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Failure of the mature hemodialysis arteriovenous fistula

Failure of the mature hemodialysis arteriovenous fistula
Literature review current through: Jan 2024.
This topic last updated: Jan 24, 2023.

INTRODUCTION — The life cycle of an arteriovenous (AV) fistula starts with its creation and evolves through phases of physiological maturation and initial clinical use, both of which can be defined using objective criteria [1]. The phase of the life cycle that is defined as sustained clinical use expresses what is meant by the term mature AV fistula. Although the time at which this state is reached cannot be precisely defined, for the purposes of our discussion we will adopt at least two months of continuous, effective, problem-free use of the access for hemodialysis as our definition. Compared with other types of vascular access, the mature hemodialysis AV fistula is associated with fewer complications, but problems can occur, and these need to be promptly recognized and managed effectively.

Failure of the mature AV fistula and its management will be reviewed here. Primary failure of the newly created hemodialysis AV fistula is reviewed separately, as are AV graft dysfunction and other types of AV fistula dysfunction, such as dialysis associated steal syndrome (DASS), aneurysm formation, infection, and excess flow leading to heart failure. (See "Primary failure of the hemodialysis arteriovenous fistula" and "Arteriovenous graft creation for hemodialysis and its complications" and "Arteriovenous fistula creation for hemodialysis and its complications".)

RISK FACTORS — The risk factors associated with failure of a hemodialysis arteriovenous (AV) fistula are reviewed separately. In addition, it is not surprising that AV fistulas requiring intervention prior to maturation are more likely to fail in the long term, even if they appear to mature and are functional following intervention [2]. (See "Primary failure of the hemodialysis arteriovenous fistula", section on 'Outcomes for fistula salvage' and "Risk factors for hemodialysis arteriovenous fistula failure".)

MONITORING THE MATURE AV FISTULA — Failure of the mature hemodialysis arteriovenous (AV) fistula is frequently suspected during monitoring designed to detect stenosis so that it can be identified and treated prior to thrombosis, usually on the basis of physical examination findings, flow measurements, or duplex ultrasound [3]. Lesions associated with the mature hemodialysis AV fistula can include arterial or venous stenosis (preexisting or acquired) and collateral veins. These are described in more detail elsewhere. (See "Endovascular intervention for the treatment of stenosis in the arteriovenous access", section on 'Specific AV access lesions'.)

Findings on physical examination associated with vascular stenotic lesions or thrombosis are listed briefly below, and these, along with other methods for monitoring and surveillance of fistulas, are discussed in detail elsewhere. (See "Physical examination of the mature hemodialysis arteriovenous fistula" and "Clinical monitoring and surveillance of the mature hemodialysis arteriovenous fistula".)

Findings of extremity edema (central vein obstruction), AV fistula hyperpulsatility, and lack of AV fistula collapse when raising the extremity are indicative of an outflow problem. (See "Physical examination of the mature hemodialysis arteriovenous fistula", section on 'Detection of specific problems'.)

The presence of poor pulse augmentation within the access can be indicative of an inflow problem. While on dialysis, abnormalities in direct flow measurements or inflow or outflow pressure may signal a problem. (See "Physical examination of the mature hemodialysis arteriovenous fistula", section on 'Detection of specific problems'.)

The AV fistula without a pulse or thrill may be thrombosed or have a stenotic lesion so severe that it reduces flow to an undetectable level. Duplex ultrasound distinguishes between these possibilities. (See "Physical examination of the mature hemodialysis arteriovenous fistula", section on 'Thrombosed AV fistula'.)

Patients with abnormalities on physical examination or other problems with dialysis that are consistent with AV fistula stenosis or thrombosis (in the absence of contraindications for AV fistula salvage) should be referred for more detailed evaluation and possibly intervention [3,4].

STENOTIC VASCULAR LESIONS — Stenotic vascular lesions in a mature arteriovenous (AV) fistula can develop anywhere within the access circuit, which starts and ends at the level of the heart [5]. Although either venous or arterial lesions may be seen, venous stenosis is by far the most common. Venous lesions have a predilection for sites characterized by turbulent flow such as bifurcations, venous valves [6-11], and areas that have been referred to as "swing points" [7]. In addition, there are some stenotic lesions that appear to be related to or at least influenced in their clinical manifestations by high blood flow rates, which are more common in patients with an AV fistula. These include central vein stenosis and cephalic arch stenosis [10,12,13].

