Causes of hemodialysis access failure

Abstract

Complications of hemodialysis access remain significant problems in the population receiving renal replacement therapy. The causes of access loss must be recognized before appropriate interventions can be designed. The native primary arteriovenous fistula is the access of choice because of its good survival characteristics and low rate of complications. Unfortunately, a substantial number of patients have vasculature insufficient to create and maintain this access. Once a primary fistula is established, thrombosis is the leading cause of failure: its causes can be divided into early (less than 6 weeks) and late complications. In patients unable to have fistulas, arteriovenous conduits of expanded polytetrafluoroethylene (ePTFE) are now the prostheses of choice. Again thrombosis is the leading cause of this access loss but there is also a substantial rate of failure from infection, pseudoaneurysms, perigraft hematomas, and simple attrition of the prosthesis. Thrombosis of ePTFE grafts is usually associated with anatomic stenosis at the venous anastomosis, within the graft itself, or in the central venous system. Graft thromboses cannot always be attributed to anatomic lesions: in these circumstances, thrombosis has been attributed to low-flow states. It is possible that the normal balance between endothelial procoagulant and anticoagulant forces are disrupted within the arteriovenous conduit. Recurrent venipuncture, hemodialysis therapy itself, or pathophysiological forces inherent in the access may all favor hemostasis. Infection also causes significant hemodialysis access morbidity. The causative organism is usually Staphylococcus aureus but several other pathogens have been reported. Ideally, all prostheses should be removed when infected, but this approach must be tempered by the reality of limited hemodialysis access sites. There is no consensus as to the best therapeutic approach to access infection.