AVF failure can be discussed in terms of primary (early) failure or late failure. A review of current literature reveals variability in the definition of primary failure1<\/sup>; however, late AVF failure is frequently defined as failure that occurs after three months of use2<\/sup>. \u00a0The causes of access failure can typically be diagnosed by imaging either through angiography or by duplex ultrasound3,4<\/sup>. Use of these technologies is important because the etiology of access problems must be identified before appropriate interventions can be designed. It is important to realize that the lesions typical of early failure are also commonly seen during the later period either because they were not addressed in a timely fashion or because the lesions have progressed and are now the source of dysfunction2<\/sup>.<\/p>\n Thrombosis in the first month after access placement is usually due to technical errors in fistula construction or vessel selection5<\/sup>. Principal causes of late fistula thrombosis include venous stenosis, excessive post dialysis fistula compression, hypotension, fistula compression due to sleeping position, hypercoagulability and occasionally arterial stenosis5<\/sup>. \u00a0Venous stenosis is the most common cause of late AVF loss2,6<\/sup>. In one study, 63 mature fistulas required 209 procedures to maintain patency2,7<\/sup>. Eighty-three percent (174\/209) of the procedures were venous angioplasty to correct venous stenosis2,7<\/sup>. \u00a0Although a consistent definition for stenosis does not exist, a narrowing equal to or exceeding a 50% diameter reduction as compared to the adjacent vessel has been used8<\/sup>.<\/p>\n Approximately 50-60% of stenoses develop at or near the arterial anastomosis (juxta-anastomotic) of the fistula, whereas the rest occur more proximally in the venous circulation, including up to 20% that involve central veins5,9<\/sup>. Lesions at the arterial anastomosis develop from progressive neointimal hyperplasia (NH)9<\/sup>. Pathogenic mechanisms of NH include formation by smooth muscle cells, fibroblasts and microvessels and cytokine modulation9,10<\/sup>. The pathogenesis of NH is initiated by endothelial cell injury, possibly from turbulent blood flow, vascular damage from angioplasty, calcification of fibrosis of venous valves, or endothelial trauma at certain anatomic pressure points such as elbow or axilla5,9<\/sup>.<\/p>\n Lesions within the fistula may also include organized clots at the sites of frequent cannulation; however, approximately one third of access thrombosis occurs in the absence of an anatomic lesion5<\/sup>. Decreased fistula blood flow due to inadequate inflow, failure to adequately dilate, hypotension, decreased cardiac output, hypovolemia, or prolonged compression of the fistula during sleep may all contribute to thrombosis in the absence of a focal anatomic lesion5,8<\/sup>. Non-stenosis-associated access thrombosis is often due to excessive fistula compression to achieve hemostasis after dialysis5<\/sup>. Dialysis staff and patients should be educated and trained in preventing this avoidable complication.<\/p>\n Though stenosis is an undesirable AVF complication, AVF are less likely than grafts to develop stenosis and thrombosis11,12<\/sup>. In a 2004 study of 543 fistulograms (358 in grafts and 185 in fistulas), Maya et al determined that the likelihood of finding a significant stenosis was substantially lower in fistulae than grafts (39.4% versus 68.7% p<\/em><0.001). Furthermore, among patients with significant stenosis, those with fistulae were less likely to have 2 or more stenotic lesions. (12.5% versus 33.1%; p<\/em><0.001) 11<\/sup>. The long term patency of AVF is superior to AV grafts because the risk of secondary failure is much lower.<\/p>\n P\/N 101048-01 Rev A 03\/2021<\/p>\nReferences<\/h4>\n
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