Swing-point stenosis — A swing-point stenosis is a unique point where the course of the vein involved in the AV fistula or its drainage makes an extreme angle [7]. This is seen in the juxta-anastomotic region of the AV fistula, the angle of transposition in a transposed brachial-basilic AV fistula, and at the cephalic arch.

Flow at these points is nonlaminar and associated with decreased shear stress and oscillatory shear stress [14]. These anomalies result in a cascade of events that result in neointimal hyperplasia causing venous stenosis. Except for the cephalic arch lesion, these swing-point stenoses are unique to the AV fistula. In addition, the frequency of each of the three lesions tends to be specific to an AV fistula type:

Juxta-anastomotic stenosis is seen most frequently in the radial-cephalic AV fistula (although not exclusive to it) [4,7,15].

Cephalic arch stenosis is seen most commonly with a brachial-cephalic AV fistula.

The angle of transposition lesion is specific for a brachial-basilic AV fistula.

In a study involving 127 cases with venous stenosis, 46 percent were swing-point lesions. Of these, the most common was juxta-anastomotic stenosis, accounting for 63 percent of that subgroup. Cephalic arch and brachial-basilic angle of transposition lesions accounted for 19 and 18 percent, respectively. Overall, swing-point stenosis was present in 35.4 percent of brachial-cephalic, 33.9 percent of radial-cephalic, and 30.7 percent of brachial-basilic AV fistulas [8].

Juxta-anastomotic stenosis — Juxta-anastomotic stenosis is defined as stenosis occurring within the first 3 to 4 cm of the AV fistula, immediately adjacent to the arterial anastomosis (image 1). It is the most common type of lesion associated with primary AV fistula failure [6,14,16-22] and is also a very common lesion associated with failure of a mature AV fistula [15,23,24]. Three variations of this lesion may be observed: juxta-anastomotic stenosis only, anastomotic stenosis only, and a combination of the two. Since this is an inflow lesion, its main clinical effect is to reduce access blood flow.

Brachial-basilic angle of transposition stenosis — For a brachial-basilic AV fistula to be easily accessible for cannulation once the AV fistula develops, it must be superficialized and transposed laterally. The problem that can lead to venous stenosis relates to the angle of transposition (ie, the angle created when the vein is moved to its optimal position) (image 2). Since the proximal portion is bound down by the brachial fascia, a sharp angle (angle of transposition) can be created when the lower portion is moved superficially and laterally. A stenosis can develop here related to turbulence, although surgical manipulation and mechanical factors related to the brachial fascia may also be contributory. Frequently, this is a high-grade stenosis associated with an increase in intraluminal pressure followed by progressively decreasing blood flow, which promotes thrombosis. The increased pressure also causes the vessel to dilate, leading to aneurysm formation.

Stenosis at this site is reported to be the most common complication associated with a brachial-basilic AV fistula [25,26]; however, the frequency with which it is observed varies depending upon local practices since it is at least in part iatrogenic. In one series, the incidence in failing brachial-basilic AV fistulas was 60 percent [7], and in another, the incidence was 74 percent and accounted for 87 percent of all interventions on this type of access [25].

Cephalic arch — The cephalic arch is a unique vascular structure, anatomically and hemodynamically, and a particularly problematic area [9,23,27,28]. In the upper arm, the cephalic vein lies in the deltopectoral groove where, just below the clavicle, it turns to run deeper to empty into the axillary vein. This creates an angle of insertion approaching 90 degrees and referred to as the cephalic arch. At this point, it passes through the clavipectoral fascia. This is a dense membrane occupying the interval between the pectoralis minor and the subclavian vessels. In addition to the cephalic vein, it is also pierced by the thoracoacromial artery and vein and lateral pectoral nerve. In addition to having the swing-point anatomical configuration, this unique anatomy tends to interfere with the dilatation of the vein in response to the increased flow associated with vascular access drainage.

Although cephalic arch stenosis (image 3 and image 4) accounted for 50 percent of stenoses in upper arm AV fistulas in one study [15], more typically it has been reported in 15 to 18 percent of cases of AV fistula failure (all types) [8,9]. Since the cephalic arch contributes to the drainage of both the brachial-cephalic and the radial-cephalic AV fistula, cephalic arch stenosis can be seen with either type of access. Since the cephalic vein is not involved in the drainage of a brachial-basilic AV fistula, it goes without saying that cephalic arch stenosis is not seen with this type of AV fistula.

