Revascularization using distal inflow such as the radial or ulnar artery for dialysis access creation was first described by Minion et al. in 2005 [24]. This technique involves ligation of the access at the anastomosis and relocating the inflow to the proximal radial artery using an interposition vein graft or primary anastomosis with the existing matured vein if length permits (Fig. 37.2). This configuration allows for antegrade flow via the ulnar artery, thereby improving perfusion pressures in the hand. Minion et al. reported complete resolution of ischemic symptoms in all four patients treated with RUDI with functioning fistulae during a follow-up period ranging 4–14 months [24]. Leake and coworkers recently reported their 10-year surgical experience with steal. Among a total of 201 surgically treated patients, 21 underwent RUDI which resulted in preservation of access in 95 % of the cases and improvement in steal symptoms in 89 %; however, a 30-day complication rate of 37 % was observed [23]. Although limited experience with RUDI has shown clinical benefit for symptomatic steal syndrome, it has been suggested that this technique may compromise maturation and long-term access survival in women and patients with diabetes, the two groups most likely to develop steal syndrome [25, 26]. More experience with this technique may better characterize which patients will benefit most from RUDI over other similar alternatives to address symptomatic steal syndrome.

In 1988, Schanzer and his colleagues developed a novel approach to the treatment of dialysis access-associated steal syndrome [5]. The technique involves ligation of the artery immediately distal to the anastomosis to eliminate retrograde flow from the hand and construction of a bypass using autogenous conduit distal to the flow interruption using a more proximal inflow source (Fig. 37.3). Over the following decade, this technique was increasingly used to manage dialysis-associated steal syndrome, and the acronym DRIL was later coined by Berman et al. in 1997 to describe critical features of this technique [7]. The bypass component effectively functions as a low-resistance collateral to the distal arm and restores the flow pattern to more physiologic conditions [4]. Illig et al. have quantified the hemodynamics of brachial artery-based AV accesses and demonstrated that a pressure sink that exists in the brachial artery proximal to the anastomosis is reversed with the DRIL procedure [4, 27]. Therefore, the antegrade bypass component in DRIL should originate as proximal as possible with a minimum of 10 cm proximal to the anastomosis to maximize arterial perfusion to the distal extremity and maintain adequate flow through the access.

Revascularization of the distal extremity coupled with interval ligation not only effectively addresses the ischemic component of steal but also preserves the existing access so that dialysis may continue immediately following DRIL. In 2004 Schanzer reported updated outcomes from his initial report using DRIL. Thirty-four of 42 patients had complete symptom resolution from steal with partial improvement in the remaining 8 patients, which was attributed to permanent neurologic deficits. Patency rates at 1 year were 96 % for bypass grafts, 100 % for AVFs, and 73 % for prosthetic accesses [28]. Knox and colleagues reported their experience with DRIL in 52 patients with hemodialysis access-induced ischemic steal syndrome in 2013. Substantial or complete relief of ischemic hand symptoms was achieved in 90 % of patients with an 80 % primary patency of bypass grafts at 4 years and 1-year AV access primary patency rate of 83 %. Fifteen of 20 patients with digital tissue loss had complete healing on follow-up [10]. A more recent experience by Scali et al. demonstrated symptom resolution in 82 % of patients and 85 % functional accesses following 132 DRIL procedures in 126 patients [29]. Several other single institutional case series with a moderately large number of patients have demonstrated the clinical effectiveness and durability of the DRIL procedure [7, 12, 23, 30, 31].

In 1994, we adopted the DRIL procedure as our preferred method for treating dialysis access-induced steal syndrome. Over an 18-year period, 81 DRIL procedures were performed on 77 patients for symptomatic steal syndrome associated with dialysis access. Complete symptom resolution was seen in 82 % for rest pain, 91 % for digital ulceration, 56 % for neurological deficits, and 83 % for digital gangrene. Fistula and bypass graft survival 5 years following DRIL was 56 % and 97 %, respectively. All patients not effectively treated by DRIL had resolution of ischemic-related complications following fistula ligation, local amputation, or repeat bypass.

