Chronic unilateral leg swelling caused by iliac vein compression (Cockett's) syndrome in an elderly patient

نویسندگان

  • Hitoshi Sugawara
  • Katsuhiko Matsuura
  • Akira Ishii
  • Takeshi Yamashita
چکیده

The causes of chronic unilateral leg swelling include common manifestations such as venous insufficiency, varicosis, deep vein thrombosis, and persistent cellulitis, less commonly are secondary lymphedema (tumor, radiation, and surgery), pelvic tumors or lymphoma causing pressure on the veins, and reflex sympathetic dystrophy, and rarely congenital venous malformation, pregnancy, and iliac vein compression syndrome.1,2 Here, we describe a 78yearold nonsmoking man with history of type 2 diabetes mellitus, dyslipidemia, and hypertension presented with left leg swelling that had been getting worse over several months. On the physical examination, the patient was alert in no acute distress, and 165 cm tall, weighing 50 kg with a body mass index of 18.4 kg/m2. His temperature was 36.7°C, blood pressure 120/54 mm Hg, pulse rate 90 beats/min (regular), respiratory rate 12 breaths/min, and oxygen saturation 97% on room air. There were right lateral inguinal hernia, bilateral hydrocele testis, superficial venous varicosity in left inguinal area, and painless nonpitting left leg swelling with localized redness, warmth, and several small blisters on the lower left leg. The bilateral differences of circumference of the thigh and lower leg were 9 cm and 11 cm around, respectively. The palpation of posterior tibial arteries was good, and anklebrachial index was as follows: right 1.03 and left 0.94. Digital rectal examination revealed an enlarged prostate. The remainder of the physical examination was unremarkable. Laboratory findings were as follows: white blood cell count, 4080/μL; hemoglobin (Hb), 14.0 g/dL; platelet count, 140 000/μL; HbA1c, 6.0%; blood urea nitrogen, 19 mg/dL; creatinine, 1.01 mg/ dL; lowdensity lipoprotein cholesterol, 124 mg/dL; triglyceride, 124 mg/dL; Creactive protein, 2.12 mg/dL; occasional plasma glucose, 124 mg/dL; Ddimer, less than 1.0 μg/mL; and no proteinuria. Chest radiograph showed cardiomegaly, and the cardiothoracic ratio was 56% with bilateral sharp costophrenic angles. Electrocardiogram showed normal sinus rhythm without STT segment abnormalities. Contrastenhanced wholebody computed tomography (Figure 1) demonstrated complete compression with calcification of the left common iliac vein (LCIV) between the overlying right common iliac artery (RCIA) anteriorly and the fifth lumbar vertebra posteriorly, known as iliac vein compression syndrome, resulting in both obstruction of venous outflow and twisting venous dilatations distal from the LCIV (white arrowheads) and venous thrombosis only in the left soleus veins with no evidence of pulmonary embolism. Iliac vein compression syndrome was clinically overviewed as one of the causes for postphlebitic syndrome by Cockett.3 We do not confuse iliac vein compression syndrome with the original MayThurner description4 which indicates anatomical spurlike formations at the lesion of the LCIV by the overlying RCIA.5 Iliac vein compression syndrome could cause left unilateral leg swelling and leftsided deep venous thrombosis in elderly patients.6

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عنوان ژورنال:

دوره 18  شماره 

صفحات  -

تاریخ انتشار 2017