Differences in long-term patency of a brachial-cephalic AV fistula and radial-cephalic AV fistula have been attributed, at least in part, to the higher incidence of cephalic arch stenosis brachial-cephalic AV fistula [8-11,29,30]. In one report, the incidence of cephalic arch stenosis was 39 percent for brachial-cephalic AV fistula and only 2 percent in radial-cephalic AV fistulas [8]. In other reports, the incidences ranged from 77 to 97 percent compared with 3 to 20 percent, respectively [11,31]. The explanation for this difference in incidence is thought to be related to differences in blood flow in the cephalic arch [2]. Blood flow through the cephalic arch is generally higher with a brachial-cephalic compared with a radial-cephalic AV fistula because blood flow through the brachial artery is greater, and all the blood flow of a brachial-cephalic fistula goes through the cephalic arch. By comparison, flow through the radial artery is less and with a radial-cephalic AV fistula blood flow can drain into either the basilic vein or the cephalic vein. In some cases, a large portion of the blood flow misses the cephalic arch.

Central vein stenosis — Stenotic lesions can occur anywhere within the thoracic central venous system, including the subclavian or brachiocephalic veins (image 5) or the superior vena cava. (See "Overview of thoracic outlet syndromes", section on 'Anatomy' and "Central vein obstruction associated with upper extremity hemodialysis access".)

The overall incidence of central vein stenosis is not known for certain given that asymptomatic cases are generally not recognized. Published reports describe an incidence ranging from 3 to 41 percent [5,32-34]. Much of this variability relates to the frequency of the use of central venous catheters in the population being studied.

In a study of hemodialysis patients who underwent angiography for AV access-related concerns, 55 of 133 (41 percent) had evidence of significant central vein stenosis [32]. Affected patients had a significantly longer duration on dialysis (43 versus 34 months) and a history of a previous dialysis catheter insertion (95 versus 76 percent). The number of prior catheters was a significant factor, even after excluding subclavian insertions.

In another study of 69 consecutive patients undergoing percutaneous placement of tunneled right internal jugular vein catheters, venography was performed prior to insertion of the guidewire [35]. Evidence of unexpected stenosis and/or angulation of the central veins was found in 29 cases (42 percent). Patients who had previously received tunneled internal jugular catheters had more than double the incidence of such abnormalities compared with those who had not.

A significant number of central vein stenotic lesions occur at the junction of the first rib and the clavicle, at the costoclavicular junction (image 6). After passing over the first rib, the subclavian vein and associated neurovascular structures pass through the costoclavicular space beneath the clavicle, which is a confined space through which the subclavian vein passes. The exact mechanism for this lesion is not known. It appears that as the vein enlarges as a result of increased AV access blood flow, the vein becomes increasingly vulnerable to constriction. It has also been postulated that turbulent blood flow occurs at this unique area, promoting the development of neointimal hyperplasia [36]. Subclavian vein stenosis due to costoclavicular compression is not rare [36-38]; however, the exact incidence is not fully known. Frequently, the problem goes unrecognized. Costoclavicular compression has been the subject of extensive study in the context of venous thoracic outlet syndrome, with which it shares many features. (See "Overview of thoracic outlet syndromes", section on 'Venous TOS'.)

Arterial stenosis — The arterial segment of the dialysis access circuit includes all arteries leading to the AV fistula (feeding arteries) and the anastomosis (image 7) (ie, the inflow portion of the circuit). Arterial stenosis is a much less common cause of AV fistula failure compared with venous stenosis. Reports of inflow stenosis in dysfunctional AV fistula cases are reported to be in the range of 6 to 29 percent [18,39,40]. These lesions can develop at any point within the arterial segment; however, stenosis of the anastomosis is by far the most common. Anastomotic stenosis is seen most frequently in association with juxta-anastomotic stenosis (see 'Juxta-anastomotic stenosis' above). In a cohort study of 101 dysfunctional AV fistula cases, 8 percent had lesions in the feeding artery and 21 percent had stenosis of the arterial anastomosis [40]. In addition, a higher incidence of inflow stenosis has been reported for forearm compared with upper arm AV fistulas [40]. Stenotic lesions within the arterial segment of dialysis access circuit lead to decreased blood flow to the AV fistula, which can result in inadequate dialysis and eventually thrombosis of the access.

