Arteriovenous fistula (AVF) late complications: Stenosis

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; however, late AVF failure is frequently defined as failure that occurs after three months of use².  The causes of access failure can typically be diagnosed by imaging either through angiography or by duplex ultrasound^3,4. 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.

Thrombosis in the first month after access placement is usually due to technical errors in fistula construction or vessel selection⁵. 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.  Venous stenosis is the most common cause of late AVF loss^2,6. In one study, 63 mature fistulas required 209 procedures to maintain patency^2,7. Eighty-three percent (174/209) of the procedures were venous angioplasty to correct venous stenosis^2,7.  Although 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.

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 veins^5,9. Lesions at the arterial anastomosis develop from progressive neointimal hyperplasia (NH)⁹. Pathogenic mechanisms of NH include formation by smooth muscle cells, fibroblasts and microvessels and cytokine modulation^9,10. 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 axilla^5,9.

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. 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 lesion^5,8. Non-stenosis-associated access thrombosis is often due to excessive fistula compression to achieve hemostasis after dialysis⁵. Dialysis staff and patients should be educated and trained in preventing this avoidable complication.

Though stenosis is an undesirable AVF complication, AVF are less likely than grafts to develop stenosis and thrombosis^11,12. 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<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<0.001) ¹¹. The long term patency of AVF is superior to AV grafts because the risk of secondary failure is much lower.

References

1. Ravani P, Spergel LM, Asif A, Roy-Chaudhury P, Besarab A. Clinical epidemiology of arteriovenous fistula in 2007. J Nephrol. 2007;20(2):141-149. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17514618.
2. MacRae JM, Dipchand C, Oliver M, et al. Arteriovenous Access Failure, Stenosis, and Thrombosis. Can J kidney Heal Dis. 2016;3:2054358116669126. Available from: http://www.ncbi.nlm.nih.gov/pubmed/28270918.
3. Sands JJ, Ferrell LM, Perry MA. The role of color flow Doppler ultrasound in dialysis access. Semin Nephrol. 2002;22(3):195-201. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12012305.
4. Malik J, Slavikova M, Malikova H, Maskova J. Many clinically silent access stenoses can be identified by ultrasonography. J Nephrol. 2002;15(6):661-665. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12495280.
5. P Y Fan SJS. Vascular access: concepts for the 1990s – PubMed. J Am Soc Nephrol . Available from: https://pubmed.ncbi.nlm.nih.gov/1391700/.
6. Roy-Chaudhury P, Spergel LM, Besarab A, Asif A, Ravani P. Biology of arteriovenous fistula failure. J Nephrol. 2007;20(2):150-163. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17514619.
7. Falk A. Maintenance and salvage of arteriovenous fistulas. J Vasc Interv Radiol. 2006;17(5):807-813. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16687746.
8. Asif A, Gadalean FN, Merrill D, et al. Inflow stenosis in arteriovenous fistulas and grafts: a multicenter, prospective study. Kidney Int. 2005;67(5):1986-1992. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15840048.
9. Maya ID, Allon M. Vascular Access: Core Curriculum 2008. Am J Kidney Dis. 2008;51(4):702-708. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18371547.
10. Roy-Chaudhury P, Sukhatme VP, Cheung AK. Hemodialysis vascular access dysfunction: a cellular and molecular viewpoint. J Am Soc Nephrol. 2006;17(4):1112-1127. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16565259.
11. Maya ID, Oser R, Saddekni S, Barker J, Allon M. Vascular access stenosis: comparison of arteriovenous grafts and fistulas. Am J Kidney Dis. 2004;44(5):859-865. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15492952.
12. Allon M, Robbin ML. Increasing arteriovenous fistulas in hemodialysis patients: Problems and solutions. Kidney Int. 2002;62(4):1109-1124. Available from: https://pubmed.ncbi.nlm.nih.gov/12234281/.

P/N 101048-01 Rev A 03/2021