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Overview of hemodialysis arteriovenous graft maintenance and thrombosis prevention

Overview of hemodialysis arteriovenous graft maintenance and thrombosis prevention
Literature review current through: Jan 2024.
This topic last updated: Jan 24, 2023.

INTRODUCTION — This topic review provides an overview of general issues regarding arteriovenous (AV) graft maintenance, including measures to prevent AV graft thrombosis and management of the high-risk AV graft. These same considerations with respect to AV fistulas are reviewed separately. (See "Overview of hemodialysis arteriovenous fistula maintenance and thrombosis prevention".)

RISK FACTORS FOR AV GRAFT THROMBOSIS — Arteriovenous (AV) graft thrombosis can occur immediately following AV graft creation, usually related to technical issues, or later after using the access for a variable period of time predominantly due to stenotic lesions that develop from intimal hyperplasia. More than 90 percent of thrombosed grafts have a stenotic lesion. (See "Hemodialysis arteriovenous graft dysfunction and failure".)

Stenosis of a hemodialysis AV graft is initiated by endothelial cell injury, which leads to the upregulation of adhesion molecules on the endothelial cell surface. Subsequent leukocyte adherence to damaged and activated endothelium causes the release of chemotactic and mitogenic factors for vascular smooth muscle cells, thereby enhancing smooth muscle cell migration and proliferation [1-3]. Additional factors that contribute to the neointimal proliferation and fibromuscular hyperplasia include shear stress generated by the turbulent blood flow [4,5] and the mismatch in elastic properties around the anastomosis leading to excessive mechanical stretch [6]. Activated platelets and inflammatory cells also secrete oxidants and other toxins that directly injure the vessel wall [7]. Measures aimed at reducing neointimal hyperplasia as well as other pharmacologic agents that address other elements underlying vascular stenosis may help prevent stenosis. (See 'High-risk AV grafts' below.)

Other factors that can lead to AV graft dysfunction and thrombosis include:

Preexisting stenotic lesions

Cannulation injury/more frequent cannulation (eg, daily hemodialysis)

Infiltration/hematoma formation

Recurrent stenosis after angioplasty

Prior stenting

Hypercoagulable states

Thrombosis of a pseudoaneurysm

Pseudoaneurysms, which may result from repeated cannulation at one site, can rupture, thrombose, or become infected. The clinical features and management of pseudoaneurysms associated with AV hemodialysis are reviewed separately. (See "Arteriovenous graft creation for hemodialysis and its complications", section on 'Pseudoaneurysm' and "Arteriovenous graft creation for hemodialysis and its complications" and "Arteriovenous fistula creation for hemodialysis and its complications".)

ROUTINE GRAFT MAINTENANCE AND CARE — Proper graft maintenance and graft cannulation technique are important for preventing complications that might lead to thrombosis [8].

Following arteriovenous (AV) graft creation, the access arm should be elevated as much as possible until swelling subsides, which may take as long as six weeks but usually takes less. Symptoms, such as increased swelling or severe pain, require urgent evaluation. (See "Arteriovenous graft creation for hemodialysis and its complications" and "Arteriovenous fistula creation for hemodialysis and its complications".)

Monitoring — AV grafts are initially evaluated after their creation for usability. Once in use, the AV graft should be examined at each dialysis session and monitored for any problems with dialysis. (See "Physical examination of the arteriovenous graft" and "Clinical monitoring and surveillance of hemodialysis arteriovenous grafts to prevent thrombosis".)

Patients should be taught to examine the AV graft between dialysis sessions for a thrill. If a thrill cannot be felt, there is a change from the prior examination, or there is redness or swelling of the arm, the patient should inform the staff at the dialysis unit as soon as possible [9,10]. There are no data to suggest that a delay in addressing AV graft thrombosis affects outcomes of intervention. However, detecting and reporting possible thrombosis as soon as possible may allow intervention prior to the next dialysis session. This reduces the risk of missing or delaying the dialysis session, which can lead to hyperkalemia and volume overload. Early thrombectomy may also decrease the need of requiring a temporary catheter.

Cannulation and decannulation — Proper cannulation and decannulation are important for preventing complications that can cause AV graft thrombosis. Hemodialysis staff should be appropriately trained, and only those with technical mastery should be allowed to cannulate a newly created graft [9].

Inspection prior to initial cannulation — The newly created AV graft should be examined by an experienced clinician to determine if it is clinically usable [11]. The AV graft must have an appropriate depth and location that allows cannulation with a minimal risk for infiltration and the ability to deliver adequate blood flow. (See "Approach to the adult patient needing vascular access for chronic hemodialysis".)

New AV grafts can usually be cannulated two weeks after placement. If the AV graft is judged to be ready, cannulation and hemodialysis can be initiated. However, the initial cannulation should be delayed if there is residual postoperative edema over the graft. (See 'General procedure' below.)