Treatment of vascular stenosis — Prospective treatment of physiologically significant stenosis before thrombosis can occur and will materially prolong access survival. Percutaneous angioplasty has come to be the treatment of choice for these lesions and has a greater than 95 percent technical success rate. Long-term primary patency rates are reported in the range of 92 percent at three months, 57 to 77 percent at six months, and 35 to 69 percent at one year [15,41]. The treatment of venous stenosis in AV fistulas presents no unique problems when compared with lesions seen in association with AV grafts. The treatment of vascular stenosis and associated complications are reviewed separately. (See "Endovascular intervention for the treatment of stenosis in the arteriovenous access" and "Techniques for angioplasty of the arteriovenous hemodialysis access" and "Techniques for angioplasty of the arteriovenous hemodialysis access", section on 'Procedure-related complications'.)

THROMBOSED FISTULA — The rate of thrombosis for arteriovenous (AV) fistulas is approximately one sixth of that of AV grafts [41]. In a multicenter study in which 302 newly created AV fistulas matured and were successfully used for dialysis, a thrombosis rate of 0.14 patients/year was observed during a follow-up period of 0.72 years following first successful use of the access [18]. From a clinical perspective, when an AV fistula no longer has detectable flow in the dialysis facility, it is generally labeled by the facility staff as a thrombosed AV fistula. Whether the fistula is thrombosed, how much thrombus is present, and whether the thrombus can be resolved requires further investigation.

Virtually all thrombosed AV fistulas have associated pathological anatomy contributing to the thrombosis. Any of the lesions described above can be seen in association with fistula thrombosis. Venous lesions cause an increase in resistance to blood flow, and arterial lesions result in a decrease in blood inflow. These lesions tend to be progressive, resulting in a progressive decrease in blood flow and eventually thrombosis. The thrombosed AV fistula can vary considerably in its clinical appearance, so much so that these cases must almost be considered individually when planning an approach to treatment [42].

The amount of thrombus, when thrombus is present (image 8), varies considerably [43]. At one extreme, no thrombus is found when the access is imaged. In this case, stenosis within the AV fistula has progressed to the point that blood flow is so diminished that it is not detectable. At the other extreme is the large aneurysmal AV fistula that contains a very large volume of thrombus [43]. A large volume of thrombus is more likely to be seen in an upper arm AV fistula, especially those associated with a central venous lesion, and in one that is large and ectatic.

AV fistula thrombosis differs from thrombosis associated with AV graft:

Because an AV fistula is lined with native endothelium, which is inherently less thrombogenic than synthetic material even with very low blood flow, thrombosis occurs late in the progression of a stenotic lesion in an AV fistula. As a result, the associated stenotic lesions have longer to develop and tend to be more severe, and total obstruction of the main channel is not unusual.

With increasing outflow resistance from a venous lesion, an AV fistula will generally develop collateral flow (image 9), which allows continued flow of blood even when the lesion in the main body of the AV fistula has become totally obstructive. When an angiogram is finally performed, such severely stenotic lesions frequently result in a very complex picture with their proliferation of collaterals.

Thrombus that develops within an AV fistula is mildly inflammatory [43]. It reacts with the wall of the AV fistula, becomes attached, and begins to undergo organization. This can complicate efforts directed toward treatment and removal of the thrombus. The more quickly a thrombectomy can be performed, the better. Nevertheless, one should not hesitate to at least evaluate and consider thrombectomy of a thrombosed AV fistula no matter how long it has been nonfunctional, especially if a pulse or thrill is present. It may also be possible to salvage the access by using one of the larger collaterals [44].

Treatment of thrombosis — A variety of techniques have been used to treat the thrombosed AV fistula [28,43,45-50] with no obvious best choice. It is important to adapt the technique used to the situation found when the thrombosed AV fistula is evaluated [43].

Definitions for the hemodialysis access time points used in describing outcomes (eg, primary patency, assisted primary patency, postintervention patency) are provided in the figure (figure 1 and table 1).

Reported initial success for the endovascular treatment of thrombosed AV fistulas has ranged from 88 to 100 percent [15,45-49]. Primary patency rates ranging from 20 to 56 percent at six months and 27 to 40 percent at one year have been reported. Secondary patency rates of 54 to 83 percent and 51 to 80 percent have been documented for six months and one year, respectively [43,46,47,50,51].

