Version May 2024
INTRODUCTION — Arteriovenous (AV) vascular access is necessary for the delivery of lifesaving hemodialysis therapy but is nonphysiologic and harmful with considerable downsides [1]. AV hemodialysis access exerts an adverse effect on the heart because of the increased workload demanded by the vascular access blood flow (Qa) [2]. Although this is superimposed upon the cardiopulmonary dysfunction that develops in patients with chronic kidney disease, in the absence of a pre-existing clinically significant comorbidity (heart disease, pulmonary hypertension, severe microvascular disease), it is generally tolerated [3-6]. However, Qa can reach levels that can generate adverse sequelae, some of which can be life-threatening. Early recognition and management of the inappropriately high-flow AV access is an important aspect of medical care delivered to the hemodialysis patient.
The clinical features, diagnosis, and management of the high-flow AV access are reviewed. Other complications related to AV access are reviewed separately. (See "Arteriovenous fistula creation for hemodialysis and its complications" and "Arteriovenous graft creation for hemodialysis and its complications".)
HIGH-FLOW ARTERIOVENOUS ACCESS
Definition — To define hemodialysis arteriovenous (AV) access flow (Qa), one must first define normal access Qa. Unfortunately, there is no generally accepted definition for either of these. Ideally, Qa would be the minimum that is adequate for efficient hemodialysis while still maintaining AV access patency. A physiologically mature AV fistula has been defined as having a Qa of 500 mL/min or greater [7].
Under normal circumstances, AV access blood flow is greater for a brachial artery-based AV fistula compared with a distal radial-cephalic AV fistula [8-10]. Studies documenting AV access blood flow rates in asymptomatic patients have reported values ranging from 785 to 998 mL/min in radial-cephalic AV fistulas [6,8-14] and from 1376 to 1580 mL/min in brachial-cephalic AV fistulas [8,9]. According to a survey conducted by the US Dialysis Outcomes and Practice Patterns Study (DOPPS) Practice Monitor, the mean Qa prescribed by surveyed facilities was 417 mL/min (median 400 mL/min) [15]. For effective dialysis, Qa should exceed this level by at least 100 mL/min. When blood flow has been reduced to levels no lower than 500 to 600 mL/min for AV fistulas and 600 to 700 mL/min for AV grafts, post-banding access patency rates have been reasonably good [16,17]. (See 'Target flow rate' below.)
Although the exact threshold for defining a high-flow Qa access has not been rigorously validated nor universally accepted, a Qa of 1500 mL/min, or Qa >20 percent of the cardiac output (ie, cardiopulmonary recirculation [CPR] >20 percent) has been suggested [3,15,18]. It should be noted, however, that patients with specifically related comorbidities can develop adverse sequelae from a Qa below this level. In this sense, there is an element of individuality intrinsic to the definition of excessive high flow.
Risk factors — High Qa is more commonly seen in association with an AV fistula than with an AV graft. Blood flow in an AV graft is maximal at the time of creation, and there is less of a tendency towards an increase in blood flow with the passage of time. By contrast, with an AV fistula, Qa increases rapidly during the first weeks to months after creation [10]. The blood flow rate in the access continues to increase but at a slower rate as the AV fistula ages. In some cases, it can reach levels in excess of 4000 mL/min [19].
An AV fistula associated with a larger artery (and vein) is at greater risk for the development of a high blood flow rate [20]. This being the case, brachial-cephalic and brachial-basilic accesses are much more commonly associated with this problem than a distal radial-cephalic access [21].
CLINICAL MANIFESTATIONS — There is no level of access flow volume that is without some degree of adverse physiologic consequences. While an excessively high blood flow rate (Qa) is associated with adverse sequelae, the ability to tolerate high AV access flow is variable.
The clinical manifestations associated with a high-flow hemodialysis AV access can range from an asymptomatic incidental finding to a severe, life-threatening situation. Discussions concerning this problem generally focus on conditions such as heart failure, pulmonary hypertension, and hand ischemia; however, other problems can also occur requiring attention. These are reviewed briefly below and in more detail in associated topics.
