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Johannes H. M. Smits, Joke van der Linden, Peter J. Blankestijn, Ton J. Rabelink, Coagulation and haemodialysis access thrombosis, Nephrology Dialysis Transplantation, Volume 15, Issue 11, November 2000, Pages 1755–1760, https://doi.org/10.1093/ndt/15.11.1755
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Introduction
An increased thrombotic tendency is an important cause of complications in chronic haemodialysis patients, leading not only to possibly fatal complications like ischaemic heart disease or stroke, but also to thrombosis of the vascular access [1]. This latter complication remains the main problem in vascular access for haemodialysis, particularly in polytetrafluoroethylene (PTFE) grafts. It accounts for considerable morbidity and mortality with an estimated annual cost of close to $1 billion in the United States. Moreover, vascular access complications mainly consisting of thrombotic events are responsible for 17–25% of all hospitalizations in dialysis patients [2–4].
In most cases thrombosis is associated with low access blood flow [5–7]. The most important reason for a decreasing access blood flow is intimal hyperplasia formation at the venous anastomosis or in the outflow tract of the graft [8–13]. However, not all decreases in access blood flow are related to intimal hyperplasia or stenosis formation. Other causes for low access flow leading to access thrombosis have been proposed (Table 1). Hypotension, hypovolaemia, or external compression may be involved in these non‐stenotic thrombotic events [14]. Also, there has been a growing appreciation of the role of hypercoagulability states found in these patients.
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