Nephrology Dialysis Transplantation

NDT Advance Access originally published online on September 28, 2007
Nephrology Dialysis Transplantation 2008 23(1):19-24; doi:10.1093/ndt/gfm673

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Steal syndrome—strategies to preserve vascular access and extremity

Volker Mickley

Department of Vascular Surgery, Clinical Centre Mittelbaden, Kreiskrankenhaus Rastatt, Germany

Correspondence and offprint requests to: Dr Volker Mickley, Department of Vascular Surgery, Clinical Centre Mittelbaden, Kreiskrankenhaus Rastatt, Engelstrasse 39, D-76437 Rastatt, Germany. E-mail: v.mickley{at}klinikum-mittelbaden.de

Keywords: access banding; arteriovenous access; DRIL procedure; PAVA procedure; review; steal syndrome

	Introduction

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
In access-related steal syndrome, four stages can be distinguished (Table 1, [1]). Steal syndrome stage I (retrograde inflow of blood into the access during diastole without complaints) is a frequent finding in arteriovenous (AV) fistulae and grafts [2] and needs no intervention. Patients with pain on exercise or during dialysis (stage II), however, require permanent attention in order to early detect deterioration to stage III (rest pain) or stage IV (necrosis).

View this table: [in this window] [in a new window]   Table 1. Classification of steal syndrome (modified from [1])

 
Depending on the type and location of AV access for HD, the risk of severe access-related peripheral ischaemia (steal syndrome stage III or IV) varies between 1–2% (in distal radio-cephalic AV fistulae) and 5–15% (in brachio-cephalic/basilic fistulae and grafts) [3–6]. Following the creation of a femoral (autogenous or allograft) access, an even higher incidence of steal syndrome (16 to 36%, [7,8]) has been reported. Women, diabetics and patients with known coronary or peripheral arterial occlusive disease are at higher risk than the remaining HD population [3,9–11].

The steal syndrome is likely to disappear when the access is abandoned but creation of a new AV access on another extremity is burdened with a significant risk of recurring peripheral ischaemia. Therefore correction of the steal syndrome must aim at the double goal of preserving the access and at the same time, improving peripheral arterial circulation.

	Pathophysiology

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
AV fistulae in general are constructed in a side of artery-to-end of vein (or graft) fashion. Under resting conditions, the high resistance of muscle-feeding arteries in the diastole causes a retrograde flow in the artery distal to the AV anastomosis and into the AV access. This ‘physiologic’ steal phenomenon can be observed in 73% of AV fistulae and in 91% of access grafts [2]. Approximately 75% of the blood flow through distal radio-cephalic fistulae is supplied by the proximal radial artery, but 25% comes from a patent ulnar artery via the distal radial artery and palmar arch [12]. In elbow fistulae, the periarticular arterial collaterals have the same impact.

When an AV fistula is created using healthy vessels, dilatation of the proximal and distal arteries, as well as dilatation of the collaterals around the anastomosis, compensates for enhanced systolic AV flow and also for diastolic retrograde inflow into the fistula. Any vascular pathology affecting one or several of these adaptive mechanisms can cause distal ischaemia by a steal mechanism. Arterial stenosis upstream of the anastomosis prevents the necessary flow increase in the feeding artery; severe peripheral arterial occlusive disease (PAOD) or vasculitis enhance the resistance of distal arteries and simultaneously impair the function of natural collaterals [13]. Under these conditions, during diastole virtually all blood coming from the collaterals is drained into the access [14]. Instead of a steal syndrome stage I (also named steal phenomenon), the further dreaded stages II to IV develop, with clinical signs of peripheral ischaemia. The likelihood that a steal syndrome develops depends more on the severity of arterial pathology and less on the volume of intra-access blood flow.

	Clinical findings

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
Access-related peripheral ischaemia is primarily diagnosed on the basis of the patient's complaints and clinical findings. Similar to Fontaine's classification of PAOD, four stages can be distinguished (Table 1, [1]). In critical ischaemia stage III or stage IV, transcutaneous oxygen partial pressure (tcpO₂) is lower than 30 mmHg, wrist or digital arterial pressures are below 50 mmHg and the digital(wrist)/brachial pressure index is below 0.6 [13]. With access compression, the respective values rise significantly, sometimes even to normal. These tests help to distinguish steal syndrome from other conditions causing the constellation of dystrophy, pain and necrosis, such as carpal tunnel syndrome, Sudeck's dystrophy or calciphylaxis.