Cardiopulmonary
Eccentric left ventricular hypertrophy — Left ventricular hypertrophy (LVH) is highly prevalent among patients with end-stage kidney disease and is a strong predictor of morbidity and mortality [4,22,23]. The creation of an AV access is accompanied by an increase in cardiac output, the degree of which is directly proportional to the Qa. This is accompanied by an expansion of blood volume leading to increased venous return and right atrial, pulmonary artery, and left ventricular end-diastolic pressures [24-26]. Both plasma atrial natriuretic peptide and brain natriuretic peptide concentrations increase, peaking 10 days after AV fistula creation, consistent with the presence of cardiac volume overload [27].
The chronic effects of these changes on the myocardium appear to be due primarily to volume overload, which translates into a remodeling of the cardiac muscle. This is characterized by four-chamber dilatation and what is referred to as eccentric left LVH, the development of which is proportional to the Qa [2,28]. This is distinguished from concentric LVH in which the pathogenic mechanism is a pressure overload resulting in muscle hypertrophy. In both cases, an increase in left ventricular muscle mass occurs, but with eccentric LVH, a relatively normal wall thickness is maintained, while wall thickening occurs with concentric LVH (figure 1) [24]. In one study involving predialysis patients, the incidence of LVH following AV fistula creation increased from 67 percent at baseline to 83 and 90 percent at one and three months, respectively [29]. This increase was due to the development of eccentric LVH.
High-output cardiac failure — Heart failure is a serious problem for patients with end-stage kidney disease (ESKD). Approximately 35 to 40 percent of patients with chronic kidney disease have an established diagnosis of heart failure at initiation of hemodialysis. An estimated 44 percent of patients on hemodialysis have heart failure, and cardiac disease is the most common cause of death in the dialysis patient [5,6].
The creation of an AV access increases cardiac output. As Qa increases over time with an AV fistula, it can eventually exceed the patient's cardiac functional reserve resulting in high-output cardiac failure (HOCF) [30-33]. Although this is more likely to occur at a lower Qa in patients with preexisting heart disease, even without cardiovascular disease, an excessively high Qa can adversely affect cardiac output, leading to HOCF. (See "Causes and pathophysiology of high-output heart failure", section on 'Arteriovenous fistula'.)
HOCF is characterized by dyspnea either at rest or with varying degrees of exertion, orthopnea, paroxysmal nocturnal dyspnea, and edema (pulmonary, peripheral) in the presence of an above-normal cardiac index or simply an elevated cardiac output [34,35]. (See "Clinical manifestations, diagnosis, and management of high-output heart failure".)
Because of the high incidence of heart failure in patients with chronic kidney disease, in general, and the fact that the signs and symptoms suggesting this diagnosis are often obscured by the effects of ultrafiltration during the dialysis treatment in reducing fluid and maintaining a dry weight, it is important to have a high index of suspicion for the development of HOCF [36]. Patients with intractable or worsening symptoms despite maximum medical management should undergo assessment for HOCF. (See "Evaluation and management of heart failure caused by hemodialysis arteriovenous access".)
Myocardial ischemia — Cardiovascular disease accounts for >40 percent of deaths in patients with ESKD. Atherosclerotic coronary heart disease is a large proportion of the cardiovascular disease spectrum in these patients, with the prevalence being several-fold greater than in age-matched subjects without kidney disease [37]. This high incidence is driven in large part by a clustering of traditional risk factors such as hypertension, diabetes, and age. The cardiac changes occurring with the creation of an AV access predispose the patient to an increased risk for myocardial ischemia caused by an adverse imbalance between subendocardial oxygen supply and increased oxygen demand consequent to the increased cardiac output. One study used pulse wave analysis to determine the subendocardial viability ratio (SEVR; ratio of the area under the diastolic aortic pressure curve to the area under the systolic aortic pressure curve) in a group of patients before and after AV fistula creation [25]. SEVR was used to gauge the relationship between myocardial oxygen supply and demand. Following AV fistula creation, SEVR immediately decreased and remained low throughout the six-month study period, implying a significant impact on subendocardial perfusion. A high-flow AV access predisposes to further increased risk for myocardial ischemia caused by an adverse imbalance between subendocardial oxygen supply and increased oxygen demand consequent to a greater cardiac output [38].
Pulmonary hypertension — Increased AV flow over time in the setting of altered cardiovascular physiology or pathology may also contribute to the increased risk of developing pulmonary hypertension in patients with ESKD [39]. The increase in cardiac output following AV access creation is accompanied by an increase in pulmonary arterial pressure, which correlates with Qa [11,26,40]. This change can be attenuated or resolve in some patients by AV access compression or closure [12,26,41-46].
