Abstract

Stenosis of the subclavian vein (SVS) after cannulation occurs in 15 to 50% of chronic hemodialysis patients, and impedes the placement of an arteriovenous fistula in the ipsilateral arm. Its natural history and pathogenic mechanisms are not well established. This study examined 42 consecutive chronic renal failure patients (28 men and 14 women; 46+/-19 yr) in whom subclavian catheters had been placed as the initial vascular access for hemodialysis. All patients underwent sequential venography studies: at baseline (24 to 48 h after removal of the catheter) and 1, 3, and 6 mo thereafter. Venograms were considered abnormal when there was evidence of unequivocal strictures (more than 30% narrowing), with or without collateral circulation. At baseline, 52.4% (n=22) of patients showed stenotic vein lesions (n=19) or total thrombosis (n=3), and identical lesions were also observed after 1 mo. Surprisingly, 10 of 22 patients with initial SVS (45.4%) showed spontaneous recanalization of venous lesions in the venographies performed 3 mo after removal. The patients with normal baseline venograms (n=20) showed no change during follow-up. Patients with definitive stenosis at 6 mo (n=12) had a higher number of inserted catheters (1.58+/-0.6 versus 1.2+/-0.48; P < 0.05), longer time in place (49.08+/-32.2 versus 29.03+/-26.6 d; P < 0.05), and higher number of dialysis sessions (21+/-13.8 versus 12.4+/-11.4; P < 0.05) than those without SVS or with spontaneous recanalization of venous lesions during follow-up. Furthermore, a higher number of catheter-related infections were observed in patients with definitive SVS (66.6% versus 33.3%; P < 0.05). In summary, SVS is observed in more than half of patients 24 to 48 h after catheter removal and 1 mo later. Even when recanalization occurs in many cases, a definitive stenosis is seen in 28% of patients by the third month. Thus, the creation of an ipsilateral vascular access is possible provided that venography is normal at this time. Finally, mechanical factors and catheter-related infections are the major risk factors for the development of late SVS.

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