The specific interval from creation to first AV graft cannulation depends upon the specific type of graft that is used. Guidelines for use from the various manufacturers are based on the expected time needed for tissue-to-graft incorporation to minimize the likelihood of hematoma formation from blood dissecting along the perigraft space. Advances in AV graft design may allow immediate cannulation within 24 to 72 hours of placement [12,13]. The different types of grafts, including immediate cannulation grafts, are discussed separately. (See "Arteriovenous graft creation for hemodialysis and its complications", section on 'Types of AV grafts'.)

Self-cannulation of the AV grafts is encouraged for patients who are capable and whose access is suitably positioned [14,15].

General procedure — Appropriate sterile technique should be used. We recommend wearing gloves and masks during cannulation and appropriate hand cleansing and antiseptic cleansing of the cannulation site [16,17]. Full barrier precautions (gowns, drapes) are generally not needed. Dialysis unit personnel should wear a gown if there is risk of contamination of the field (eg, uncontrolled diarrhea or wound drainage not contained by a dressing) [18].

These minimal standards reduce the transmission but are variably used in observational studies that have compared different dialysis facilities [19]. Preventing disease transmission is important, particularly given the increasing microbial resistance to mainstream antibiotics [18].

The standard technique for repeatedly cannulating an AV graft is using the "rope-ladder" technique, which simply involves rotating the cannulation sites between hemodialysis sessions. Rotation of cannulation sites is important for avoiding pseudoaneurysm formation. (See "Arteriovenous graft creation for hemodialysis and its complications", section on 'Pseudoaneurysm' and "Arteriovenous graft creation for hemodialysis and its complications" and "Arteriovenous fistula creation for hemodialysis and its complications".)

Cannulation of a new AV graft is generally performed using a 15 gauge needle and a dialysis blood flow of 450 mL/minute. Our approach for cannulating an AV graft is as follows [9]:

Locate, inspect, and palpate the needle cannulation sites prior to skin preparation.

Wash the access site using an antibacterial soap or scrub and water.

Cleanse the skin by applying 2% chlorhexidine gluconate/70% isopropyl alcohol or 70% alcohol and/or 10% povidone iodine.

If the skin is touched by the patient or staff after the skin prep has been applied but the cannulation has not been completed, repeat the preparation.

The use of a wet needle is safer and also prevents the risk for a blood spray or spill, especially for the initial cannulation. Attach a 10 mL syringe filled with 8 mL of normal saline solution to prime the AV graft needle immediately before use, then clamp the needle.

Insert the needle bevel up at an approximately 30 to 45° angle. Arterial needle direction can be antegrade or retrograde to direction of blood flow; the venous needle should be antegrade to direction of blood flow.

Once the vein has been penetrated, blood flashback will be visible (the needle may need to be unclamped to see the blood flashback); advance the needle slowly with the bevel up, or, for a deeper AV graft that is difficult to palpate, immediately rotate the needle 180° and advance slowly with the bevel down. Tape the needle onto the skin.

Confirm needle placement with a normal saline flush before connecting the needles to the blood pump and starting the pump. Blood return alone is not enough to show good needle placement. After flashback is visible, aspirate 1 to 5 mL with the 10 mL syringe, then flush the needle with the normal saline solution, looking for any signs of infiltration, then clamp the needle.

Decannulating the AV graft — Proper needle removal prevents postdialysis infiltrations. Our approach to decannulating an AV graft is as follows [9]:

Remove the needle at approximately the same angle used for insertion. Using too steep an angle during needle removal may cause the tip to puncture the back wall.

Apply the gauze dressing over the needle site, but do not apply pressure.

Apply pressure only after the needle has been completely removed.

Cannulation difficulty or failure — If the first cannulation is unsuccessful, the nurse or patient care technician may leave the needle in place and attempt a second cannulation at another portion of the graft. At the end of dialysis, all three needles are removed. However, in some cases, if cannulation is unsuccessful, recannulation should not be attempted again until the site has healed.

Infiltration associated with cannulation sites can occur at any time during dialysis. The patient should be monitored closely during the dialysis procedure for signs and symptoms of infiltration (pain, bruising, oozing) [9]. A quick response to a needle infiltration can help minimize damage to the access.

Avoid lifting up on the needle after it is in the vein and use care when taping needles in place. Improper needle placement or taping procedure can cause infiltration, as can improper decannulation.

If the graft has infiltrated, it is best to rest that access for at least one treatment, but, if this is not possible, the next cannulation should be above the site of the infiltration. If the patient still has a catheter in place, restart use of the access with one needle.

For infiltration that occurs after the administration of heparin, leaving the needle in place and cannulating at another site may be appropriate.

Care between dialysis sessions — In between dialysis sessions, patients are instructed to keep the access extremity clean and to avoid wearing any clothing or jewelry (such as wristwatches) that restricts flow to or from the access and to refrain from activities that similarly restrict flow. Bathing and other activities can be resumed as normally tolerated.