A rare but potentially devastating complication of steal is the so-called ischaemic monomelic neuropathy (IMN) [15,16]. In uraemic diabetics with pre-existing neuropathy, a reduction of the blood flow in the vasa nervorum caused by the steal phenomenon can cause severe sensorimotoric dysfunction of the ulnar, radial and median nerves without obvious tissue loss and with pressure indices above critical values. Symptoms often occur immediately after creation of the access. When the ischaemia is not reversed immediately and sufficiently, irreversible neural damage and permanent impairment of the afflicted extremity can be the consequences.

	Diagnostic evaluation

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
Access flow measurements—either with colour-coded duplex-ultrasound or with one of the dilution methods—are of minor relevance for the diagnosis of steal syndrome because—depending on the severity of arterial disease— symptoms can occur at any rate of access flow. In a recent German series [17], two-third of patients with an AV fistula and access-related ischaemia had access flows 250 ml/min. Preoperative access flow measurements, however, are indispensable in planning the optimal treatment of a steal syndrome (see below).

To detect proximal arterial stenoses, duplex-ultrasound is of limited value in patients with an AV access, as the typical post-stenotic flow pattern (bi-phasic signal) is masked because of the high diastolic flow through access-feeding arteries. However, when duplex-ultrasound is performed with the access being compressed, the post-stenotic flow pattern can be detected and thus permits the localization of a potential stenosis interfering with the arterial inflow. A pattern of minimal flow in stenotic forearm arteries suggesting severe disease of the peripheral artery as the cause of a steal syndrome can easily be demonstrated by ultrasound, whereas the palmar arch and finger arteries are better visualized angiographically [18].

In selected cases and when performed by an experienced investigator, colour-coded duplex-ultrasound alone may be sufficient to define the cause of steal syndrome and to definitely plan the corrective procedure. Most authors, however, demand angiographic visualization of the complete arterial and venous trees of the extremity. When an arterial stenosis proximal to the AV anastomosis is ruled out by duplex-ultrasonography with access compression or by MR angiography, the AV anastomosis and the venous outflow are easily visualized by a transbrachial angiography. In cases with a severe steal syndrome, forearm, hand and finger arteries can only be opacified when the access is compressed during dye injection. As a less invasive alternative to arterial puncture, contrast media can be injected directly into the access. With central compression of the access, the AV anastomosis, the feeding segment of the artery and the peripheral arterial tree can be visualized.

	Treatment options

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
Arterial inflow obstruction
Proximal arterial stenoses are the cause of access dysfunction in more than 10% of patients [19] and they have been demonstrated to be present in 25 to 50% of patients with access-related ischaemia [20,21]. Standard interventions result in immediate relief of symptoms [21]. Arterial inflow obstruction should be treated irrespective of the severity of steal-induced complaints; not only do they impair the peripheral circulation, they also cause dysfunction of the vascular access, thus reducing the efficacy of haemodialysis.

‘Classical’ steal syndrome
Only when inflow stenoses have been ruled out or successfully treated, should one classify symptoms of ischaemia as a steal syndrome in the strict sense. In AV fistulae without graft, blood flow tends to rise over time. Therefore patients with fistulae presenting with stage II steal syndrome require permanent attention by the nephrology team, in order to detect progression to stage III or stage IV in time. However, in diabetic haemodialysis patients with significant neuropathy, early correction of stage II steal syndrome should be considered in order to prevent the development of IMN. Progressive stenosis of the venous anastomosis of access grafts frequently causes flow reduction as a result of increased venous resistance. When stage II steal syndrome occurs early after the creation of a vascular access using a graft, watchful waiting is justified because symptoms of a steal syndrome will most likely disappear with time. However, if such a stenosis has to be treated in a late phase, simultaneous prophylactic correction of steal should be considered. The presence of a steal syndrome causing critical limb ischaemia (stage III or stage IV) or IMN is reason enough for urgent imaging and treatment—irrespective of the type of AV access.

Since the early 1970s, banding the access has been the preferred therapy for the steal syndrome.

Meanwhile therapeutic decisions seem to have become somewhat more difficult with the advent of surgical procedures such as DRIL and DRAL, PAVA, RUDI and MILLER. Despite being widely quoted, those techniques are not necessarily well understood. The following algorithm hopefully helps to find the most adequate solution for the problem of each individual patient. Pre-therapeutic access flow measurements, although not necessary for the diagnosis of steal syndrome, have become more and more important for a differentiated approach. Depending on the flow values measured, (i) ‘high flow’ (>800 ml/min in native fistulae, >1200 ml/min in access grafts), (ii) ‘normal flow’ and (iii) ‘low flow associated steal’ (<400 ml/min in native fistulae, <600 ml/min in access grafts) can be distinguished [22,23].

