Prevention of Early Arteriovenous Fistula Failure Due to Thromosis: Experience with Primary Thromboprophylaxis.
Authors: Sharathkumar Anjali A. , Lin Jin-Jar , Hirschl Ronald , Pipe Steven 
Published: April 2020

Abstract
Background: Arteriovenous fistula (AVF) is the preferred vascular access for children with end stage renal disease (ESRD) requiring hemodialysis. Once AVF is surgically created, it takes 6 to 12 weeks to mature. Nearly 20 to 50% of AVFs fail to mature due to development of primary or secondary thrombosis. Currently there is no uniform strategy to prevent the thrombosis at AVF. We report our experience of using primary thromboprophylaxis (PTP) for prevention of thrombosis at AVF.
Methods & Results: A strategy of PTP constituted an infusion of unfractionated heparin (UFH, 10 IU/kg/hr) for the first 24 hours after AVF surgery followed by subcutaneous injection of low molecular weight heparin (LMWH, 0.5 to 1 mg/kg/dose) twice daily until AVF was matured and successfully accessed. LMWH therapy was monitored by peak and trough anti-Xa levels. Target anti-Xa levels were maintained in therapeutic range (0.5 to 1.0 IU/ml) for those with history of thrombosis or associated risk factors for thrombosis while remaining patients were maintained in prophylactic range (0.2 to 0.5 IU/ml). Trough anti-Xa level was aimed to be les than 0.2 IU/ml. Total of 26 AVF were performed on 18 children from January 2001 to July 2006: 19 (73%) historical controls; 7 (27%) received PTP. Mean time for AVF maturation was 60 days (range: 33 to 88). Among 19 children, 14 received no thromboprophylaxis while 5 received aspirin (81 mg once daily). Eleven (79%) of 14 AVF in no treatment group failed: 9/14 (65%) due to thrombosis, 2/14 (14%) due to poor growth of venous segment. Among 5 children who received aspirin prophylaxis, 2 (40%) AVFs failed, 1 (20%) developed hematoma and 1 (20%) had poor growth. In PTP group, 2/7 (29%) AVF failed: 1 due to hematoma, 1 due to poor growth. Additional events in PTP group included: vasospasm-induced thrombosis requiring thrombectomy (n=1) and hematoma (n=2, one was salvaged by surgical evacualtion). Two children who developed hematoma had anti-Xa levels at 1.56 IU/ml and 0.6 IU/ml respectively. Presently 4/7 (57%) AVFs in PTP group are functioning well (Figure 1). The 7th patient does not require hemodialysis. Three of the 5 children in the PTP group are still on LMWH (mean duration 6 months, mean anti-Xa level 0.6 IU/ml). Mean AVF survival was higher in children who received PTP (Day 100 survival: 57.14±18.7% versus 42.10±11.32% respectively; p 0.20; Figure 2). Small sample size thus far limits the meaningful statistical analysis.
Conclusion: Our experience of LMWH thromboprophylaxis appears encouraging for prevention of AVF failure due to thrombosis. Close clinical and laboratory monitoring is required to prevent bleeding complications related to LMWH. More prospective data to expand our sample size will be required to clarify our observation.
Institutional Experience of AVF from 2001 to 2006: Comparison between heparin thromboprophylaxis and historical controls D100 AVF survial: Comparison between thromboprophylaxis & historical controls D100 AVF survial: Comparison between thromboprophylaxis & historical controls