PRIMARY THROMBOSIS PREVENTION IN NEWLY CREATED GRAFTS — Thrombosis of a newly created arteriovenous (AV) graft is often related to underlying stenosis. The mainstay of thrombosis prevention revolves around clinical monitoring of the graft and treatment of clinically significant stenosis, prior to AV graft thrombosis. (See "Clinical monitoring and surveillance of hemodialysis arteriovenous grafts to prevent thrombosis".)

We do not administer pharmacologic agents (eg, fish oil, anticoagulants, antiplatelet agents) prophylactically for the purpose of preventing thrombosis in a newly created AV graft in patients who are not considered high risk for AV graft thrombosis (ie, history of thrombosis within three months of surgery of a prior AV access, coagulation abnormality, hypercoagulable state). The management of the high-risk patient is discussed below. (See 'High-risk AV grafts' below.)

Angioplasty/stenting of underlying stenosis — Stenosis of a hemodialysis AV graft is initiated by endothelial cell injury and most often involves the venous anastomosis but may also involve the draining vein, central vein, or feeding artery; or, stenosis can be within the AV graft. (See "Endovascular intervention for the treatment of stenosis in the arteriovenous access".)

Although monitoring for and treatment of AV graft stenosis is the mainstay of preventing AV graft thrombosis, the outcomes of angioplasty/stenting for treating stenosis associated with AV grafts have been overall disappointing. Moreover, angioplasty exacerbates neointimal hyperplasia, often resulting in accelerated restenosis [20]. (See "Endovascular intervention for the treatment of stenosis in the arteriovenous access" and 'Recurrent thrombosis' below.)

Prophylactic antithrombotic therapy — Measures aimed at reducing neointimal hyperplasia as well as other mechanisms responsible for the development of vascular stenosis may help prevent AV graft thrombosis. However, no specific regimen has been proven useful. Results of the various studies have been conflicting due in part to the use of variable treatment regimens and enrollment of differing patient populations. As such, we do not prophylactically administer pharmacologic agents (eg, fish oil, anticoagulants, antiplatelet agents) for the purpose of preventing thrombosis in a newly created AV graft in patients who are not considered high risk for AV graft thrombosis (ie, history of thrombosis within three months of surgery of a prior AV access, coagulation abnormality, hypercoagulable state).

Among the many available antiplatelet agents, predominantly those that block cyclooxygenase (aspirin, sulfinpyrazone), phosphodiesterase inhibitors (dipyridamole) have been studied for reducing AV graft thrombosis [18]. Given the uncertainty concerning the benefit and the increased risk of bleeding, we do not routinely administer antiplatelet therapies to those not considered high risk for thrombosis. (See 'Dipyridamole and aspirin' below.)

Other antiplatelet therapies, including the platelet P2Y12 receptor blockers (clopidogrel, ticlopidine), the protease-activated receptor-1 antagonists (vorapaxar), and the glycoprotein IIb/IIIa receptor blockers, have not been evaluated for this clinical indication. (See 'Other antiplatelet agents' below.)

We also do not use prophylactic anticoagulation. Prophylactic anticoagulation does not prevent AV graft thrombosis and is associated with an increased risk of bleeding [21,22]. This was best shown in a multicenter clinical study in which 107 patients with new AV grafts were randomly assigned to receive low-intensity warfarin (target international normalized ratio [INR] 1.5 to 1.9) or placebo [21]. There was no difference in the rate of AV graft thrombosis between the two groups. However, 10 percent of the patients receiving warfarin developed major hemorrhage despite close monitoring of the INR. Although no well-designed, randomized studies have been performed, some retrospective and observational studies have also reported an increased morbidity and mortality among dialysis patients treated with warfarin for a number of different indications [23,24]. Anticoagulation may be considered for those with immediate (very early) AV graft thrombosis not related to technical issues. (See 'Anticoagulation for hypercoagulability' below.)

HIGH-RISK AV GRAFTS — Patients at high risk of graft failure are those with a history of thrombosis (within three months of surgery) of a previous arteriovenous (AV) graft. AV graft thrombosis can occur in the immediate postoperative period or at a later date.

Among those with a history of immediate (ie, very early, within 24 to 48 hours of surgery) or recurrent AV graft thrombosis in the absence of underlying stenosis, we initiate an evaluation for a coagulation abnormality or hypercoagulable state. Among selected patients with such abnormalities, warfarin may be appropriate. (See 'Evaluation for hypercoagulable state' below.)

For high-risk patients with a history of early AV access thrombosis who are also at low risk for bleeding, we suggest a combination of dipyridamole plus aspirin. (See 'Dipyridamole and aspirin' below.)

Immediate graft thrombosis — Patients with a history of immediate (very early) AV graft thrombosis are considered high risk for subsequent AV graft thrombosis. We define immediate (very early) thrombosis as occurring within 24 to 48 hours of AV graft creation and that which is not felt to be related to technical issues (the most common cause of immediate graft thrombosis). (See "Hemodialysis arteriovenous graft dysfunction and failure", section on 'Immediate'.)

