Complications of hemodialysis (HD) access create significant problems for renal practitioners, the healthcare system and especially for individuals living with end stage renal disease. Chronic HD access complications include thrombosis, infection, ischemic steal syndrome, aneurysms, venous hypertension, hematomas, heart failure, and prolonged bleeding and result in frequent interventions and increased morbidity and mortality¹. In addition, access interventions are often costly, challenging and may require specialized surgical expertise.

Thrombosis and infection are the most common vascular access dysfunctions² and thrombosis is the most common cause of vascular access loss. Thrombosis and infection occur more frequently in arteriovenous grafts (AVG) and dialysis catheters than in arteriovenous fistulae (AVF). The Dialysis Outcomes and Practice Patterns Study (DOPPS) reports that AVG are 3.8 times more likely to require thrombectomy and 3.0 times more likely to require access intervention than AVF^1,3. AVF thrombosis rates remain in the range of 0.2 to 0.8 per patient year and AVG thrombosis rates are typically in the range of 0.6 to 1.2 per patient year⁴. Although, the United States Renal Data System (USRDS) data confirm that AVF have the lowest complication rates of any available vascular access (0.64 procedures per patient year versus 1.61 for AVG^5,6 ; once a primary fistula is established, thrombosis is the leading cause of failure in approximately 40% of cases^1,7.

Infectious complications of vascular access are a major source of morbidity and mortality among HD patients. Previous studies have reported infection as a common cause of death; accounting for 9.5 to 36% of deaths in HD patients⁸. Vascular access infections (most commonly found in patients utilizing dialysis catheters) are reported to be the source in up to 48 to 73% of all bacteremias in HD patients⁹. The risk of bacteremia with tunnel cuffed catheters averages 2.3 per 1000 catheter days. This translates into an approximate 20 to 25% bacteremia risk over the average duration of use^{1, 10}. The risk of infection averages 10% in AVG, 5% in transposed fistulas and less than 2% in non-transposed fistulas¹.

Ischemic steal syndrome secondary to a HD arteriovenous access occurs in approximately 5 to 10% of cases^1,11. The pathophysiological basis of this condition is a marked decrease or reversal of flow in the arterial segment distal to the AVF or AVG, induced by the low resistance of the fistula outflow¹¹. Mild cases can be observed closely, as most of them will reverse in a few weeks; however, severe cases require immediate intervention to prevent severe ischemic complications including ischemic neuropathy and ischemic gangrene with the potential need for amputation. Several surgical and endovascular treatments have been used including: access ligation, banding, elongation, distal arterial ligation, and distal revascularization-interval ligation. The best reported results, for treatment of dialysis access-associated steal syndrome with maintenance of access function and reversal of symptoms, have been obtained with the distal revascularization-interval ligation (DRIL)¹¹ and the endoluminal-assisted revision (MILLER) procedures¹².

Aneurysms and pseudoaneurysms, resulting from improper needle site rotation or as complications of more proximal stenosis, are less frequent complications of vascular access. AVG peudoaneurysms can develop profuse bleeding and require emergency surgical intervention. Appropriate selection of dialysis staff for access cannulation together with cannulation training and education for staff members and patients may reduce the risk of this complication. In addition, visibly tortuous access shape is a major cosmetic concern for many patients.

Venous hypertension occurs in approximately 3% of fistulas and grafts and is usually related to central vein stenosis (CVS)¹. Percutaneous transluminal angioplasty of a CVS, supplemented by stent placement as needed, is effective and considered the primary treatment for such lesions due to the lack of viable and safe surgical options¹³.

Hematomas result from needle infiltration. Needle infiltration of new fistulae is a relatively frequent complication, which occurs most commonly in older patients¹⁴. If the access has been assessed as mature for venipuncture, poor cannulation skills are often the root cause of infiltrations. Sample policies and procedures for cannulation of new AVF are available at www.fistulafirst.org.

High-output heart failure from fistula placement occurs if fistula flow exceeds 20% of cardiac output². This complication is extremely rare (less than 1% of case series)¹.

Prolonged access bleeding should not be overlooked, and should raise suspicion of high intra-access pressure, outflow stenosis or local inflammation. Prolonged bleeding may also be caused by excessive heparinization of the blood circuit, access laceration during previous cannulation or skin atrophy¹⁵. Clinical examination of the site should be performed and previous static or dynamic venous pressure measurements should be reviewed.
Vascular access management has improved dramatically over the past decades⁴. Promising new therapies including catheter lock solutions, biological tissue engineering and the merging of current access conduits into a singular device are currently under development and evaluation. It is hoped that these and other new technologies may decrease the future incidence of vascular access complications.

References

1. Oliver MJ. Chronic hemodialysis vascular access:Types and placement. Retrieved from www.uptodate.com on January 14, 2008
2. Fan Py and Schwab SJ. Vascular access: Concepts for the 1990s. J Am Soc Nephrol 3:1-11, 1992
3. Young EW, Dykstra DM, Goodkin DA, Mapes DL, Wolfe RA, Held PJ. Hemodialysis vascular access preferences and outcomes in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Kidney Int 61: 2266-2271, 2002
4. Sands JJ. Vascular access 2007. Minerva Urol Nefrol 59:237-249, 2007
5. Sands, JJ. Vascular access: The past, present and future. Blood Purif 27:22-27, 2009
6. U.S. Renal Data System, USRDS 2007 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, 2007
7. Albers FJ. Causes of hemodialysis access failure. Adv Ren Replace Ther 1:107-118, 1994
8. Dhingra RK, Young EW, Hulbert-Shearon TE, Leavey S, Port FK. Type of vascular access and mortality in US hemodialysis patients. Kidney Int 60:1443-1451, 2001
9. Nassar GM and Ayus JC. Infectious complications of the hemodialysis access. Kidney Int 60:1-13, 2001
10. Saad TF. Bacteremia associated with tunneled, cuffed hemodialysis catheters. Am J Kidney Dis 34:1114-1118, 1999
11. Schanzer H and Eisenberg D. Management of steal syndrome resulting from dialysis access. Sem in Vascular Surgery 17:45-49, 2004
12. Goel N, Miller GA, Jotwani MC, Licht J, Schur Iand Arnold WP. Minimally invasive limited ligation endoluminal-assisted revision (MILLER) for treatment of dialysis access-associated steal syndrome. Kidney Int 70:765–770, 2006
13. Levit RD, Cohen RM, Kwak A, Shlansky-Goldberg RD, Clark TWI, Patel AA, Stavropoulos SW, Mondschein JI, Solomon JA, Tuite CM, Trerotola SO. Asymptomatic central venous stenosis in hemodialysis patients. Radiology 238:1051-1056, 2006
14. Allon M. Current management of vascular access. Clin J Am Soc Nephrol 2:786-800, 2007
15. Vascular access guidelines. Retrieved from www.vascularaccesssociety.com on February 16, 2009

P/N 101051-01 Rev. 00 3/2009