Dialysis Clinic
Blackwell
Oxford,
Seminars
SID
2004
0894-0959
Blackwell
UKin
Publishing,
Dialysis
Publishing
Ltd.
Arteriovenous Fistula Stenosis: New Terminology
What is a swing point stenosis?
A common cause of autogenous arteriovenous fistula
(AVF) failure is the presence of stenosis at sites of surgi-
cal vein mobilization (14), called swing point steno-
sis (1) (Table 1). Anastomotic swing point stenosis
occurs within a few centimeters beyond the surgical con-
nection in the vein used to create the AVF. In published
AVF failure series, this lesion is more common in fore-
arm AVFs (6477%) (13) than in upper arm AVFs (39
56%) (1,3). In addition, AVFs that require superficial-
ization of the basilic vein are subject to transposition
swing point stenosis, a finding in 60% of failing brachio-
basilic AVFs in one series (1).
The pathophysiology of swing point stenosis is
unknown. Hypotheses include technical surgical prob-
lems (axial rotation, kinking, or vein adventitial bands),
secondary changes in the vein related to extensive dis-
section, as well as devascularization, and intimal hyper-
plasia associated with increased turbulence and shear
stress following AVF creation (1).
The initial diagnosis of swing point stenosis is based
on clinical findings. The normal examination should
reveal a soft and pliable AVF with a brisk continuous
thrill at the anastomosis that diminishes gradually travel-
ing up the fistula away from the anastomosis (5). An
TABLE 1. Etiologies for AVF failure initially or after attainment of
blood flow to support dialysis
Anastomotic swing point stenosis
Transposition swing point stenosis
Outflow vein stenosis (not associated with surgical vein mobilization
sites)
Central vein stenosisa
Accessory vein (diversion of blood flow) b
Arterial insufficiency
a
Rarely if ever a primary etiology, but characteristically present with
other primary etiologies.
b
Controversial, as some investigators cite this as a primary etiology
requiring direct interruption of flow with ligation or embolization (4),
whereas others designate accessory veins as epiphenomena to stenosis
requiring extensive search for and PTA of stenosis (3).
Dysfunction of New Catheters by Old Fibrin Sheaths
Dysfunction of tunneled central vein catheters is often due
to fibrin sheath formation. I was under the impression
that the dysfunctional catheter could be exchanged over a
wire with-out concern about the sheath, which was pre-
sumably disrupted with catheter removal. I recently heard that
additional action is needed to ensure that the new catheter
is not made dysfunctional by the old sheath. Is this true?
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DIALYSIS
ialysis
AVF
VassalottiClinic
2004
CLINIC
Stenoses
anastomotic swing point stenosis appears as a firm or
hard AVF with a water hammer pulse at the surgical
connection, including an absent diastolic component
(5). Moving downstream along the fistula (away from
the anastomosis), past the stenotic lesion, the pulse
diminishes abruptly or disappears. An important sign of
anastomotic swing point lesions in an AVF supporting
dialysis is high negative arterial (prepump) pressures,
since the narrowing is generally upstream from the AVF
arterial needle. Such high negative pressures can cause
a significant reduction in actual delivered blood flow,
thereby compromising the adequacy of dialysis. Swing
point stenosis can also present with AVF thrombosis (3).
Fistulogram is the optimal technique to confirm this
lesion, allowing for subsequent percutaneous angio-
plasty (PTA) of the stenosis. Several investigators
employ PTA as the first-line therapy (1,3,4). One-year
mean primary patency rates of 50% for forearm AVFs
and 34% for upper arm AVFs were reported in one series
(3); secondary patency rates of 8086% were found
for all AVF. Alternatively, one group advocates a new
surgical anastomosis just proximal to the pathologic
area (2). When PTA fails, surgical revision is uniformly
recommended.
Joseph A. Vassalotti
New York, NY
References
1. Falk A, Teodorescu V, Lou WY, Uribarri J, Vassalotti JA: Treatment of
swing point stenoses in hemodialysis arteriovenous fistulae. Clin Nephrol
60:3541, 2003
2. Tordoir JH, Rooyens P, Dammers R, van der Sande FM, de Haan M, Yo TI:
Prospective evaluation of failure modes in autogenous radiocephalic wrist
access for haemodialysis. Nephrol Dial Transplant 18:378383, 2003
3. Turmel-Rodrigues L, Pengloan J, Baudin S, Testou D, Abaza M, Dahdah G,
Mouton A, Blanchard D: Treatment of stenosis and thrombosis in haemodia-
lysis fistulas and grafts by interventional radiology. Nephrol Dial Transplant
15:20292036, 2000
4. Beathard GA, Arnold P, Jackson J, Litchfield T: Aggressive treatment of early
fistula failure. Kidney Int 64:14871494, 2003
5. Beathard GA: Physical examination of the dialysis vascular access. Semin
Dial 11:231236, 1998
Tunneled hemodialysis catheter dysfunction occurring
after a period of optimal function is generally due to
thrombosis. Catheter-related thrombosis can be either
extrinsic, such as a mural thrombus or an intra-atrial
thrombus, or it can be intrinsic (1). This later category is
the most frequent cause of dysfunction associated with
the tunneled hemodialysis catheter, and the category
244 Beathard
referred to as a fibrin sheath is the most common
culprit.