Pulmonary hypertension is characterized by symptoms of progressive dyspnea, fatigue, syncope, and signs of right heart failure. A high index of suspicion for the development of pulmonary hypertension is critical; patients with intractable or worsening symptoms should undergo assessment for high Qa. The clinical features and diagnosis of pulmonary hypertension are provided separately. (See "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults", section on 'Clinical manifestations' and "Pulmonary hypertension in patients with end-stage kidney disease".)
Hemodialysis access-induced distal ischemia — Ischemic complications of hemodialysis AV access are uncommon but can result in significant limb dysfunction or even limb loss. Hemodialysis access-induced distal ischemia (HAIDI) occurs due to decreased perfusion pressure occurring distal to the AV access anastomosis. In most cases, compensatory mechanisms counteract this adverse effect; however, in cases where this is inadequate, hand ischemia results and can lead to gangrene and digit loss. Although Qa in these cases may be low, normal, or high, most cases are characterized by a high Qa. (See "Hemodialysis access-induced distal ischemia".)
Decreased dialysis clearance secondary to high cardiopulmonary recirculation — An excessively high Qa can have an adverse effect efficiency of dialysis because of a high level of cardiopulmonary recirculation (CPR) [47]. CPR is characterized by dialyzed blood returning to the dialyzer after traversing the cardiopulmonary circulation. A fraction of this volume that returns to the AV access has a lower blood urea nitrogen (BUN) concentration when compared with the peripheral venous BUN because it has not traversed the BUN-rich systemic microcirculation. Because of this phenomenon, blood at the dialyzer inlet has a BUN concentration lower than that of systemic venous blood, and the quantity cleared is less. A high Qa relative to cardiac output enhances CPR and can adversely affect the efficiency of the dialysis treatment [48]. Dialysis efficiency is reduced by an amount roughly equal to the ratio of CPR to cardiac output [48-50]. A fistula with a Qa of 1 L/minute will have approximately 17 percent of the cardiac output that bypasses the systemic microcirculation, while a fistula with a Qa of 2.3 L/minute will have 27 percent of the cardiac output that evades the systemic microcirculation during dialysis [8].
Accelerated central or peripheral venous stenosis — The most common complication associated with an AV access is venous outflow stenosis. This is the result of neointimal hyperplasia resulting from an adverse response of the endothelium of the vessel to a derangement in the hemodynamics of blood flow [51,52]. These lesions occur at specific sites, the anatomy of which promotes turbulent blood flow resulting in a derangement in wall shear stress. Susceptible sites include points where vessels branch, venous valves, sharply angled curved zones within the vessel, and areas of compliance mismatch. This process has a linear relationship to blood flow velocity and volume [51,52]. With the development of stenosis, blood flow through that zone increases in velocity, resulting in propagation of the stenotic lesion. Specific lesions associated with hemodialysis AV access are reviewed separately. (See "Endovascular intervention for the treatment of stenosis in the arteriovenous access", section on 'Specific AV access lesions'.).
It is not clear as to whether an excessively high Qa can also promote the development of stenosis in the central veins. This mechanism has been perceived to be the culprit in patients in whom a history of prior hemodialysis catheter placement was lacking, with a prevalence between 5 and 10 percent [53,54]. In a study of 57 hemodialysis patients [54], six (10 percent) had symptomatic de novo central vein stenosis. All six patients had massive swelling of their access arm. The access was located at the elbow in five and at the wrist in one case. Three cases had stenosis of the left subclavian vein, and three had stenosis of the left brachiocephalic vein. In the four patients in whom it was available, the mean access blood flow volume was 2347 mL/min. It has also been suggested that a high Qa from an associated AV access in a patient with a central venous catheter can increase the risk for the development of central venous stenosis. Central vein stenosis has been reported in the absence of any antecedent. In a study of 69 hemodialysis patients in whom an angiogram was done in preparation for dialysis catheter insertion, 14 of 46 (30 percent) had no antecedent central venous intervention and were found to have significant stenosis involving the venous structures through which the catheter would pass [55]. (See "Central vein obstruction associated with upper extremity hemodialysis access" and "Failure of the mature hemodialysis arteriovenous fistula", section on 'Stenotic vascular lesions'.)
