The creation of an arteriovenous hemodialysis access establishes a low-resistance pathway that always shunts a fraction of the arterial inflow into the low-pressure venous circulation. In addition, because of the extremely low resistance and high capacitance of the venous circulation, blood flow in the artery distal to the fistula origin may no longer remain antegrade but become “to and fro” or even reverse throughout the entire pulse cycle, thus becoming entirely retrograde. The net result is that the fistula “steals” arterial flow that may thereby compromise distal perfusion if intrinsic compensatory mechanisms are inadequate. Such a steal phenomenon is a common physiologic consequence of both autogenous and prosthetic hemodialysis accesses and is demonstrable in 73% to 91% of cases. “Physiologic” steal phenomenon is nearly universal and usually asymptomatic, while clinically significant steal, or ischemic steal syndrome (ISS), develops only when inherent compensatory mechanisms are inadequate to maintain or restore distal arterial perfusion pressure to a level sufficient to meet peripheral metabolic demands. Surgical creation of a proximal arteriovenous fistula always reduces the perfusion pressure of the distal vascular bed. Normal compensatory mechanisms including the development of collateral circulation and decreased peripheral vascular resistance due to vasodilation are usually sufficient to maintain adequate distal perfusion.

The ISS associated with a functioning autogenous or prosthetic arteriovenous hemodialysis access develops after 1.6% to 8% of all procedures. Risk factors for the development of this access-induced ISS include female gender, age greater than 60 years, diabetes mellitus, multiple-access operations on the ipsilateral limb, the construction of an autogenous access, and the use of the brachial artery as the donor vessel. To date, however, no specific pre-operative criteria have been identified that accurately predict the development of clinically significant arterial steal in an individual patient. Therefore, a significant challenge remains to develop criteria allowing prospective identification of those patients in whom steal is most likely to become clinically significant.

Symptoms associated with the ISS range over a broad spectrum; some are mild, such as vague neurosensory deficits, and are frequently mistaken for diabetic neuropathy, while others are more severe, such as ischemic rest pain or tissue loss. Involvement of the median nerve can mimic carpal tunnel syndrome. Because of the nonspecificity of many of these signs and symptoms, the physician must maintain a high index of suspicion when treating patients with a functioning arteriovenous hemodialysis access. Prompt recognition is crucial to prevent finger necrosis and permanent neurologic damage. Although it is a relatively uncommon complication of dialysis access, ISS poses two difficult management challenges: maintenance of functional hemodialysis access and relief of distal ischemia.

In order to understand the onset and management of ISS, a thorough understanding of the hemodynamics and circulatory physiology of the arteriovenous hemodialysis access is necessary. The basic components of an arteriovenous fistula include an inflow artery and outflow vein that are connected by two parallel circuits; a low-flow, high-resistance connection (peripheral vascular bed) via collateral vessels, and a high-flow, low resistance connection (the fistula) via a donor artery, most commonly the brachial artery. Two parallel circuits are interconnected by the segment of the artery distal to the fistula, which allows communication between the collateral circulation and the fistula. Because the venous circulation has much lower resistance, overall flow is from the arterial to the venous side. The direction of blood flow in the artery distal to the fistula, however, is variable and governed by the overall resistance created by the two sides of the circuit. For example, increasing peripheral vascular resistance would favor the development of steal by encouraging the collateral flow into fistula (low-resistance system). Increasing fistula resistance would favor antegrade flow in the distal artery.

In general, overall resistance on the fistula side is lower, because both the inflow artery and the fistula itself have relatively large diameters and low resistances. The peripheral vascular bed, in contrast, is of much higher resistance and fed by a number of smaller collateral vessels, which, in general, offer higher resistance compared to the single large inflow vessel of the fistula circuit. Therefore, it should come as no surprise that physiologic steal is observed in most instances following arteriovenous hemodialysis access creation. The presence of a large arteriovenous fistula almost always reduces distal perfusion; this is evidenced by the fact that a lower perfusion pressure is always present distal to an arteriovenous fistula. Under usual circumstances, arterial collaterals and compensatory peripheral vasodilatation develop to maintain peripheral perfusion at adequate
levels. Practically speaking, as long as there is enough distal perfusion to meet the metabolic demands of the peripheral tissues, the direction of the flow in the artery distal to the fistula is irrelevant. However, understanding the hemodynamics is vital to the management of the ISS. Successful treatment mandates recognition that there is a disparity between the resistances of the peripheral circulation and the fistula.

