jeff

I have seen several such cases . when I was doing my static pressures with Kevin Sullivan in the late 80's early 90 we did sequential angiograms. I too noted that accessory veins present after initial maturation of BC AVF would over time have the accessory veins pruned off  even though the static pressures remained unchanged. Even when central stenosis at the arch occurred in some and intra access pressure increased,  the accessory veins were still not visible. I always wondered whether the change in shear forces did something at the orifice of the accessory veins. On the other hand I remember a patient with complete central occlusion and evidence of "collateral" flow with veins over the shoulder, the intercostals etc who was carrying 3 L of fluid in his arm but who maintained a flow through the system if you can believe it of 1.7 L (measured by US at the brachial artery) which basically did not change after his obstructed portion was "recanulized". so is there a difference among patients or how much pressure does it take to make the accessories open up and carry flow.

I really do not know and there are no studies to study the natural Hx since we can't do flow, pressure and angiographic studies under current re-imbursement rules.

Anatole Besarab

Dear all,

A surgeon told me that as a fistula enlarges there will be more accessory vein flow. Not sure what his point was.  Certainly we think that fistulas will not clot at lower  access flow rates  as compared to grafts  because of these accessory ( “ collateral”)  veins maintaining outflow.   I am perplexed how frequently the accessory veins  involute  in larger fistulas.   Classic example is a well -developed BC avf that presents with  subtotal  occlusion of the cephalic arch and there are no longer any accessory/collateral veins draining to the basilic/brachial  veins.   What caused the attrition of these collateral pathways that were present when the fistula was created?   The fistula  vein became the pathway of least resistance  to flow  as the fistula matured.   Early in the maturation of the fistula, one could still demonstrate that  the accessory veins were still there if a  reflux study  was done with outflow compression.   But  later as the fistula became much larger and one discovers  an outflow occlusion  or  development of  high inflow  the accessory/collateral veins  did not enlarge to accommodate the outflow.  What causes this attrition; thrombosis in the  much smaller veins?

  I guess the other  question is why don’t some accessory veins involute when there is no longer an outflow  restriction in a developing immature fistula.   I see this more commonly in an immature forearm RC avf that has now been dilated to 8 mm and  multiple  accessory veins  remain even a year later.     Seems like the physics of  flow don’t   explain all the findings of the shunts that are man- made.

Does anyone know of any anatomy/pathology studies that document the presence of valves in these small  accessory  veins. I would assume they have valves but I don’t know.

Thank you for any thoughts or feedback about accessory veins.

Jeff

Jeffrey Hoggard MD

Capital Nephrology Assoc

3031 New Bern Ave

Suite 100

Raleigh, NC  27610

Office: 919-747-7820

Cell:  252 -531-9556

Dear All,

Have fun reading the January Articles of Interest...

Abigail 

https://sites.google.com/site/abigailsarticles/january-2015-articles