Aneurysmal enlargement of the AV access — The increase in blood flow at the time of AV fistula creation results in a proportional increase in wall shear stress. This promotes the secretion of mediators that promote vasodilatation and remodeling of the vein. The result is an increase in the diameter of the vessel restoring shear stress to baseline levels. This sequence of events has a linear relationship with blood flow velocity and volume [51,52]. With excessively high Qa, progressive remodeling of the vessel results in progressive enlargement of the AV fistula, reaching a size significantly greater than occurs with lower levels of Qa. The possible development of downstream venous stenosis, also promoted by an excessively high Qa, has an additive effect on vessel enlargement due to increased pressure within the vein. If allowed to progress unabated, the end result can be a diffusely ectatic, tortuous AV fistula commonly referred to as a "megafistula" (picture 1 and picture 2).
The effects of hypervolemic pressure associated with excessively high Qa invoke the principles of Laplace Law, which defines the relationship between wall tension and both pressure and size (radius). This relationship is such that either an increase in size, an increase in pressure, or both will result in an increase in wall tension. Under normal circumstances, the vessel responds to this increase in tension by wall thickening. As a result, the process of vessel enlargement tends to be uniform except in areas where the vein is injured by repetitive cannulation. Frequently, thickening does not occur in these areas. The vessel wall in that zone becomes progressively thinner, creating a weak area in the access. This tends to bulge, resulting in aneurysmal dilatation. Development of an associated downstream venous stenosis can aggravate this process. Repetitive injury to the site eventually results in replacement of healthy tissue with scar formation. Pressure within the aneurysm increases progressively as the aneurysm enlarges because of Bernoulli principle, which states that a decrease in the velocity of the flow of the fluid results in higher pressures. In other words, with the blood flow through the access being constant, flow through the larger diameter of the aneurysm results in a lower velocity, creating higher pressure within that zone. As a result, there is a tendency for the aneurysm to continue to increase in size over time. The tendency for this process to occur has a linear relationship with Qa. (See "Arteriovenous fistula creation for hemodialysis and its complications", section on 'Aneurysm/pseudoaneurysm/megafistula'.)
DIAGNOSIS — Although not always the case, clinical manifestations of problems caused by a high blood flow rate (Qa) generally begin with minimal signs and symptoms but tend to be progressive. Early diagnosis and management are important. An enlarging AV fistula may not be noted because the change is gradual. Enlarging aneurysms may be simply attributed to poor cannulation technique. Even serious complications such as high-output cardiac failure and pulmonary edema are underdiagnosed because the dialysis treatment removes fluid and masks early signs and symptoms. For these reasons, a high index of suspicion is important so that the goal of early diagnosis and management can be achieved.
An excessive Qa should be suspected in any patient who develops any of the clinical manifestations listed below (discussed in further detail above and in associated topics). (See 'Clinical manifestations' above.)
●Eccentric left ventricular hypertrophy. (See 'Eccentric left ventricular hypertrophy' above.)
●High-output cardiac failure. (See 'High-output cardiac failure' above.)
●Myocardial ischemia. (See 'Myocardial ischemia' above.)
●Pulmonary hypertension. (See 'Pulmonary hypertension' above.)
●Hemodialysis access-induced distal ischemia. (See 'Hemodialysis access-induced distal ischemia' above.)
●Decreased dialysis clearance secondary to high cardiopulmonary recirculation. (See 'Decreased dialysis clearance secondary to high cardiopulmonary recirculation' above.)
●Peripheral and central venous stenosis. (See 'Accelerated central or peripheral venous stenosis' above.)
●Aneurysmal enlargement of the access (megafistula (picture 2)), aneurysm/pseudoaneurysms. (See 'Aneurysmal enlargement of the AV access' above.)
Physical examination of the access — While the measured Qa is the defining feature for defining an AV access with an excessively high Qa, at least a suspicion of the problem can be ascertained by a careful physical examination of the access. Typically, high Qa is much more common in association with an AV fistula compared with an AV graft and more commonly seen in AV access of the upper arm.
The AV fistula in these cases is generally quite large. While not hyperpulsatile unless there is a significant downstream obstruction, the thrill and bruit are continuous and more prominent in the high-flow AV access than in an access with a lower Qa. Normally, as one progresses up the vein, the prominence of the background thrill and bruit becomes somewhat less. With a high-flow Qa access, this is not the case.