Evaluation for hypercoagulable state — Some patients with early AV graft thrombosis may have an underlying hypercoagulable state [25-28].

Multiple acquired and inherited thrombophilias have been associated with AV graft thrombosis, including protein C deficiency, protein S deficiency, antithrombin 3 deficiency, antiphospholipid antibodies, factor V Leiden, prothrombin gene mutation, hyperhomocystinemia, anticardiolipin antibody, and a lupus anticoagulant.

In one retrospective review of 419 hemodialysis patients with and without vascular access thrombosis, a genetic or acquired thrombophilia was identified in a higher proportion of patients with access thrombosis compared with those without access thrombosis (55 versus 39 percent) [29]. In a review of patients on maintenance hemodialysis, those with lupus anticoagulant activity (16 of 97) had a higher frequency of vascular access thrombosis compared with patients without lupus anticoagulant (62 versus 26 percent) [26].

Among patients with immediate AV graft thrombosis, we initiate an evaluation for a coagulation abnormality or hypercoagulable state [26-28,30]. In general, the assessment should include evaluation for abnormalities in protein C, protein S, antithrombin-3, the presence of antiphospholipid antibodies, and possibly others depending upon clinical history. (See "Protein C deficiency" and "Protein S deficiency" and "Antithrombin deficiency" and "Diagnosis of antiphospholipid syndrome".)

Anticoagulation for hypercoagulability — Although thrombophilias are associated with very early graft thrombosis, there is no published literature on whether anticoagulating patients with thrombophilia would actually prevent thrombosis or whether such an approach is safe [31]. Although entirely opinion based, we consider anticoagulating selected patients with hypercoagulable states typically using warfarin; other agents have not been adequately studied in this setting [22,25,31]. The decision to treat with warfarin is dependent upon the relative risks of AV graft thrombosis versus the risks of anticoagulation.

General management issues related to individual coagulation disorders are discussed in more detail separately. (See "Protein C deficiency", section on 'Management' and "Protein S deficiency", section on 'Management' and "Antithrombin deficiency", section on 'Management' and "Management of antiphospholipid syndrome".)

Early graft thrombosis — Patients with a history of early thrombosis (within three months of surgery) of a previous AV graft are at high risk of failure of the new AV graft. We define early thrombosis as occurring after the immediate postoperative period (ie, 24 to 48 hours) up to three months after graft creation. Based upon randomized trials showing a modest benefit, we suggest extended-release dipyridamole (200 mg twice daily) plus aspirin (25 mg twice daily) among those in whom the bleeding risk is low [32-34]. We do not administer fish oil to those with AV grafts for the sole purpose of preventing thrombosis. (See 'Dipyridamole and aspirin' below and 'Fish oil' below.)

Dipyridamole and aspirin — Dipyridamole is a phosphodiesterase inhibitor that reduces proliferation of vascular smooth muscle and may prevent neointimal hyperplasia, stenosis, and thrombosis in AV grafts [35,36].

In a small trial, 84 patients were randomly assigned to receive dipyridamole (75 mg, three times/day) and/or aspirin (325 mg/day) for the prevention of thrombosis [32]. Neither therapy appeared to be effective in patients with AV grafts that had a previous thrombosis as the recurrence rate was 78 percent within 18 months. In patients with new grafts, the relative risk of thrombosis with dipyridamole was reduced compared with placebo at 0.35 (95% CI 0.15-0.80; after adjustment for subgroup analysis). Dipyridamole lowered graft thrombosis whether it was administered alone or in conjunction with aspirin.

In a large, multicenter study, long-acting dipyridamole plus aspirin improved primary patency [33]. In this trial, 649 patients with a new AV graft were randomly assigned to aspirin (25 mg twice daily) plus extended-release dipyridamole (200 mg twice daily) or placebo [33]. For approximately one half of the patients in each group, the AV graft was their first AV access. Dipyridamole plus aspirin was associated with a modest but significant increase in primary patency at one year (28 versus 23 percent). Both groups had a similar incidence of adverse events (particularly bleeding), AV graft failure, and death. Although no significant differences were seen between the groups, the incidence of bleeding in this study that was associated with the combination of dipyridamole plus aspirin may have been lower than anticipated because of the exclusion of patients with an increased bleeding risk and the short duration of use of the drugs. Forty-three percent of patients were taking aspirin prior to trial entry and were allowed to continue for the duration of the trial.

In a secondary analysis, at one year, aspirin use compared with no aspirin use at baseline (ie, prior to trial entry) was associated with a trend toward an increase in AV graft patency (30 versus 23 percent) and, after adjusting for multiple covariates, a 17 percent lower rate of loss of patency (adjusted hazard ratio 0.83, 95% CI 0.68-1.01) [34]. There was no difference between groups in the overall rate of bleeding, death, hospitalization, or vascular access events. These data suggest that aspirin alone may safely prevent loss of AV graft patency, although, as noted above, patients at high risk for bleeding were excluded from the trial.