Some investigators have advocated surgical therapy for the thrombosed AV fistula [40,52-56]. Success rates ranging from 70 to 90 percent have been documented using this approach. Primary patency rates ranging from 51 to 84 percent at six months and in the range of 75 percent at one year have been reported. Secondary patency rates of 69 to 88 percent and in the range of 77 percent have been documented for six months and one year, respectively. When these data are compared with that obtained with endovascular therapy, it is apparent that no significant differences exist between these two modalities.

Not infrequently, an AV fistula thrombectomy is complicated by the presence of old, partially organized adherent thrombus, especially in areas of aneurysmal dilatation. The thrombus may be very resistant to removal but can be approached using a hybrid technique, which has been shown to be very effective [56-58]. This technique involves making a small incision and removing thrombus either with forceps and/or by milking method followed by angioplasty to treat the associated stenotic lesion [59]. Every effort should be made to extract, lyse, or at least macerate the thrombus, rather than allowing it to embolize to the lungs as a large mass. Regardless of the approach to the salvage of a thrombosed AV fistula, long-term patency postintervention is reduced in comparison to an AV fistula that has prospective treatment of a vascular lesion [60].

Contraindications to attempted salvage — There are absolute and relative contraindications to the salvage of thrombosed AV fistulas, some of which are more absolute for endovascular techniques [43,61-65].

Infection — Infection is not seen with AV fistulas with the same frequency as for synthetic grafts. In one study of 4500 dialysis patients, the incidence of infection related to the vascular access (all types) was 2.18 per 100 patient-months. Of these, 0.95 per 100 patient-months occurred in AV grafts in contrast to 1.6 in AV fistulas [56]. In another study of 239 patients over a seven-year period, 148 bacteremic episodes occurred in 102 patients with an overall rate of 0.52 per 1000 patient-days. The rate for AV fistulas was 0.18 per 1000 patient-days in contrast to 0.39 per 1000 patient days for AV grafts [60].

These data offer an indication of the frequency of infection associated with an AV fistula; however, they do not indicate the frequency of infection associated with thrombosis, which is not a common occurrence. When it does occur, its presentation is very similar to that of a vasculitis. The thrombus will contain a variable amount of infectious material, which will be released into the circulation if endovascular thrombectomy is attempted. This can lead to serious complications, including septic shock. (See "Physical examination of the mature hemodialysis arteriovenous fistula", section on 'Infection'.)

Right-to-left shunt — Embolization of thrombus fragments associated with any type of thrombectomy is not uncommon [63,64,66]. A probe patent foramen ovale has been reported to be present in 27 percent of the general population at autopsy [67,68]. These individuals do not have right-to-left shunts normally; however, they are at risk if the patient develops severe pulmonary hypertension. The high incidence of pulmonary hypertension in dialysis patients [69] places them at risk of developing paradoxical emboli when endovascular thrombectomy techniques are used to manage a thrombosed AV access [70]. (See "Clinical manifestations and diagnosis of patent ductus arteriosus (PDA) in term infants, children, and adults", section on 'Diagnosis'.)

Chronic occlusion — Thrombus within an AV fistula is somewhat inflammatory, and as a result it becomes attached to the wall of the vessel and begins to organize very early. With time, the thrombus becomes completely organized. While attempting salvage on such a case is not an absolute contraindication, clinical judgment should be used in attempting salvage. There are two features that can contribute to success: the amount of thrombus that was present when patency was lost, and the fact that there is a tendency for collaterals to form as patency is lost. These can be evaluated with ultrasound. If this evaluation reveals the presence of anatomy that could be used to reestablish a usable conduit, an attempt at salvage should be made. No AV fistula should be abandoned without first making such an evaluation.

Excess thrombus burden — The amount of thrombus, when it is present, is variable. However, in some cases, the thrombus load can be very large. This is more likely with an upper arm AV fistula, an AV fistula associated with a central vein stenosis, and for large dilated aneurysmal AV fistulas referred to as a "mega-fistula." Some of these can have over 200 mL of thrombus. Additionally, thrombus of several different ages is frequently present. Some of this may even be partially organized. These fistulas can be treated, but it is time-consuming and associated with a significant risk for pulmonary embolism. In some cases, salvage of such an AV fistula is not warranted. If treatment is elected, a surgical approach is recommended.