When the normal-flow AV fistula is associated with a significant downstream stenosis, the access is markedly hyperpulsatile. The thrill is shortened and may be systolic only. This is also true for the bruit, which may also increase in pitch, at times taking on a whistling character. In the high-flow AV fistula with a downstream obstruction, the most obvious physical finding is the large size of the access. The fistula is hyperpulsatile but may not be to the degree noted in an AV fistula with a normal Qa because of the increased diameter of the vessel. The thrill and bruit tend to be longer and in some cases may be continuous [11].
Radiographic appearance — The key to distinguishing between the high-flow Qa and normal Qa access lies in recognition of the diameter of the vessel at the site of narrowing compared with the adjacent "normal" vessel. Practice guidelines recommend that a lesion should represent a 50 percent stenosis to justify treatment. An access having a diameter of 8 mm with a narrowed zone of 4 mm and an access of 14 mm with a narrowing of 7 mm both represent 50 percent stenosis. However, the latter case would suggest an inflow problem (high Qa), while the former would suggest an outflow problem. Optimal treatment of the two cases would be different: angioplasty versus flow reduction.
Access flow measurement — The diagnosis of a high Qa is dependent upon its measurement. This can be easily quantitated using Doppler ultrasound. Measurement should be made from the brachial artery at least 5 cm proximal to the anastomosis regardless of whether one is dealing with a radial or brachial artery-based AV fistula [7,47-50,56-60]. In cases of high bifurcation of the brachial artery, the measurement should be made from the brachial artery proximal to the bifurcation. Blood flow measurements made from the access itself are fraught with errors because of the variation in the diameter of the access and its easy compressibility. The brachial artery measurement overestimates the Qa in that it includes that which perfuses the hand; however, this amount is not enough to materially affect decisions made relating to management. Since Qa is directly proportional to the mean inflow blood pressure [61], clinical judgment is necessary in dealing with patients with a systemic blood pressure that is either high or low.
MANAGEMENT — The sequelae resulting from the various problems caused by a high blood flow rate (Qa) range from those that can affect the efficiency of dialysis or the viability of the vascular access to those that can result in the loss of a digit or endanger the life of the patient. For this reason, clinical judgment and consideration of the severity of the patient's individual condition is critical. Treatment is individualized based on the clinical presentation, including patient comorbidities, symptoms, and projected longevity.
Flow reduction — The ideal goal of treatment is to alleviate adverse effects by reducing Qa (ie, flow reduction) while preserving the AV access. Even when dealing with the more serious complications such as high-output cardiac failure, pulmonary hypertension, and hemodialysis access-induced distal ischemia (HAIDI), this goal can generally be achieved if treatment is instituted early. Most patients with severe manifestations of high Qa will require AV access ligation.
General considerations — Treatment criteria for flow reduction for conditions such as cardiopulmonary disease (heart failure, pulmonary hypertension, hemodialysis access-induced distal ischemia) associated with excessively high Qa are well documented. Beyond these conditions, criteria for treatment are less well defined. (See "Pulmonary hypertension in patients with end-stage kidney disease" and "Evaluation and management of heart failure caused by hemodialysis arteriovenous access" and "Hemodialysis access-induced distal ischemia".)
For patients with venous stenosis associated with a hemodialysis AV access, clinical manifestations are the result of an inflow-outflow imbalance. Qa can be normal, low, or high. When the Qa is high, flow reduction rather than angioplasty should be performed. When angioplasty is used to treat a stenotic lesion, Qa can be expected to increase (except for treatment of a central venous stenosis) [62]. In patients with either a marginal or a high Qa, this increased flow following angioplasty can worsen or precipitate problems such as heart failure, pulmonary edema, or hand ischemia [63].
Target flow rate — There is no generally accepted target value for flow reduction. The goal is to reduce Qa to the maximal degree possible without risking the loss of patency. Some studies have used levels of 800 mL/min for an AV fistula and 1000 mL/min for an AV graft as threshold levels for a patient with a normal blood pressure [7,64]. In other reports, Qa has been reduced to levels below this. In a report of 398 cases of precision banding, the target for intraprocedural Qa for AV fistulas was in the 400 to 600 mL/min range and 600 to 800 mL/min in AV grafts [65]. Some degree of rebound post-banding was observed, which was less pronounced in AV grafts. Even when reduced to these levels, post-banding access patency rates have been reasonably good [16,17,65]. These Qa levels are adequate for efficient, effective dialysis.