Until relatively recently, arteriovenous hemodialysis access-associated ISS was treated using methods focused on increasing the resistance on the fistula side of the circuit. Two basic premises underlie this approach. First, by increasing the overall resistance in the fistula, which encourages antegrade flow in the artery distal to the fistula, the blood flow to the peripheral vascular system is enhanced. Second, increasing the fistula resistance also decreases the brachial shunt fraction and shifts more blood flow into collateral systems and subsequently into the peripheral circulation. These techniques include banding, plication, and lengthening of the prosthetic graft, as well as use of a tapered prosthetic graft. The theoretical objective is to narrow the prosthetic graft sufficiently to achieve a delicate balance of distal perfusion and adequate access flow. A number of intra-operative maneuvers, including digital photoplethysmographic (PPG) monitoring and pressure measurement, have been used to achieve this subtle balance. However, despite these physiologic measures, reviews of clinical series in which these techniques have been used demonstrate not only inconsistent restoration of distal perfusion but also strikingly high rates of hemodialysis access thrombosis. Inconsistency of symptomatic relief may be partially explained by the dynamic aspect of the in vivo circulation. Because anatomy and physiology change over time with the development of new collaterals, disease progression, and blood pressure fluctuations, the fine balance created by intra-operative measurements may not hold steady in the long run.

The other issue is that operations that amplify fistula resistance change the nature of the fistula itself. Fistulas have been classified based on their diameter relative to that of the inflow artery. Small fistulas are defined as having a diameter less than 75% of the diameter of the donor artery. The primary determinant of the blood flow in the small variety is the fistula resistance, which varies with the fourth power of fistula diameter. The natural history of small fistulas is that the relatively sluggish flow through the fistula eventually leads to thrombosis. Large fistulas, on the other hand, are those with a diameter exceeding 75% of that of the donor artery; in such large fistulas, the magnitude of blood flow tends to be independent of fistula resistance and diameter (Fig. 88-1). Most surgically created fistulas are of the large variety, in order to ensure sufficient blood flow to maintain patency and support hemodialysis (400 to 600 mL/min). Based upon these considerations, techniques directed at increasing the fistula resistance in order to diminish flow must convert a large functional fistula to a small one, the predictable result of which is thrombosis and a loss of hemodialysis access.

The best currently available technique to treat ISS is the distal revascularization-interval ligation (DRIL) procedure; this operation is soundly based on the recognition of the discordant resistances between two circuits (the fistula itself and the peripheral vascular circulation). Schanzer and colleagues often observed poorly developed collateral circulations in patients with true ISS. They recognized a potential mechanism of inadequate tissue perfusion due to poor arterial supply to the periphery. In usual circumstances, the distal arterial bed is supplied by arterial collaterals that prevent ischemia in the distal limb following access placement. When this compensatory mechanism fails, distal ischemia results. Instead of increasing the resistance on the fistula side of the circuit, a bypass created between the artery proximal to the fistula and the artery distal to the fistula reduces the overall resistance on the peripheral vascular side of the equation. This reduced resistance ratio between the peripheral circulation and the fistula decreases the brachial shunt fraction and directs greater blood flow toward periphery while maintaining sufficient flow through the fistula. The artery distal to the fistula is ligated to eliminate a potential pathway of steal via retrograde flow in the arterial segment distal to the arteriovenous fistula (Figs. 88-2A and 88-2B).

Onset of ischemic symptoms may be either acute (<30 days) or chronic (>30 days). Manifestations of ischemia following arteriovenous hemodialysis access may be mild and include hand coolness, mild paresthesias/numbness, pallor, or pain only during dialysis. Severe symptoms include rest pain, cyanosis, severe paresthesias, paralysis, ischemic ulcers, and gangrene. In the absence of motor dysfunction, patients with mild sensory symptoms that develop acutely after the creation of an arteriovenous hemodialysis access may safely be observed. Over time, the chronic distal ischemia tends to maximize peripheral vasodilation and stimulates the maturation of a rich collateral network. Mild symptoms, therefore, frequently resolve over a period of several weeks to months as collateral circulation develops.