein sclerosis into the popliteal vein, which all occurred when the small saphenous vein connected directly into the popliteal vein, were identified by systematic Duplex ultrasound examination in asymptomatic patients. Medial gastrocnemius veins thrombosis were more frequent (p = 0.02) in patients with medial gastrocnemius veins perforator. A common outlet or channel between the small saphenous vein and the medial gastrocnemius veins did not increase the risk of deep vein thrombosis. CONCLUSION: Deep vein thrombosis after foam sclerotherapy of the small saphenous vein are very rare. Only 0.6% medial gastrocnemius veins thrombosis occurred in symptomatic patients. However, the anatomical pattern of the small saphenous vein should be taken into account and patients with medial gastrocnemius veins perforators and the small saphenous vein connected directly into the popliteal vein should be checked by Duplex ultrasound one or two weeks after the procedure. Recommendations based on our everyday practice and the findings of this study are suggested to prevent and treat deep vein thrombosis.

Pathophysiology of visual disturbances occurring after foam sclerotherapy.

BACKGROUND: Visual disturbances (VDs) are reported with an average rate of 1.4% after foam sclerotherapy (FS). Some clinical clues indicate that they could correspond to migraine with aura (MA). AIMS: To validate the hypothesis that VDs occurring after FS correspond to MA and are not transient ischaemic cerebro-vascular events. METHOD: A prospective multicentre study was carried out by the French Society of Phlebology in collaboration with the Neurology Department of the Marseille University Hospital (France). We included prospectively and consecutively all patients who experienced VDs after FS using air to make the foam. The patients were assessed (1) clinically with a specific form describing procedures of FS and recording neurological symptoms, later analysed by a neurologist specialized in migraine; and (2) by a brain diffusion-weighted magnetic resonance imaging (MRI) (T1, T2, T2*, diffusion) carried out within two weeks and analysed by a neuroradiologist. RESULTS: Twenty patients, 16 women and four men, were included in 11 phlebology clinics. All kinds of veins were treated. VDs occurred in average seven minutes after FS. Clinical assessment showed that VDs presented characteristics of MA in all patients, with headache in 10 and without in 10. Paresthesia was observed in five patients and dysphasic speech disturbance in one. Fifteen patients (75%) had a personal history of migraine. Fifteen MRIs were performed within two weeks (mean: 8 days) and three were late (26 days). All of them were normal. MRI was not performed in two patients. CONCLUSION: These results show that VDs occurring after FS correspond to MA and are not transient ischaemic cerebro-vascular events. We suggest a pathophysiological hypothesis resting on the release of endothelin that would reach the cerebral cortex through a paten foramen ovale.

A splice site variant in the sodium channel gene SCN1A confers risk of febrile seizures.

OBJECTIVE: Our aim was to investigate whether the risk of febrile seizures is influenced by a common functional polymorphism in the sodium channel gene SCN1A. This single nucleotide polymorphism (IVS5N+5 G>A, rs3812718) was shown to modify the proportion of two alternative transcripts of the channel. METHODS: We performed an exploratory case-control association analysis in 90 adult epilepsy patients with childhood febrile seizures vs 486 epilepsy patients without a history of febrile seizures and also vs 701 population controls. In the replication step, we investigated children with febrile seizures without concomitant epilepsy at the time of their inclusion. We compared the genotypes of 55 of those children against population controls and performed a within-family association analysis in an additional 88 child-parent trios with febrile seizures. RESULTS: We observed a significant association of the splice-site interrupting A-allele with febrile seizures (p value in the exploratory step: 0.000017; joint p value of the replication: 0.00069). Our data suggest that the A-allele of this variant confers a threefold genotype relative risk in homozygotes and accounts for a population attributable fraction of up to 50% for the etiology of febrile seizures. CONCLUSIONS: The A-allele of the SCN1A single nucleotide polymorphism IVS5N+5 G>A (rs3812718) represents a common and relevant risk factor for febrile seizures. A limitation of the present study is that patients of the exploratory and replication steps differed in aspects of their phenotype (febrile seizures with and without additional epilepsy).