Options for flow reduction — Three approaches are available for flow reduction, including ligation of a large venous tributaries, precision banding or its equivalent (surgical, endovascular), and revascularization procedures such as revision of distal inflow (RUDI) (figure 2) [66-68].
Ligation of venous tributaries — Venous tributaries associated with an AV fistula have an additive effect on Qa volume. Limited studies have shown that in cases demonstrating this type of vascular anatomy, ligation of these contributing veins may be effective in relieving the symptoms of hand ischemia [69].
However, it should be noted that there are limitations to this approach. Large tributaries are not commonly seen with either brachial-cephalic or brachial-basilic AV fistulas. Reports advocating ligation of these veins have primarily dealt with Gracz AV fistulas, so this method of flow reduction may be somewhat specific to that type of access.
The role large venous tributaries might play in the pathogenesis of hand ischemia associated with a radial-cephalic fistula has not been studied.
Precision banding — Although other banding techniques have been used in the past, the standard of practice is termed "precision-banding." This technique is safe and effective and can be easily done and undone until the desired Qa volume reduction is achieved, or repeated, as needed. The procedure is accomplished by using a sizing device placed intraluminally or extraluminally to ensure that a controlled degree of luminal restriction is achieved [70-72]. For this purpose, an intravascular dilator or angioplasty balloon is generally used. However, there are reports of instances in which an angioplasty balloon has been partially compressed by tying the ligature too tightly, creating a risk of thrombosis [65]. To ensure success, accurate intraoperative Doppler ultrasound flow measurements to judge the degree of access flow restriction should be considered mandatory [17,70,73]. In one report, significant changes in Qa were noted, with only 0.5 mm variations in lumen diameter achieved with banding [70].
In selecting an intraoperative post-banding Qa, the relationship between blood flow and blood pressure must be taken into consideration. The values quoted in these recommendations are based upon a normalized blood pressure maintained during the procedure for the final Qa measurement. Since the effect of a stenotic lesion on Qa is directly proportional to the mean inflow pressure [61], clinical judgment is necessary in dealing with patients with a systemic blood pressure that is either high or low.
Revision using distal inflow — The RUDI procedure (figure 2) is based upon the concept that a radial artery-based access is associated with a lower Qa than one associated with the brachial artery. The RUDI procedure is accomplished by closing the original AV anastomosis with the distal brachial artery and moving it to the more distal proximal radial or ulnar artery. This can be accomplished either by direct anastomosis of the outflow vein to the new inflow artery if possible or with an interposition graft (saphenous vein or expanded polytetrafluoroethylene [ePTFE]) [74,75].
Outcomes of flow reduction — As indicated above, flow reduction is not successful in all cases initially or in longer-term follow-up. However, in most cases it is effective in either improving or eliminating the clinical signs and symptoms of the condition for which it was performed.
●Cardiopulmonary – For patients with cardiac or pulmonary manifestations, flow reduction improves heart structure and function and reduces pulmonary artery pressure [76-78]. Beneficial effects of flow reduction are present even in patients without symptoms of heart failure. Symptomatic and structural improvements have been noted within weeks of the procedure [70,77]. (See "Evaluation and management of heart failure caused by hemodialysis arteriovenous access".)
There are no studies available assessing the effect of flow reduction on myocardial ischemia.
●Hand ischemia – Hemodialysis access-induced distal ischemia (HAIDI) can be associated with high, normal, or low flow, which determines treatment (algorithm 1). For cases related to high flow, flow reduction has a high degree of success in relieving symptoms of hand ischemia [9,79,80]. In a review of surgical techniques used to treat HAIDI associated with high flow, 12 studies involving 255 cases used precision banding [80]. The pooled rate for symptomatic relief was 90.2 percent (95% CI 80.5 to 97.3 percent), and early thrombosis of the vascular access was 8.2 percent (95% CI 0.6 to 20.4 percent). The surgical procedure RUDI, in which the anastomosis of a brachial artery associated with upper arm access is moved distally to the proximal radial or ulnar artery, has also been used to treat a high Qa-associated HAIDI. In the study referred to above [80], only two reports were found, involving 26 cases. The pooled rate for symptomatic relief was 93.1 percent, and early thrombosis of the vascular access was 12.1 percent. (See "Hemodialysis access-induced distal ischemia".)
