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

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 78‐year‐old 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 ankle‐brachial 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; low‐density lipoprotein cholesterol, 124 mg/dL; triglyceride, 124 mg/dL; C‐reactive protein, 2.12 mg/dL; occasional plasma glucose, 124 mg/dL; D‐dimer, 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 ST‐T segment abnormalities.

Contrast‐enhanced whole‐body 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.

Figure 1

The left panel is three‐dimensional computed tomography (CT) angiography with volume rendering from the pelvis to the upper thigh. The right upper panel is the coronal view of the pelvis by multi‐planar reconstruction. The right lower panel is the axial view at the line A. These CT panels demonstrate 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, resulting in both obstruction of venous outflow and twisting venous dilatations distal from the LCIV (white arrowheads). LCIA, left common iliac artery; RCIV, right common iliac vein

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 May‐Thurner description4 which indicates anatomical spur‐like formations at the lesion of the LCIV by the overlying RCIA.5 Iliac vein compression syndrome could cause left unilateral leg swelling and left‐sided deep venous thrombosis in elderly patients.6

Recently, percutaneous balloon angioplasty and off‐label use stenting are being tried for the recanalization of chronic iliac vein compression syndrome.7 The patient did not undergo this procedure due to both the complete obstruction of LCIV with calcification and the risk of a major tearing of the LCIV during the procedure of guidewire recanalization. We are following this patient under anticoagulation therapy.

Conflict of Interest

The authors have stated explicitly that there are no conflicts of interest in connection with this article.