A severe cause of pulsating varicose veins

A severe cause of pulsating varicose veins

Case Report A severe cause of pulsating varicose veins Pietro Rispoli, Gianfranco Varetto, Davide Santovito, Claudio Castagno, Caterina Tallia Lancet...

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Case Report

A severe cause of pulsating varicose veins Pietro Rispoli, Gianfranco Varetto, Davide Santovito, Claudio Castagno, Caterina Tallia Lancet 2011; 378: 2138 University of Turin, Department of Medical and Surgical Disciplines, Division of Vascular Surgery, Turin, Italy (Prof P Rispoli PhD, G Varetto MD, D Santovito MD, C Castagno MD, C Tallia MD) Correspondence to: Prof Pietro Rispoli, University of Turin, Department of Medical and Surgical Disciplines, Division of Vascular Surgery, Molinette Hospital. Corso A.M. Dogliotti 14, 10126-Torino, Italy [email protected]

In June, 2010, a 66-year-old woman presented to us with a 2 month history of a bilateral pulsatile swelling in her groin. On examination she was in chronic atrial fibrillation. She had been on oral anticoagulant therapy since a mitral valve replacement in 1998. Her medical history also included arterial hypertension and bilateral varices along both great saphenous veins, but without oedema, skin dyschromia or phlebostatic ulcers. Physical examination showed abnormal bilateral pulsatile groin swelling, with holosystolic thrill and pulsating varices along the entire course of the great saphenous veins. Cardiac auscultation showed severe tricuspid insufficiency, although she was still in class 1 of the New York Heart Association (NYHA) classification system. Doppler sonography showed bilateral incontinence of the saphenofemoral junction and the entire course of the great saphenous vein, with dilatation of the iliaco-caval segment and the suprahepatic veins associated with hepatomegaly. A reversed arteriallike pulsating flow was seen in the veins of the abdomen and of the limbs, and in particular in the great saphenous veins. Neither arteriovenous fistula nor an apparent pulsatile flow transmitted by an artery was detected. The arterial trunks were normal. Transthoracic echocardiography showed an ejection fraction of 55%, confirming the presence of severe tricuspid insufficiency (figure), with dilatation of the tricuspid annulus (44 mm), the inferior vena cava (39 mm), and the suprahepatic veins with reverse systolic flow. On the basis of clinical and sonography findings, we diagnosed severe tricuspid insufficiency with repercussions on the

peripheral venous system. Initially, the differential diagnosis included arteriovenous fistula,1–5 which was ruled out because of the absence of a typical auscultatory pattern at any level of the abdominal and peripheral vasculature. In our patient, symptoms were bilateral and symmetrical; a fistula would have been localised to the vena cava if it were due to a congenital malformation or of iatrogenic origin following a bilateral invasive procedure, which our patient had not received. Clinical and imaging evidence of a relevant hyperflow towards the right heart, or of a steal syndrome due to an arteriovenous short-circuit, were not present. Because the condition was well tolerated by our patient (class 2 according to Clinical Etiology Anatomy Pathophysiology classification of venous diseases), and there were no signs of worsening venous insufficiency of the lower limbs, we temporarily opted for clinical and imaging follow-up every 6 months. Compression therapy with class 3 graduated elastic stockings was prescribed according to the results of the continuous wave doppler measurement of the peripheral venous pressure, which was 65 mm Hg in the orthostatic position. In July, 2011, at final follow-up our patient was well. We considered ligation of both saphenofemoral junctions with saphenectomy or preferably endovenous laser treatment to reduce venous hypertension in the superficial peripheral veins. When no symptoms of severe venous disease resulting from haemodynamic failure are present, prophylactic compression therapy, after measurement of peripheral venous pressure, might be required. Primary varicose veins of the lower limbs is a common condition, especially among women. Pulsating varicose ectasias are rarely reported. Severe tricuspid insufficiency should be suspected when pulsating varices of the lower limbs are present. Echo-colour-doppler ultrasound of the lower limb veins and the iliaco-caval segment, together with transthoracic echocardiography, are the imaging studies of choice. In our patient, accurate history taking and clinical assessment were sufficient to raise diagnostic suspicion of severe tricuspid insufficiency. Contributors All authors looked after the patient and wrote the report. Written consent to publish was obtained.

Figure: Transthoracic echocardiography showing severe tricuspid insufficiency

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References 1 Chow W-H, Cheung K-L. Pulsating varicose veins—a sign of tricuspid regurgitation. Br J Clin Pract 1990; 44: 669. 2 Abbas M, Hamilton M, Yahya M, Mwipatayi P, Sieunarine K. Pulsating varicose veins!! The diagnosis lies in the heart. ANZ J Surg 2006; 76: 264–66. 3 Blackett RL, Heard GE. Pulsatile varicose veins. Br J Surg 1988; 75: 865. 4 Barnett N, Collyer TC, Weston M, Spark JI. Pulsatile varicose veins. J R Soc Med 2000; 93: 29–30. 5 Moawad MR, Blair SD. Pulsating varicose veins. Lancet 1998; 352: 1030.

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