●Peripheral and central venous stenosis — The literature as it relates to this complication associated with high Qa consists of only a few small case series reports. Flow reduction in these cases has been prompted by the frequency of symptomatic recurrence of these lesions after successful treatment, especially the cephalic arch and central veins. The benefit of the procedure has been judged by a significant decrease in the frequency of recurrence [81,82]. (See "Endovascular intervention for the treatment of stenosis in the arteriovenous access" and "Central vein obstruction associated with upper extremity hemodialysis access".)
●Decrease dialysis clearance secondary to high cardiopulmonary recirculation — There are no publications available that address this problem directly. In a study of 10 patients with high-output cardiac function who underwent surgical flow reduction [77], Qa (adjusted to L/min/1.73 m2) was 2.4 before the procedure and was reduced after the procedure to 0.9. Cardiopulmonary resuscitation (CPR) dropped from 41 to 16 percent at one month. Although the effect on dialysis clearance was not assessed, this problem is related to a high CPR. With this decrease, the cause for the problem would have been removed.
●Anatomical abnormalities of vascular access — Although a high Qa plays a role in the formation and progression of aneurysms, pseudoaneurysms, and vascular ectasia, removing the stimulus by reducing Qa does not result in regression. With the removal of the stimulus, the further advancement is only arrested. (See "Arteriovenous fistula creation for hemodialysis and its complications", section on 'Aneurysm/pseudoaneurysm/megafistula'.)
AV access ligation — Some patients present with severe symptoms, and for others the situation is not recognized until signs and symptoms have advanced to a critical state. In these patients, access ligation, rather than attempts at flow reduction, may be required.
It should be noted that a patient with severe cardiopulmonary disease has a short life expectancy, and dialysis therapy is palliative. In these situations, hemodialysis with a central venous catheter or peritoneal dialysis represents the best choice.
FOLLOW-UP — After flow reduction, patient follow-up is important to determine the course of the patient's symptoms. If symptoms improve, the patient should continue to be monitored. The interval for evaluation should be determined by the patient's individual situation.
Repeat banding — Experience with precision banding for flow reduction has shown a small but significant incidence of thrombosis as well as a small but significant incidence of cases requiring rebanding. In a large study of precision banding, target for intraprocedural blow flow rate (Qa) for AV fistulas was in the 400 to 600 mL/min range and 600 to 800 mL/min in AV grafts [65]. With a median follow-up of 157 days (range 52 to 373 days), rebanding was required in 54 of 398 cases (14 percent), with the median time to rebanding of 134 days (range 56 to 224 days). Early banding failure occurred in 9/398 (2.3 percent) of patients, typically associated with an increase of the angiographic diameter at the banding site postprocedure to rebanding, suggesting that the knots of the banding suture had slipped. The 30-day thrombosis rate after banding was 15 of 397 cases (3.8 percent), with a median time to event of 5.5 days (range 2 to 102 days).
Treatment failure — If symptoms do not improve after flow reduction in those treated for cardiopulmonary disease, the access should be ligated. In general, these patients have a short life expectancy, and dialysis treatments are palliative.
For the patient with HAIDI, an alternative surgical procedure to salvage the access may be possible. If not, the access should be ligated. In these patients, if dialysis is to be continued, the creation of a new AV access may be possible after a detailed clinical evaluation.
SUMMARY AND RECOMMENDATIONS
●Effects of AV access flow – Arteriovenous (AV) vascular access is necessary for the delivery of lifesaving hemodialysis therapy but is nonphysiologic. The increased blood flow generated by the AV access increases the workload of the cardiopulmonary system and reduces flow to the hand. While compensatory mechanisms reduce some of these effects, excessive blood flow rate (Qa) can cause serious complications, some of which can be life- or limb-threatening. Thus, early recognition and management of the high-flow AV access is an important aspect of medical care delivered to the hemodialysis patient. (See 'Introduction' above and 'High-flow arteriovenous access' above.)