Based on animal (24), postmortem studies (5,6), and
the histologic examination of fragments of sheath that
adhere to catheters that have been removed, it seems
apparent that for many patients, the term fibrin sheath is
a misnomer. The sheath is actually composed primarily
of fibrous connective tissue. The formation of the sheath
begins at the venous insertion site and propagates down
the catheter from that point. Initially it is fibrin; however,
it becomes organized and is progressively converted to
fibrous connective tissue as it migrates down the catheter
toward the tip. While the leading edge is fibrin, it is fol-
lowed by a transition zone where the thrombus becomes
organized; the remainder is connective tissue. The extent
of the organization depends upon the age of the catheter.
As the sheath extends downward, it eventually closes over
the tip of the catheter. In this position, it can be disrupted
by inward pressure, creating a flap-valve that will allow
injection but prevents withdrawal of blood and fluid.
The sheath is only loosely attached to the catheter. In
the case of an early sheath, in association with a catheter
that has been in place for only a short period of time, the
sheath is composed predominantly of fibrin and may be
very fragile. Manipulation of the catheter can result in its
disruption. We have seen an instance in which a com-
plete fibrin sheath developed around a catheter in place
for only 5 days. The sheath was observed when radio-
contrast was injected through the catheter as it was being
removed. When a second injection was made, it was
completely gone. In the case of a chronic sheath, one that
has become organized, it is possible to remove the cath-
eter and leave the sheath in place where it may persist for
weeks (7). In this instance it is possible to remove the old
catheter and place a new one back into the same sheath
that has remained intact.
There have been three basic approaches to the treat-
ment of the fibrin sheath: lytic enzymes, stripping, and
catheter exchange. All have had their proponents. In gen-
eral, the use of lytic enzymes is viewed to be primarily of
temporary value for use in the dialysis unit, thus allow-
ing the patient with a dysfunctional catheter to receive
their scheduled dialysis treatment. Fibrin sheath strip-
ping is falling out of favor with many interventionalists
because it has no advantage and adds significantly to the
cost of treatment. Catheter exchange has emerged as the
preferred treatment.
The presence and persistence of a fibrin sheath is easily
demonstrated during the course of catheter exchange.
As the old catheter is being removed, an injection of
radiocontrast made when the tip of the catheter is at the
level of the venous entry site, will demonstrate the struc-
ture quite well. In our experience a sheath is present in
approximately 50% of the catheter dysfunction cases.
Variability in its detection may be largely dependent
upon the age of the catheter being exchanged. Early
sheaths will be predominantly fibrin and can be dis-
rupted by catheter manipulation and never seen. Older,
more chronic sheaths are more organized and resistant.
Unfortunately the evidence supporting the value
of disrupting the fibrin sheath prior to placing the new
catheter is largely anecdotal. There is a need for a
well-designed prospective controlled study. Nevertheless,
prior to routinely looking for and disrupting the fibrin
sheath, we had many instances in which early recurrence
of catheter dysfunction was found to be associated with
a prominent fibrin sheath after a period too short to allow
for its de novo development.
It has become common practice on the part of most
interventionalists to routinely look for the presence of a
fibrin sheath and avoid inserting the new catheter into
the old, retained sheath. In order to avoid this eventuality,
it is necessary to either recannulate the vein so as to avoid
entering the sheath or use some mechanism for disrupt-
ing the structure prior to the insertion of the new catheter.
Gerald A. Beathard, MD, PhD
Austin, TX
References
1. Beathard GA: The use and complications of catheters for hemodialysis vascu-
lar access: introduction. Semin Dial 14:410, 2001
2. OFarrell L, Griffith JW, Lang CM: Histologic development of the sheath that
forms around long-term implanted central venous catheters. J Parenter
Enteral Nutr 20:156 158, 1996
3. Xiang DZ, Verbeken EK, Van Lommel AT, Stas M, De Wever I: Composition
and formation of the sleeve enveloping a central venous catheter. J Vasc Surg
28:260 271, 1998
4. Xiang DZ, Verbeken EK, Van Lommel AT, Stas M, De Wever I: Sleeve-
related thrombosis: a new form of catheter-related thrombosis. Thromb Res
104:714, 2001
5. Grossi C, Mangano S, Zani MB, Tettamanzi F, Scalia P: Tessio catheters: findings
in post-mortem examination. Nephrol Dial Transplant 11:1363 1364, 1996
6. Forauer AR, Theoharis C: Histologic changes in the human vein wall adjacent
to indwelling central venous catheters. J Vasc Interv Radiol 14:11631168, 2003
7. Hoshal VJ, Ause RG, Hoskins PA: Fibrin sleeve formation on indwelling sub-
clavian central venous catheters. Arch Surg 102:253 258, 1971