Complications following DRIL are most commonly wound related involving the vein harvest site. A feared complication following the DRIL procedure is bypass graft thrombosis with subsequent acute limb ischemia. Although the effectiveness DRIL is predicated on interval ligation of the native artery distal to the AV anastomosis, bypass graft thrombosis in this setting rarely leads to acute, irreversible ischemia. In our series, the overall complication rate following DRIL was 17 % with the majority being wound related. Among the 81 DRIL procedures performed, three bypass grafts occluded all within the first 4 months. The saphenous vein and prosthetic graft occlusions resulted in the development of ischemic rest pain, and in both cases, a repeat bypass with saphenous vein led to complete resolution of symptoms. The basilic vein bypass failure was discovered when a patient with digital gangrene was unable to heal from a local amputation. Fistula ligation resulted in prompt healing of the amputation site. Therefore, we believe the reticence in interval ligation of the axial artery in DRIL is not justified. Our experience has demonstrated excellent brachial bypass patency, especially when saphenous vein was used as conduit. In the rare instance of bypass graft occlusion, irreversible ischemia is unusual, and limb salvage can be achieved with a repeat bypass procedure or fistula ligation.

Ischemic monomelic neuropathy (IMN) is a rare but devastating complication following access creation that is distinguished by profound neurologic dysfunction in the distribution of the median, radial, and ulnar nerves in the absence of profound hand ischemia. The condition was first described by Bolton et al. in 1979 and later coined ischemic monomelic neuropathy in 1983 by Wilbourn and colleagues [32, 33]. Risk factors that have been consistently identified to be associated with those that develop IMN include older females with diabetes and accesses created using brachial artery as inflow. IMN is not observed with access creation based on radial or ulnar artery inflow. The pathogenesis of IMN is not entirely understood; however, some hypothesize that IMN is a result of transient ischemia exclusively to the nerve trunks due to flow diversion following access creation [34]. Some have demonstrated loss of flow through the vasa vasorum or an inherent watershed zone for the vasa nervosum in the antecubital fossa as possible mechanisms to explain IMN [34, 35]. It is generally believed that the threshold for ischemia is less for peripheral nerves than that of muscle, similar to the natural progression of symptoms seen in acute lower extremity ischemia with neurologic deficits precede soft tissue ischemic changes which may explain why some have describe IMN as steal syndrome isolated to nerves with preservation of the soft tissues of the distal upper extremity [33].

Patients who develop IMN do so within hours of access creation and present with acute hand pain; numbness in the distribution of the median, radial, and ulnar nerves in the distal upper extremity; and weakness or paralysis of the hand and forearm. The hand is typically warm with a palpable pulse often present without evidence of any skin or muscle ischemia. The diagnosis of IMN is often delayed, with the neurologic deficits usually being attributed to intraoperative positioning or from the effects of a regional nerve block. Any motor or sensory deficit recognized immediately following an access creation procedure should prompt an expeditious evaluation of the patient, and other potential causes to explain the deficits ruled out, including surgical nerve trauma or hematoma. Therefore, the use of regional blocks as an anesthetic for dialysis access procedures is controversial.

Treatment of IMN involves immediate action to improve arterial flow to the distal upper extremity by access ligation or revision such as DRIL, in order to expeditiously eliminate steal phenomena and maximize chances for neurologic recovery. Although access ligation achieves preoperative baseline arterial flow, neurologic recovery has been inconsistent with evidence of improvement in some and permanent loss in sensory-motor function of the affected limb in others. In our series, four of the seven patients with neurological deficits not responding to the DRIL procedure presented within 24 h of access creation with severe sensory and motor deficits out of proportion to the degree of ischemia observed. A number of these patients almost certainly had IMN, which might explain the inability of the DRIL procedure to improve their neurologic symptoms. The optimal management for IMN is still controversial since neurologic recovery has been inconsistent despite prompt recognition and immediate access ligation. We preferentially address IMN with DRIL so that the access is preserved for continued dialysis regardless of the degree of recovery.