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A reduction of > 50 % of
the lumen diameter in association with haemodynamic change is
recommended as the triggering point
for treatment of stenosis 1.
The impact of the
stenosis is more obvious in prescribed blood flows as high as
500 ml/min than in 200 ml/min. The
stenosis can lead to a reduction in the adequacy of the dialysis
therapy 2. The progression of the narrowing is quite
different in individual patients and, therefore,
repeated measurements are necessary
to decide whether and how the stenosis should be treated.
Multiple stenoses and longer
stenoses are probably better treated surgically.
*2 Stenosis at the arterial anastomosis
Like in A/V fistulas,
most arterial inflow stenoses can successfully be treated by
angioplasty.
Stenosis of
the arterial anastomosis itself can be dilated, if only the
afferent artery and the graft at the anastomosis is affected but
the efferent artery is not stenosed.
If there is an additional stenosis of the
efferent artery, angioplasty of the anastomosis alone will
enhance graft flow with the risk of peripheral ischaemia due to
reduced peripheral arterial perfusion.
In these patients, either dilatation of the efferent artery by
interventional radiology or through
surgical revision of the anastomosis, may resolve the
problem.
Intra-graft (or
mid-graft) stenoses are found in the cannulation segment of
access grafts which have been in use for at least some months.
They result from excessive in-growth of fibrous tissue through
puncture holes. These stenoses can be treated by percutaneous
transluminal angioplasty (PTA) 3, graft curettage
4, and segmental graft replacement.
Replacing the
damaged graft segment is not only
the most straight-forward but also the most durable means to
restore or maintain graft patency 5. When only part
of the cannulation segment is replaced (the remaining can be
treated by curettage or intraoperative PTA if necessary), the
access can be used for further haemodialysis without the need of
a central venous catheter.
When re-stenosis occurs
in a non-exchanged part of the graft, this can be replaced after
healing of the new segment (i.e. after two weeks), again without
the need for central venous access.
*4 Stenosis at the venous anastomosis
The most frequent cause
for access graft dysfunction and thrombosis is venous
anastomotic stenosis 3 6 7. As
access grafts should be implanted only in patients with
exhausted peripheral veins, vein saving procedures like PTA or
patch angioplasty should be preferred to graft extensions to
more central vein segments, although the latter may provide
superior patency rates 8 9.
When PTA repeatedly
fails, additional stent implantation can be considered 10
11. When stent or a patch fail, graft extension is
still possible. This staged application of different therapeutic
options is very likely to enhance cumulative graft function to a
greater extent than primary use of the best option.
When the interval
between the recurrence of stenosis
becomes shorter, surgery should be considered.
Frequent graft occlusion
can occur in severely hypotensive patients, in certain types of
thrombophilia, and in subclinical graft infections. These
conditions have to be excluded if no or mild stenosis (< 50 %)
is found at graft thrombectomy.
After successful
percutaneous transluminal angioplasty (PTA) the access blood
flow (Qa) usually increases almost twofold, but in
half of the grafts the blood flow decreases to baseline within
three months 12. There is no correlation between the
change in blood flow and the residual stenosis 13
14. In 20 30 % of the grafts, PTA does not increase
blood flow to more than 600 ml/min, indicating insufficient
dilatation with an undersized balloon, immediate recurrence of
stenosis, or the existence of unidentified and not corrected
stenosis either more centrally or at the arterial inflow.
Long-term outcomes did not
correlate with angiographic results, but with Qa
values before PTA and the increase in Qa due to the
procedure 14. However, it may be argued, that the
dilatation has not been sufficient in these grafts.
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