Update of the SFMV (French society of vascular medicine) guidelines on the conditions and safety measures necessary for thermal ablation of the saphenous veins and proposals for unresolved issues.

Venous insufficiency is a very common disease affecting about 25% of the French population (if we combine all stages of its progression). It is a complex disease and its aetiology has not yet been fully elucidated. Some of its causes are well known, such as valvular dysfunction, vein wall defect, and the suctioning effect common to all varicose veins. These factors are generally associated and together lead to dysfunction of one or more of the saphenous veins. Saphenous vein dysfunction is revealed by ultrasound scan, a reflux lasting more than 0.5 seconds indicating venous incompetence. The potential consequences of saphenous vein dysfunction over time include: symptoms (heaviness, swellings, restlessness, cramps, itching of the lower limbs), acute complications (superficial venous thrombosis, varicose bleeding), chronic complications (changes in skin texture and colour, stasis dermatitis, eczema, vein atresia, leg ulcer), and appearance of unaesthetic varicose veins. It is not possible to repair an incompetent saphenous vein. The only therapeutic options at present are ultrasound-guided foam sclerotherapy, physical removal of the vein (saphenous stripping), or its thermal ablation (by laser or radiofrequency treatment), the latter strategy having now become the gold standard as recommended by international guidelines. Recommendations concerning thermal ablation of saphenous veins were published in 2014 by the Société française de médecine vasculaire. Our society has now decided to update these recommendations, taking this opportunity to discuss unresolved issues and issues not addressed in the original guidelines. Thermal ablation of an incompetent saphenous vein consists in destroying this by means of a heating element introduced via ultrasound-guided venous puncture. The heating element comprises either a laser fibre or a radiofrequency catheter. The practitioner must provide the patient with full information about the procedure and obtain his/her consent prior to its implementation. The checklist concerning the interventional procedure issued by the HAS should be validated for each patient (see the appended document).

[Paroxysmal nocturnal hemoglobinuria: An unknown cause of thrombosis?]. / L'hémoglobinurie paroxystique nocturne : une cause méconnue de thrombose ?

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired disorder of hematopoietic stem cells. Somatic mutation in the phosphatidylinositol glycan class A (PIG-A), X-linked gene, is responsible for a deficiency in glycosphosphatidylinositol-anchored proteins (GPI-AP). The lack of one of the GPI-AP complement regulatory proteins (CD55, CD59) leads to hemolysis. The disease is diagnosed with hemolytic anemia, marrow failure and thrombosis. Thromboembolic complication occurs in 30% of patient after 10 years of follow-up and is the first event in one out of 10 patients. The two most common sites are hepatic and cerebral veins. These locations are correlated with high risk of death. Currently, these data are balanced with the use of a monoclonal antibody (Eculizumab), which has significantly improved the prognosis with a survival similar to general population after 36 months of follow-up. Anticoagulant treatment is recommended after a thromboembolic event but has no place in primary prophylaxis.

[Henoch-Schonlein purpura and prostate cancer]. / Purpura rhumatoïde et cancer de la prostate.

INTRODUCTION: The association between adult Henoch-Schonlein purpura and prostatic carcinoma is exceptional. We report a new case. EXEGESIS: The diagnosis of prostatic adenocarcinoma, suspected because of prostatic induration is made after anatomopathological study. The patient has all the clinical (purpura, polyarthralgia), biological (circulating monocmonal IgA), and histological (leukocytoclastic vasculitis, with IgA and C3 deposits) criteria of Henoch-Schonlein purpura too. The simultaneous appearance of vasculitis and neoplasia is known. The association between adult Henoch-Schonlein purpura and malignant neoplasm like lung carcinoma or lymphoma exists too. The initial events leading to the development of these vasculitis could be tumor antigens or abnormal IgA production. CONCLUSION: The simultaneous appearance of these two disease asks here the question of mechanisms implicated in these association.

[Lower limb occlusive arteriopathy: retrospective analysis of 73 patients with onset before the age of 50 years]. / Les artériopathies des membres inférieurs débutant avant 50 ans.