Other antiplatelet agents — Many other antiplatelet agents, including sulfinpyrazone, clopidogrel, and ticlopidine, as well as many combination therapies, have been used in an attempt to prevent AV graft thrombosis in those with a prior failed hemodialysis access [31-34,37-39]. As examples:

A single-center clinical trial compared dipyridamole (75 mg, three times/day) and/or aspirin (325 mg/day) for the prevention of thrombosis in expanded polytetrafluoroethylene (PTFE) AV grafts [32]. Neither therapy appeared to be effective in patients with previous thrombosis, as the recurrence rate was 78 percent within 18 months.

A well-designed, multicenter study with 200 patients evaluated the effectiveness of aspirin plus clopidogrel versus placebo in preventing AV graft thrombosis [39]. Aspirin plus clopidogrel did not prevent AV graft thrombosis but doubled the frequency of bleeding complications. The study was stopped due to the doubled risk of bleeding among those receiving aspirin plus clopidogrel (hazard ratio 1.98, 95% CI 1.19-3.28).

Fish oil — Fish oil is an option for patients who are considered at high risk for graft thrombosis. Omega-3-acid-ethyl esters, which are the active component of fish oil, may help to prevent AV graft thrombosis, possibly related to antiproliferative and antioxidant properties [40]. However, we suggest not administering fish oil to those with AV grafts for the sole purpose of preventing thrombosis. Nevertheless, the administration of fish oil is associated with other clinically relevant cardiovascular benefits (eg, blood pressure lowering, adverse cardiovascular events), particularly among individuals with coronary heart disease and its risk equivalents [41]. Additional information on available preparations is provided separately. (See "Fish oil: Physiologic effects and administration".)

A systematic review identified 13 trials involving 916 subjects [42]. The risk of AV graft events (four trials [43-45]) was reduced for fish oil compared with placebo (risk ratio [RR] 0.71, 95% CI 0.52-0.97].

In an early study, the efficacy of fish oil for preventing AV graft thrombosis was assessed in 24 patients who were randomly assigned to 4000 mg of fish oil or 4000 mg of control oil [45]. At 12 months, primary patency was higher among those who received fish oil (77 versus 15 percent).

In a later trial, 29 patients with newly created AV grafts (PTFE) were randomly assigned to receive over-the-counter omega-3 (n-3) fatty acid supplements or corn oil [43]. There was no significant difference in survival time between the n-3 fatty acid group compared with control (mean AV graft primary patency rate 254.2 days [standard error of the mean (SEM) = 51.8] versus 254.1 days [SEM = 34.6]).

In the largest trial, 201 patients with new AV grafts were randomly assigned to receive fish oil (4 g/day) or placebo starting seven days after AV graft creation [44]. At 12 month follow-up, the proportion of individuals who had AV graft thrombosis or radiologic or surgical intervention was lower among the patients taking fish oil, with a difference that trended toward being significant (48 versus 62 percent, RR 0.78, 95% CI 0.60-1.03). Compared with placebo, fish oil was associated with the following predefined secondary endpoints:

A lower rate of AV graft failure (5.95 versus 3.43 per 1000 access-days, respectively; incidence rate ratio [IRR] 0.58, 95% CI 0.44-0.75).

Fewer thromboses (3.41 versus 1.71 per 1000 access-days, respectively; IRR 0.50, 95% CI 0.35-0.72).

Fewer interventions (4.92 versus 2.89 per 1000 access-days, respectively; IRR 0.59, 95% CI 0.44-0.78).

However, in a large, well-designed, multicenter trial that included 567 patients with newly created AV fistulas, there was no benefit of fish oil in preventing thrombosis [46]. Since AV fistula and AV graft thrombosis are both mediated by neointimal hyperplasia, we believe that conclusions from this study are applicable to patients with AV grafts as well. (See "Overview of hemodialysis arteriovenous fistula maintenance and thrombosis prevention", section on 'Fish oil'.)

RECURRENT THROMBOSIS

Recurrent stenotic lesions — Recurrent graft thrombosis due to recurrent stenotic lesions is initially treated with thrombolysis and repeat angioplasty. (See "Hemodialysis arteriovenous graft dysfunction and failure" and "Endovascular intervention for the treatment of stenosis in the arteriovenous access" and "Techniques for angioplasty of the arteriovenous hemodialysis access".)

Surgical management of stenotic lesions is a less desirable alternative but may be necessary for refractory stenosis. Alternatively, creation of a secondary arteriovenous (AV) fistula or new AV graft may be necessary (algorithm 1). (See "Hemodialysis arteriovenous graft dysfunction and failure", section on 'Surgical revision'.)

Recurrence in the absence of a stenotic lesion — Among patients who experience recurrent AV graft thrombosis in the absence of underlying stenosis, we initiate an evaluation for a coagulation abnormality or hypercoagulable state because such patients may differ from those with less frequent AV graft thrombosis [26-28,30]. (See 'Evaluation for hypercoagulable state' above and 'Anticoagulation for hypercoagulability' above.)