●Definition of high flow – A high-flow AV access can be defined as having a Qa >1500 mL/min, or Qa >20 percent of the cardiac output (ie, cardiopulmonary circulation [CPR] >20 percent) has been suggested. However, the exact threshold for defining a high Qa access has not been rigorously validated nor universally accepted. Patients with specifically related comorbidities can develop adverse sequelae from a Qa below these levels. (See 'Definition' above.)
●Risk factors for high-flow AV access – High Qa is more commonly seen in association with an AV fistula than with an AV graft. Brachial-cephalic and brachial-basilic AV accesses are much more commonly associated with this problem compared with distal radial-cephalic AV access. (See 'Risk factors' above.)
●Clinical manifestations – Clinical manifestations of high Qa are generally related to the development of, or worsening of, cardiopulmonary dysfunction or distal ischemia. Clinical manifestations generally begin with minimal symptoms and signs but tend to be progressive. A careful physical examination of the AV access may help confirm a suspicion. Excessive Qa should be suspected in any patient who develops any of the clinical manifestations listed below. (See 'Clinical manifestations' above.)
•High-output cardiac failure – High-output cardiac failure (HOCF) results when Qa exceeds the patient's cardiac functional reserve. HOCF is characterized by dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and edema (pulmonary, peripheral) in the presence of an above-normal cardiac index or simply an elevated cardiac output.
•Pulmonary hypertension – The increase in cardiac output following AV access creation is accompanied by an increase in pulmonary arterial pressure, which correlates with Qa. Pulmonary hypertension is characterized by progressive dyspnea, fatigue, syncope, and signs of right heart failure.
•Hemodialysis access-induced distal ischemia – Hemodialysis access-induced distal ischemia (HAIDI) can occur due to decreased perfusion pressure occurring distal to the AV access anastomosis. While compensatory mechanisms counteract this adverse effect, ischemia can result in significant limb dysfunction or even limb loss.
•Aneurysmal enlargement of the AV access – Increased flow proportionally increases wall shear stress, which promotes vasodilatation and remodeling of the vein to increase diameter. Further diameter increases can result from downstream venous stenosis. The result can be a diffusely ectatic, tortuous AV fistula commonly referred to as a "megafistula."
•Others – Other manifestations may include eccentric left ventricular hypertrophy, myocardial ischemia, reduced efficiency of hemodialysis from cardiopulmonary circulation, and peripheral or central venous stenosis.
●Diagnosis – The diagnosis of a high Qa relies on flow measurement, which is performed using ultrasound. The measurement is made from the brachial artery at least 5 cm proximal to the AV access anastomosis, rather than from the access itself. Since Qa is directly proportional to the mean inflow blood pressure, clinical judgment is necessary in determining if Qa is high in patients with higher or lower than normal blood pressure. (See 'Diagnosis' above.)
●Management – Management of high Qa is individualized based on the clinical presentation and including patient comorbidities, symptoms, and anticipated lifespan. In general (see 'Management' above):
•Most patients with severe manifestations of high Qa will require AV access ligation.
•For all other symptomatic patients, we suggest a flow reduction procedure, rather than AV access ligation (Grade 2C).
•For patients with persistent cardiopulmonary symptoms following flow reduction, we ligate the AV access. However, for patients with HAIDI, an alternative surgical procedure to salvage the access may be possible before consideration of AV access ligation.
●Flow reduction – Flow reduction aims to alleviate symptoms by reducing flow while preserving the AV access. This goal can generally be achieved if treatment is instituted early even when dealing with serious clinical manifestations. Flow reduction effectively improves or eliminates the clinical signs and symptoms associated with high Qa. (See 'Flow reduction' above.)
•Target flow rate – There is no generally accepted target value for flow reduction. The goal is to reduce Qa to the degree possible without risking loss of AV access patency. Some studies have used levels of 800 mL/min for an AV fistula and 1000 mL/min for an AV graft as threshold levels for a patient with a normal blood pressure. Using these values, post-banding access patency rates have been reasonably good. (See 'Target flow rate' above.)
•Options for flow reduction – Three approaches are available for flow reduction, including precision banding or its equivalent (surgical, endovascular), ligation of large venous tributaries, and revascularization procedures such as revision using distal inflow (RUDI) (figure 2). Rebanding is an option for initial banding failures. (See 'Options for flow reduction' above.)
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