OBJECTIVES: Juvenile peripheral obstructive arterial diseases (POAD) have been poorly investigated but account for 1 to 7% of POAD. We analyzed retrospectively a cohort of patients with onset before the age of 50 years. PATIENTS AND METHODS: Seventy-three patients (60 males and 13 females) were divided into 4 groups (Buerger's disease: TAO, atheromatous PAOD, auto-immune POAD, arteriopathy of undetermined origin). RESULTS: The first symptoms occurred at 38 +/- 8 years of age. Fourteen patients (20%) had TAO, 51 (70%) atheromatous POAD, 4 (5%) POAD with systemic or autoimmune disease, and 4 (5%) undetermined POAD. Age of onset was earlier in TAO (35 +/- 8 vs 40 +/- 8 years, p=0.046), smoking greater in the atheroma group (33 +/- 16 vs 24 +/- 14 pack-years, p=0.033). Fifty-three POAD patients had dyslipidaemia and 26% hypertension. Regular cannabis intake was more frequent in the TAO group (21 vs 8%). At the time of medical care, Fontaine's stage was more frequently stage II in atheroma patients (57 vs 14%) and stage IV in TAO patients (86 vs 35%). TAO was diagnosed in 43% cannabis users and in 19% non users. CONCLUSION: The main etiology of juvenile POAD is atheroma, followed by TAO. Cannabis users account for at least 10% of these patients. They are characterized by lower tobacco intake, more distal lesions, more frequent involvement of the upper limbs. They present more frequently as TAO.

Clinical prediction of lower limb deep vein thrombosis in symptomatic hospitalized patients.

We evaluated two clinical scores for the prediction of deep venous thrombosis (DVT) in hospitalized patients (Wells' and Kahn's). We included 273 patients referred to the vascular exploration unit for the suspicion of DVT. A clinical questionnaire was tilled in by the practitioner and the scores were calculated from this form. 66 of the 273 patients had a DVT. When Wells' score was 3, a DVT was found by duplex echography in 51% patients; when the score was 0, a DVT was found in 9%. Kahn's score was not adapted to this population. We then developed a new simple score (cancer, palsy or plaster immobilization, warmth, superficial venous dilation, unilateral pitting edema, other diagnosis). A DVT was found in 76% patients with a score of 3 and in 11% in those with a score of 0. We therefore propose a 6-item score whose main advantages are simplicity and usefulness in routine practice.

[Upper extremity deep venous thrombosis. 40 hospitalized patients]. / Thromboses veineuses profondes des membres supérieurs: à propos de 40 patients hospitalisés.

Deep venous thrombosis is 50 times less frequent in upper than in lower limbs. Data remain poor in the literature. Forty consecutive patients (24 males, 16 females, mean age: 54.5 years) were retrospectively analysed from 161 subjects who underwent venous explorations of the upper extremity for a 3.5 year period in the same center. Diagnosis of thrombosis was made by duplex ultrasonography (n =37) or phlebography (n =3). Main clinical manifestations were edema (n =36) and pain (n =29). Location of thrombosis was humeral (n =1), axillary (n =2), or sub-clavian (n =37, 2 bilateral). The majority of thrombosis (n =29) were secondary to cancer and venous catheter (n =19, 15 implanted ports), to central catheter alone (n =3) or cancer alone (n =7). The 11 others were associated with thoracic outlet syndrome (n =6) or apparent primary thrombosis (n =5). Thrombophilia was identified in 6 out of these 11. During follow up [mean of 9 months (0,5-36)], two patients developed pulmonary embolism, 14 a post-thrombotic syndrome and 16 patients died. Initial therapy included heparin (n =36) or fibrinolysis (n =4). Upper extremity deep venous thrombosis are mostly associated with cancers and venous catheters. Thrombophilia is frequent in the other cases. Heparin followed by oral anticoagulation is the optimal therapy whose duration depends upon underlying condition. Fibrinolysis has not been useful for preventing post-thrombotic syndrome in our study.

[Inflammatory arteriopathy of the arms in the course of Horton disease. Report of six cases]. / Artériopathie inflammatoire des membres supérieurs au cours de la maladie de Horton. A propos de six cas.

We report 6 cases of upper limb involvement in giant cell arteritis; upper limb involvement revealed the disease in 4 cases and clinical symptoms were present in 5 (upper limb pain, Raynaud's phenomenon). Upper limb pulses were not palpable and blood pressure unmeasurable in all. Duplex ultrasonography found signs of inflammatory arteriopathy in 4 cases (hypoechogenous halo of the arterial wall and acceleration of flow velocity). Arteriography was performed in 5 cases and showed long and regular stenoses. In the last case, arteriography was not done because the duplex exploration gave an easier diagnosis. With this technique, the diagnosis of upper limb involvement, frequent in autopsy series of giant cell arteritis, might be made more often. Corticosteroid therapy is indicated and surgery should be discussed only in emergency situations.