EXPERIMENTAL THERAPIES

Vitamin B – Vascular access thrombosis has been associated with elevated homocysteine levels [47]. Based upon this observation, some have suggested that decreasing plasma homocysteine may prevent vascular access thrombosis. However, in two trials, administration of high doses of vitamin B failed to reduce the risk of arteriovenous (AV) graft thrombosis even though homocysteine levels were reduced [31,48,49].

Local antiproliferative drug delivery – Provision of a high concentration of an antiproliferative drug locally at the site of stenosis has been beneficial in a number of experimental animal models of AV grafts, but no large-scale clinical trials have been completed [50]. Local drug delivery can be achieved using a drug-eluting (eg, paclitaxel, rapamycin) wrap, depot, or other material. Drug eluting stents (DES) that provide high local concentrations of antiproliferative drugs such as paclitaxel and rapamycin are also being studied [51]. DES are reviewed separately. (See "Endovascular intervention for the treatment of stenosis in the arteriovenous access", section on 'Options for unsuccessful angioplasty'.)

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

Many factors predispose to arteriovenous (AV) graft failure. Proper routine AV graft care and maintenance can help prevent problems that can lead to graft dysfunction and thrombosis. (See 'Risk factors for AV graft thrombosis' above and 'Routine graft maintenance and care' above.)

The newly created AV graft should be examined by an experienced clinician to determine if it is clinically usable. The timeframe for this examination depends on the type of graft that is placed. If the AV graft is judged to be ready, cannulation and hemodialysis can be initiated. (See 'Inspection prior to initial cannulation' above.)

Proper cannulation and decannulation are important for preventing complications, and only those with technical proficiency should be allowed to cannulate an AV graft. The proper technique for cannulating and decannulating an AV graft is described above. (See 'Cannulation and decannulation' above.)

Sterile precautions should be used when accessing the AV graft, including appropriate hand cleansing, antiseptic cleansing of the cannulation site, and the use of gloves and masks during cannulation. Full barrier precautions (gowns, drapes) are generally not needed. (See 'General procedure' above.)

In addition to routine monitoring in the dialysis unit, patients should be taught to examine their AV graft routinely, and, if a thrill cannot be felt or if there is redness or swelling of the arm, the patient should inform the staff at the dialysis unit. Patients are instructed to keep the AV graft site clean and to avoid wearing any clothing, jewelry, or other activities that restrict flow to or from the access. (See 'Monitoring' above and 'Care between dialysis sessions' above and "Clinical monitoring and surveillance of hemodialysis arteriovenous grafts to prevent thrombosis".)

Vascular access stenosis, particularly at the venous anastomosis, is the most common cause of AV graft failure. Angioplasty of stenosis is the mainstay for preventing AV graft thrombosis and for treating recurrent stenosis causing thrombosis, but outcomes have been overall disappointing. Measures aimed at preventing neointimal hyperplasia may help prevent stenosis. (See 'Primary thrombosis prevention in newly created grafts' above.)

Among hemodialysis patients at high risk for AV graft failure who are also at low risk for bleeding, we suggest dipyridamole plus aspirin (Grade 2C). Patients at high risk of AV graft failure are those with a history of early thrombosis (within three months of surgery) of a previous AV graft. It is reasonable for patients to forego such therapy given the uncertainty concerning the benefit and the increased risk of bleeding.

For patients with a newly created AV graft who are not considered high risk for AV graft thrombosis, we do not prophylactically administer pharmacologic agents (ie, antiplatelet agents, antithrombotic therapies, fish oil). (See 'Primary thrombosis prevention in newly created grafts' above.)

Although we do not administer fish oil for the sole purpose of preventing AV graft thrombosis, fish oil is associated with other clinically relevant cardiovascular benefits (eg, blood pressure lowering, adverse cardiovascular events), particularly among individuals with coronary heart disease and its risk equivalents. (See 'Fish oil' above and "Fish oil: Physiologic effects and administration".)

Among the general hemodialysis patient, we recommend not giving warfarin for the prevention of thrombosis and failure of an AV graft (Grade 1B). Among high-risk patients with immediate (ie, very early, within 24 to 48 hours of surgery) or recurrent AV graft thrombosis in the absence of underlying stenosis, we initiate an evaluation for a coagulation abnormality or hypercoagulable state. Among selected patients with such abnormalities, warfarin may be appropriate. (See 'Immediate graft thrombosis' above.)