Complications of thrombectomy — Since thrombectomy generally involves an angioplasty as part of the combined procedure, angioplasty-associated complications are also seen here. In addition, the major complication encountered is the occurrence of arterial emboli. Arterial embolization of thrombus fragments associated with thrombectomy performed using any technique is not uncommon [63,64,66]. These are generally small and asymptomatic and therefore frequently unrecognized [63,71].

What is generally reported is symptomatic emboli. The reported incidence of symptomatic arterial embolization following thrombectomy in general has been in the range of 0 and 9.3 percent of total cases [72,73]. The incidence of this complication is significantly higher with an AV graft compared with an AV fistula [45]. Since the wall of the AV fistula is native vessel and the thrombus is mildly inflammatory, it adheres to the wall and begins the process of organization. This renders it less likely to break loose and embolize during the thrombectomy procedure. In a review of 12,169 AV fistula thrombectomy cases, the incidence of arterial embolization was 0.17 percent (21 cases) in contrast to 0.349 percent, which occurred in 102,737 (358 cases) AV graft thrombectomies.

The symptoms of embolization are those of hand ischemia. The hand and especially the fingers turn cold and take on a bluish discoloration that becomes mottled. These changes generally come on with the sudden onset of pain. In evaluating a patient's hand for a suspected embolus, it is important to compare it with the opposite hand. If both are cold and mottled, it is not likely that the hand in question reflects an acute problem. The pulses at the wrist are generally absent or considerably diminished, a change that can be appreciated only if the patient was carefully evaluated prior to having the thrombectomy procedure. A Doppler signal is generally present over the arteries at the wrist even when the pulse is not palpable, although it is frequently diminished. If nothing is detected with Doppler examination, the urgency for immediate treatment to avoid tissue damage is even greater than usual. Symptomatic emboli must be treated in a timely fashion in order to prevent permanent sequelae. Treatment should be directed at restoring flow to the ischemic hand as quickly as possible in order to relieve the patient's pain and preserve hand function by avoiding secondary muscle ischemia and necrosis. Outcomes and prognosis largely depend on a rapid diagnosis and initiation of appropriate and effective therapy [57]. (See "Clinical features and diagnosis of acute lower extremity ischemia".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dialysis" and "Society guideline links: Hemodialysis vascular access".)

SUMMARY AND RECOMMENDATIONS

Late arteriovenous (AV) fistula failure is defined as the inability to use a matured AV fistula after at least three months of normal usage. The lesions most typical of this later period are acquired venous (most common) and arterial stenoses. (See 'Introduction' above.)

We use physical examination, duplex ultrasound, and direct flow measurements to identify patients with possible stenotic lesions associated with hemodialysis AV fistulas. (See 'Monitoring the mature AV fistula' above and "Clinical monitoring and surveillance of the mature hemodialysis arteriovenous fistula".)

Findings of extremity edema (central venous stenosis), AV fistula hyperpulsatility, and lack of AV fistula collapse when raising the extremity is indicative of an outflow problem.

The presence of poor pulse augmentation within the access is indicative of an inflow problem. While on dialysis, abnormalities in direct flow measurements, inflow pressure, or outflow pressure may signal a problem.

The AV fistula without a pulse or thrill may be thrombosed or have a severe stenosis. Duplex ultrasound distinguishes between these possibilities.

Patients with abnormalities consistent with stenotic vascular lesions or AV fistula thrombosis should be referred for an angiogram (in the absence of contraindications for AV fistula salvage). (See 'Monitoring the mature AV fistula' above.)

For patients with ≥50 percent arterial stenosis in conjunction with hemodynamic, functional, or clinical abnormalities, such as a previous thrombotic episode, abnormal physical findings, or decreased access flow, we suggest percutaneous intervention, rather than surgical repair (Grade 2C). Similarly, for patients with ≥50 percent venous stenosis in conjunction with clinical or physiological abnormalities, we suggest initial treatment using percutaneous transluminal angioplasty rather than surgical revision (Grade 2C). (See 'Arterial stenosis' above and 'Treatment of vascular stenosis' above.)

For patients with a thrombosed AV fistula, we suggest initial treatment with endovascular thrombectomy (Grade 2C). For patients with significant adherent thrombus that is resistant to percutaneous removal, we suggest using a hybrid technique (Grade 2C). If there are contraindications, either absolute or relative, or if the endovascular procedure is not successful, the patient should be referred to surgery before considering abandoning the access. (See 'Thrombosed fistula' above.)

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References

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