	Ligation

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
Access ligation will lead to an immediate improvement of steal syndrome and also to the loss of the access with the need to create another one, again running the risk of provoking a steal syndrome. Access ligation may be considered in severe ischaemia or IMN to gain time for a thorough diagnostic work-up and preferably in a way that later reactivation of the access with simultaneous treatment of the steal syndrome is possible. However, after ligation, reactivation of the fistula will not be possible in many cases due to thrombosis. Thus a better alternative to ligation seems to be to quickly perform the examinations needed for planning the treatment, and to treat the steal syndrome immediately afterwards with one of the procedures described below.

Access ligation can of course be performed when a steal syndrome develops after successful kidney transplantation. It is imperative when other corrective procedures are not suitable or have failed.

	Banding

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
Access banding aims at creating a narrow vessel segment within the access, close to or at the AV anastomosis. Native fistulae can be banded by non-absorbable sutures, small caliber interposition grafts or by narrowing the vein with a tight Dacron or polytetrafluoroethylene (PTFE) cuff. In prosthetic accesses, interposition of a short tapered graft segment has been suggested [5,6,17,20,22,24].

Banding aims at a reduction of access flow. Thus it can successfully be performed only in patients with a high flow associated steal syndrome. Banding a low flow access to a degree where steal syndrome disappears will result in inefficient dialysis or even access thrombosis. In some earlier series, banding was controlled only by intraoperative tcpO₂ measurements. Steal was cured in 90 to 100% of patients, but only 10 to 40% of the banded accesses remained patent (Table 2, [5,6,20]). When the use of banding is restricted to high flow associated steal syndromes and when the degree of banding is controlled by intraoperative flow measurements (aiming at 400 ml/min in native fistulae and 600 ml/min in access grafts), postoperative access patency rates are obviously much better (Table 2, [22,25]).

View this table: [in this window] [in a new window]   Table 2. Treatment results of steal syndrome

 

	DRIL and DRAL

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
In 1988, Schanzer et al. introduced the distal revascularization-interval ligation (DRIL) procedure [26] to the treatment of access-associated steal syndrome. The artery distal to the access anastomosis is ligated. Thereby retrograde diastolic inflow into the fistula—the pathophysiologic principle of steal—is stopped. This first part of the DRIL procedure is completely sufficient for the treatment of steal syndrome in distal radio-cephalic fistulae (distal radial artery ligation, DRAL), as long as the ulnar artery and the palmar arch are patent, thereby providing sufficient blood flow to the hand [27]. In brachial AV fistulae and grafts, a (vein) bypass is additionally implanted, connecting the brachial artery above the anastomosis with the antecubital artery (or one of the forearm arteries) distal to the ligation, which now is situated in the ‘interval’ between the access anastomosis and the distal bypass anastomosis. Functioning vein valves in the graft and a reasonable distance (>5 cm) between the proximal bypass anastomosis and the access anastomosis prevent retrograde diastolic flow in the graft. The DRIL procedure has been shown to result in immediate relief of signs and symptoms of the steal syndrome in the great majority of patients, and provides excellent long-term patency rates for both vein bypasses and accesses (Table 2, [4,9–11,14,28–31]).

From a pathophysiologic point of view, DRIL seems to be the ideal treatment of steal syndrome. There are, however, several disadvantages. DRIL is a rather complex and time-consuming procedure, which is possible only when a suitable vein can be harvested. Blocking retrograde inflow into the access and bypassing blood around it might reduce access flow by 25% or even more. This makes the DRIL procedure a valuable option only for patients with high flow and normal flow associated steal syndrome. In low flow associated steal syndrome, it has been suggested to perform the bypass without interval ligation [32]. Clinical results, however, have not been published thus far.

	PAVA

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
Another method to treat the steal syndrome is to create a new, markedly more proximal arteriovenous anastomosis (PAVA). The original AV anastomosis is ligated and an interposition graft is used to connect the access vein or graft with the feeding artery far centrally, the distal brachial artery in the case of a wrist fistula, the proximal brachial or even the axillary artery in the case of an upper arm access. Thereby larger collaterals from the upper arm are recruited enhancing peripheral blood supply. Although the PAVA procedure has been widely used to treat steal syndrome, systematic studies have rarely been published. In their outstanding prospective series of 30 patients, Zanow et al. [23] reported a complete relief of ischaemic symptoms in 84% of their patients with excellent access patency rates (Table 2).