  1. Swedberg SH, Brown BG, Sigley R, et al. Intimal fibromuscular hyperplasia at the venous anastomosis of PTFE grafts in hemodialysis patients. Clinical, immunocytochemical, light and electron microscopic assessment. Circulation 1989; 80:1726.
  2. Rekhter M, Nicholls S, Ferguson M, Gordon D. Cell proliferation in human arteriovenous fistulas used for hemodialysis. Arterioscler Thromb 1993; 13:609.
  3. Stracke S, Konner K, Köstlin I, et al. Increased expression of TGF-beta1 and IGF-I in inflammatory stenotic lesions of hemodialysis fistulas. Kidney Int 2002; 61:1011.
  4. Sterpetti AV, Cucina A, Santoro L, et al. Modulation of arterial smooth muscle cell growth by haemodynamic forces. Eur J Vasc Surg 1992; 6:16.
  5. Hsieh HJ, Li NQ, Frangos JA. Shear stress increases endothelial platelet-derived growth factor mRNA levels. Am J Physiol 1991; 260:H642.
  6. Hofstra L, Bergmans DC, Hoeks AP, et al. Mismatch in elastic properties around anastomoses of interposition grafts for hemodialysis access. J Am Soc Nephrol 1994; 5:1243.
  7. Himmelfarb J. Pharmacologic prevention of vascular access stenosis. Curr Opin Nephrol Hypertens 1999; 8:569.
  8. Lok CE, Huber TS, Lee T, et al. KDOQI Vascular Access Guidelines Work Group. KDOQI clinical practice guideline for vascular access: 2019 update. Am J Kidney Dis 2020; 75:S1.
  9. https://www.kidney.org/sites/default/files/docs/12-50-0210_jag_dcp_guidelines-va_oct06_sectionc_ofc.pdf (Accessed on March 13, 2017).
  10. https://www.pennmedicine.org/departments-and-centers/department-of-radiology/patient-care/radiology/interventional-radiology/procedures-and-services/hemodialysis-access (Accessed on March 13, 2017).
  11. Saran R, Dykstra DM, Pisoni RL, et al. Timing of first cannulation and vascular access failure in haemodialysis: an analysis of practice patterns at dialysis facilities in the DOPPS. Nephrol Dial Transplant 2004; 19:2334.
  12. Sottiurai VS, Stephens A, Champagne L, et al. Comparative results of early and delayed cannulation of arteriovenous graft in haemodialysis. Eur J Vasc Endovasc Surg 1997; 13:139.
  13. Schild AF, Schuman ES, Noicely K, et al. Early cannulation prosthetic graft (Flixene™) for arteriovenous access. J Vasc Access 2011; 12:248.
  14. Jayanti A, Foden P, Wearden A, et al. Self-cannulation for haemodialysis: patient attributes, clinical correlates and self-cannulation predilection models. PLoS One 2015; 10:e0125606.
  15. Donato-Moore S. Self cannulation for home hemodialysis: strategies for success. Nephrol Nurs J 2013; 40:37.
  16. https://www.cdc.gov/dialysis/PDFs/collaborative/AV-Fistula-Graft-Can-Decannulation-Observations-AT.pdf (Accessed on August 22, 2017).
  17. Tokars JI, Arduino MJ, Alter MJ. Infection control in hemodialysis units. Infect Dis Clin North Am 2001; 15:797.
  18. https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5005a1.htm (Accessed on March 13, 2017).
  19. Arenas MD, Sánchez-Payá J, Barril G, et al. A multicentric survey of the practice of hand hygiene in haemodialysis units: factors affecting compliance. Nephrol Dial Transplant 2005; 20:1164.
  20. Chang CJ, Ko PJ, Hsu LA, et al. Highly increased cell proliferation activity in the restenotic hemodialysis vascular access after percutaneous transluminal angioplasty: implication in prevention of restenosis. Am J Kidney Dis 2004; 43:74.
  21. Crowther MA, Clase CM, Margetts PJ, et al. Low-intensity warfarin is ineffective for the prevention of PTFE graft failure in patients on hemodialysis: a randomized controlled trial. J Am Soc Nephrol 2002; 13:2331.
  22. D'Ayala M, Smith RM, Martone C, et al. The effect of systemic anticoagulation in patients undergoing angioaccess surgery. Ann Vasc Surg 2008; 22:11.
  23. Chan KE, Lazarus JM, Thadhani R, Hakim RM. Anticoagulant and antiplatelet usage associates with mortality among hemodialysis patients. J Am Soc Nephrol 2009; 20:872.
  24. Morgan CL, McEwan P, Tukiendorf A, et al. Warfarin treatment in patients with atrial fibrillation: observing outcomes associated with varying levels of INR control. Thromb Res 2009; 124:37.
  25. O'shea SI, Lawson JH, Reddan D, et al. Hypercoagulable states and antithrombotic strategies in recurrent vascular access site thrombosis. J Vasc Surg 2003; 38:541.
  26. Brunet P, Aillaud MF, San Marco M, et al. Antiphospholipids in hemodialysis patients: relationship between lupus anticoagulant and thrombosis. Kidney Int 1995; 48:794.
