Overview of hemodialysis arteriovenous graft maintenance and thrombosis prevention
- Michael Allon, MD
Michael Allon, MD
- Professor of Medicine
- University of Alabama at Birmingham
- Section Editors
- Jeffrey S Berns, MD
Jeffrey S Berns, MD
- Editor-in-Chief — Nephrology
- Section Editor — Dialysis
- Professor of Medicine
- Perelman School of Medicine at the University of Pennsylvania
- David L Cull, MD
David L Cull, MD
- Section Editor — Arterial and Venous Access
- Clinical Professor, Department of Surgery
- University of South Carolina School of Medicine
This topic review provides an overview of general issues regarding arteriovenous (AV) graft maintenance, including measures to prevent AV graft thrombosis and management of the high-risk AV graft. These same considerations with respect to AV fistulas are reviewed separately. (See "Overview of hemodialysis arteriovenous fistula maintenance and thrombosis prevention".)
RISK FACTORS FOR AV GRAFT THROMBOSIS
Arteriovenous (AV) graft thrombosis can occur immediately following AV graft creation, usually related to technical issues, or later after using the access for a variable period of time predominantly due to stenotic lesions that develop from intimal hyperplasia. More than 90 percent of thrombosed grafts have a stenotic lesion. (See "Hemodialysis arteriovenous graft dysfunction and failure".)
Stenosis of a hemodialysis AV graft is initiated by endothelial cell injury, which leads to the upregulation of adhesion molecules on the endothelial cell surface. Subsequent leukocyte adherence to damaged and activated endothelium causes the release of chemotactic and mitogenic factors for vascular smooth muscle cells, thereby enhancing smooth muscle cell migration and proliferation [1-3]. Additional factors that contribute to the neointimal proliferation and fibromuscular hyperplasia include shear stress generated by the turbulent blood flow [4,5] and the mismatch in elastic properties around the anastomosis leading to excessive mechanical stretch . Activated platelets and inflammatory cells also secrete oxidants and other toxins that directly injure the vessel wall . Measures aimed at reducing neointimal hyperplasia as well as other pharmacologic agents that address other elements underlying vascular stenosis may help prevent stenosis. (See 'High-risk AV grafts' below.)
Other factors that can lead to AV graft dysfunction and thrombosis include:
●Preexisting stenotic lesions
Subscribers log in hereLiterature review current through: Jul 2017. | This topic last updated: Jun 28, 2017.References
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- RISK FACTORS FOR AV GRAFT THROMBOSIS
- ROUTINE GRAFT MAINTENANCE AND CARE
- Cannulation and decannulation
- - Inspection prior to initial cannulation
- - General procedure
- - Decannulating the AV graft
- - Cannulation difficulty or failure
- Care between dialysis sessions
- PRIMARY THROMBOSIS PREVENTION IN NEWLY CREATED GRAFTS
- Angioplasty/stenting of underlying stenosis
- Prophylactic antithrombotic therapy
- HIGH-RISK AV GRAFTS
- Immediate graft thrombosis
- - Evaluation for hypercoagulable state
- - Anticoagulation for hypercoagulabity
- Early graft thrombosis
- - Dipyramidole and aspirin
- - Other antiplatelet agents
- - Fish oil
- RECURRENT THROMBOSIS
- Recurrent stenotic lesions
- Recurrence in the absence of a stenotic lesion
- EXPERIMENTAL THERAPIES
- SUMMARY AND RECOMMENDATIONS