The PAVA procedure has several advantages over DRIL. There is no need for vein harvesting because a PTFE graft can be used for proximal feeding of the access. The anastomoses of the graft to the larger vessels are easier to suture than those of the vein bypass to tiny and often calcified forearm vessels in DRIL. Thus PAVA is a valuable alternative to DRIL in normal flow associated steal syndrome, especially in patients without a suitable bypass vein and in patients with a graft access. A potential drawback of the method is that when it is applied to an autogenous fistula, the fistula is turned into a semi-prosthetic access with the consecutive risk of stenosis at the graft-to-vein anastomosis. On the other hand, there should also be a considerable risk of stenosis at the distal anastomosis of the vein bypass in DRIL. Comparative studies are lacking.

Haemodynamically, PAVA is very similar to DRIL because as in DRIL, a proximal diversion of flow is created. However, when the central anastomosis of the interposition graft in PAVA is created on the central brachial or axillary artery and when the graft used for feeding the access has a diameter of 5 or 6 mm, PAVA enhances access flow [23,32]. Therefore in low flow associated steal syndrome, PAVA seems to be the best if not the only option to preserve both the access and the extremity.

	RUDI

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
In the case of high flow induced cardiac failure due to a brachial AV access, closing the anastomosis in the antecubital fossa and interposing a graft between the forearm ulnar or radial artery has been shown to effectively reduce access flow by more than 50% [33]. Minion et al. [34] recently published a small series of four patients with brachial AV access-induced steal syndrome, in whom they successfully used the same technique, which they called ‘revision using distal inflow’ (RUDI). Unfortunately pre- and postoperative flow rates were not reported.

The RUDI procedure may be an alternative to banding in high flow associated steal syndrome, but it should be used only if the forearm artery not used for distal inflow is patent; otherwise there would be a high risk of persisting steal. RUDI is somewhat more invasive than most banding procedures, and flow reduction cannot be tailored to the individual patient's needs, but it lengthens the needling area of the access.

	MILLER

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
Minimally invasive limited ligation endoluminal-assisted revision (MILLER) for the treatment of access-induced steal syndrome was recently described by a group of US interventional nephrologists [35]. In 16 patients with brachial AV accesses, they exposed the access vein or graft proximal to its anatomosis to the artery and performed banding by tying a non-resorbable suture around the access over an inflated 4 or 5 mm dilatation balloon under fluoroscopic control to gain a defined reduction in the vessel diameter. Pre- and postoperative flows were not measured.

The MILLER procedure is no more than a simplified banding procedure and should therefore (if at all) be used only in high flow associated steal. It can be performed quickly and easily in the radiology unit immediately after diagnostic angiography for the evaluation of steal. Banding an access to a defined diameter, however, bears the risk of inadequate post-interventional access flow or inadequate therapy of steal symptoms. As already stated above, pre- and per-interventional flow measurements would enhance therapeutic certainty.

	Conclusion

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 
Due to the rise in the median ages of incident and prevalent haemodialysis patients and due to the growing percentages of diabetics among them, access-related ischaemia has become a growing problem. While arterial inflow obstructions causing ischaemia and access failure can often be treated interventionally, the ‘classical’ steal syndrome mostly requires surgery. Access-associated steal syndrome in this strict sense is basically caused by a significant rise in peripheral arterial resistance. Pre- and intraoperative flow measurements are essential for differentiated and successful therapy aiming at the preservation of access and extremity.

Banding the access is only indicated in high flow associated steal syndrome. The DRIL procedure is very effective in the treatment of high flow and normal flow associated ischaemia, but is rather complex and time-consuming. PAVA is equally effective and at the same time less invasive and easier to perform than DRIL. PAVA is the only option to optimize both access flow and peripheral circulation in low flow associated steal syndrome, which is becoming more and more frequent among our haemodialysis population due to the rising proportion of elderly and diabetic patients. A potential drawback of the method is that when it is applied to an autogenous fistula, the fistula is turned into a semi-prosthetic access, with the consecutive risk of stenosis at the graft-to-vein anastomosis. RUDI and MILLER are modifications of the typical banding procedures. Their relative importance in the treatment of steal syndrome remains to be defined.

Conflict of interest statement. None to declare.

	References

Top Introduction Pathophysiology Clinical findings Diagnostic evaluation Treatment options Ligation Banding DRIL and DRAL PAVA RUDI MILLER Conclusion References

 

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Received for publication: 9. 1.07
Accepted in revised form: 4. 9.07

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