  27. Prakash R, Miller CC 3rd, Suki WN. Anticardiolipin antibody in patients on maintenance hemodialysis and its association with recurrent arteriovenous graft thrombosis. Am J Kidney Dis 1995; 26:347.
  28. Molino D, De Lucia D, Marotta R, et al. In uremia, plasma levels of anti-protein C and anti-protein S antibodies are associated with thrombosis. Kidney Int 2005; 68:1223.
  29. Knoll GA, Wells PS, Young D, et al. Thrombophilia and the risk for hemodialysis vascular access thrombosis. J Am Soc Nephrol 2005; 16:1108.
  30. Schwab SJ, Harrington JT, Singh A, et al. Vascular access for hemodialysis. Kidney Int 1999; 55:2078.
  31. Allon M. A Patient with Recurrent Arteriovenous Graft Thrombosis. Clin J Am Soc Nephrol 2015; 10:2255.
  32. Sreedhara R, Himmelfarb J, Lazarus JM, Hakim RM. Anti-platelet therapy in graft thrombosis: results of a prospective, randomized, double-blind study. Kidney Int 1994; 45:1477.
  33. Dixon BS, Beck GJ, Vazquez MA, et al. Effect of dipyridamole plus aspirin on hemodialysis graft patency. N Engl J Med 2009; 360:2191.
  34. Dixon BS, Beck GJ, Dember LM, et al. Use of aspirin associates with longer primary patency of hemodialysis grafts. J Am Soc Nephrol 2011; 22:773.
  35. Harker LA, Kadatz RA. Mechanism of action of dipyridamole. Thromb Res Suppl 1983; 4:39.
  36. Himmelfarb J, Couper L. Dipyridamole inhibits PDGF- and bFGF-induced vascular smooth muscle cell proliferation. Kidney Int 1997; 52:1671.
  37. Mohamed I, Kamarizan MFA, Da Silva A. Medical adjuvant treatment to increase patency of arteriovenous fistulae and grafts. Cochrane Database Syst Rev 2021; 7:CD002786.
  38. Domoto DT, Bauman JE, Joist JH. Combined aspirin and sulfinpyrazone in the prevention of recurrent hemodialysis vascular access thrombosis. Thromb Res 1991; 62:737.
  39. Kaufman JS, O'Connor TZ, Zhang JH, et al. Randomized controlled trial of clopidogrel plus aspirin to prevent hemodialysis access graft thrombosis. J Am Soc Nephrol 2003; 14:2313.
  40. Hung AM, Booker C, Ellis CD, et al. Omega-3 fatty acids inhibit the up-regulation of endothelial chemokines in maintenance hemodialysis patients. Nephrol Dial Transplant 2015; 30:266.
  41. Dixon BS. Fish oil and hemodialysis graft patency: does time matter? JAMA 2012; 307:1859.
  42. He L, Li MS, Lin M, et al. Effect of fish oil supplement in maintenance hemodialysis patients: a systematic review and meta-analysis of published randomized controlled trials. Eur J Clin Pharmacol 2016; 72:129.
  43. Bowden RG, Wilson RL, Gentile M, et al. Effects of omega-3 fatty acid supplementation on vascular access thrombosis in polytetrafluorethylene grafts. J Ren Nutr 2007; 17:126.
  44. Lok CE, Moist L, Hemmelgarn BR, et al. Effect of fish oil supplementation on graft patency and cardiovascular events among patients with new synthetic arteriovenous hemodialysis grafts: a randomized controlled trial. JAMA 2012; 307:1809.
  45. Schmitz PG, McCloud LK, Reikes ST, et al. Prophylaxis of hemodialysis graft thrombosis with fish oil: double-blind, randomized, prospective trial. J Am Soc Nephrol 2002; 13:184.
  46. Irish AB, Viecelli AK, Hawley CM, et al. Effect of Fish Oil Supplementation and Aspirin Use on Arteriovenous Fistula Failure in Patients Requiring Hemodialysis: A Randomized Clinical Trial. JAMA Intern Med 2017; 177:184.
  47. Shemin D, Lapane KL, Bausserman L, et al. Plasma total homocysteine and hemodialysis access thrombosis: a prospective study. J Am Soc Nephrol 1999; 10:1095.
  48. Wrone EM, Hornberger JM, Zehnder JL, et al. Randomized trial of folic acid for prevention of cardiovascular events in end-stage renal disease. J Am Soc Nephrol 2004; 15:420.
  49. Jamison RL, Hartigan P, Kaufman JS, et al. Effect of homocysteine lowering on mortality and vascular disease in advanced chronic kidney disease and end-stage renal disease: a randomized controlled trial. JAMA 2007; 298:1163.
  50. Rotmans JI, Pattynama PM, Verhagen HJ, et al. Sirolimus-eluting stents to abolish intimal hyperplasia and improve flow in porcine arteriovenous grafts: a 4-week follow-up study. Circulation 2005; 111:1537.
  51. Cheung AK, Terry C, Li L. Pathogenesis and local drug delivery for prevention of vascular access stenosis. J Ren Nutr 2008; 18:140.
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