AVF Stenosis

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 ultrasound3,4. 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 loss2,6. In one study, 63 mature fistulas required 209 procedures to maintain patency2,7. Eighty-three percent (174/209) of the procedures were venous angioplasty to correct venous stenosis2,7. 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 veins5,9. 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 modulation9,10. 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 axilla5,9.

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 lesion5,8. 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 thrombosis11,12. 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. The 5-year and 10-year cumulative patency for radiocephalic fistulae are reported to be 53 and 45 percent respectively13. By comparison, cumulative patency for PTFE grafts at one, two and four years are approximately 67, 50 and 43 percent respectively13. These results are indicative of the reasons that AVF are considered the hemodialysis access of choice14.

References

  1. Ravani P, Spergel LM, Asif A, Roy-Chaudhury P, Besarab A. Clinical Epidemiology of arteriovenous fistula in 2007. J Nephrol 20:141-149,2007
  2. Beathard GA. Early and late hemodialysis arteriovenous fistula failure. Retrieved from www.uptodate.com on February 23, 2009
  3. Sands JJ, Ferrell LM, Perry MA. The role of color flow Doppler ultrasound in dialysis access. Semin Nephrol 22:195-201, 2002
  4. Malik J, Slavikova M, Malikova H, Maskova J. Many clinically silent access stenoses can be identified by ultrasonography. J Nephrol 15:661-665, 2002
  5. Fan Py and Schwab SJ. Vascular access: Concepts for the 1990s. J Am Soc Nephrol 3:1-11, 1992
  6. Roy-Chaudhury P, Spergel LM, Besarab A, Asif A, Ravani P. Biology of arteriovenous fistula failure. J Nephrol 20:150-163, 2007
  7. Falk A. Maintenance and salvage of arteriovenous fistulas. J Vasc Interv Radiol 17:807-814, 2006
  8. Schwab SJ. Thrombotic complications of chronic hemodialysis vascular access: Fistulas and grafts. Retrieved from www.uptodate.com on February 23, 2009
  9. Maya ID and Allon M. Vascular access:Core curriculum 2008. Am J Kid Dis 51:702-708, 2008
  10. Roy-Chaudhury P, Sukhatme VP, Cheung AK. Hemodialysis vascular access dysfunction: A cellular and molecular viewpoint. J Am Soc Nephrol 17:1112-1127, 2006
  11. Maya ID, Oser R, Saddekni S, Barker J, Allon M. Vascular access stenosis: Comparison of arteriovenous grafts and fistulas. Am J Kid Dis 44:859-865, 2004
  12. Allon M and Robbin ML. Increasing arteriovenous fistulas in hemodialysis patients: Problems and solutions. Kidney Int 62:1109-1124, 2002
  13. Oliver MJ. Chronic hemodialysis vascular access: Types and placement. Retrieved from www.uptodate.com on January 13, 2009
  14. Sands, JJ. Vascular access 2007. Minerva Urol Nefrol 59:237-249, 2007

P/N 101048-01 03/2009