ASDIN white paper: Management of cephalic arch stenosis endorsed by the American Society of Diagnostic and Interventional Nephrology

Author:

Beathard Gerald A1ORCID,Jennings William C2ORCID,Wasse Haimanot3ORCID,Shenoy Surendra4,Falk Abigail5,Urbanes Aris6,Ross John7ORCID,Nassar George8,Hentschel Dirk M9ORCID,Sachdeva Bharat10,Chan Micah R11,Salman Loay12,Asif Arif13

Affiliation:

1. University of Texas Medical Branch at Galveston, Houston, TX, USA

2. School of Community Medicine, The University of Oklahoma, Tulsa, OK, USA

3. Rush University Medical Center, Chicago, IL. USA

4. Washington University and Barnes-Jewish Hospital, Saint Louis, MO, USA

5. New York, NY, USA

6. Internal Medicine, Wayne State University, Detroit, MI, USA

7. Regional Medical Center of Orangeburg and Calhoun Counties, Dialysis Access Institute, Orangeburg, SC, USA

8. Weill Cornell Medicine and Houston Methodist Hospital, Houston, TX, USA

9. Renal Division, Brigham Health, Boston, MA, USA

10. LSU Health Shreveport School of Medicine, Shreveport, LA, USA

11. University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, USA

12. Albany Medical Center, Albany, NY, USA

13. Department of Internal Medicine, Hackensack Meridian School of Medicine at Seton Hall University, Neptune, NJ, USA

Abstract

Brachiocephalic arteriovenous fistulas (AVF) makeup approximately one third of prevalent dialysis vascular accesses. The most common cause of malfunction with this access is cephalic arch stenosis (CAS). The accepted requirement for treatment of a venous stenosis lesion is ⩾50% stenosis associated with hemodynamically abnormalities. However, the correlation between percentage stenosis and a clinically significant decrease in access blood flow (Qa) is low. The critical parameter is the absolute minimal luminal diameter (MLD) of the lesion. This is the parameter that exerts the key restrictive effect on Qa and results in hemodynamic and functional implications for the access. CAS is the result of low wall shear stress (WSS) resulting from the effects of increased blood flow and the unique anatomical configuration of the CAS. Decrease in WSS has a linear relationship to increased blood flow velocity and neointimal hyperplasia exhibits an inverse relationship with WSS. The result is a stenotic lesion. The presence of downstream venous stenosis causes an inflow-outflow mismatch resulting in increased pressure within the access. Qa in this situation may be decreased, increased, or within a normal range. Over time, the increased intraluminal pressure can result in marked aneurysmal changes within the AVF, difficulties with cannulation and the dialysis treatment, and ultimately, increasing risk of access thrombosis. Complete characterization of the lesion both hemodynamically and anatomically should be the first step in developing a strategy for management. This requires both access flow measurement and angiographic imaging. Patients with CAS present a relatively broad spectrum as relates to both of these parameters. These data should be used to determine whether primary treatment of CAS should be directed toward the anatomical lesion (small MLD and low Qa) or the pathophysiology (large MLD and high Qa).

Publisher

SAGE Publications

Subject

Nephrology,Surgery

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