23 Vascular Access Monnie Wasse, MD, MPH, FASN, and Gerald A. Beathard, MD, PhD, FASN OUTLINE Arteriovenous Fistula, 361 Types of Arteriovenous Fistulas, 361 Classification of Fistulas, 361 Fistula Types Based on Anatomy, 362 Life Cycle of the Arteriovenous Fistula, 362 Complications Associated with Arteriovenous Fistulas, 364 Failure to Mature, 364 Late Arteriovenous Fistula Failure, 365 Excessive Flow, 365 Secondary Arteriovenous Fistulas, 368
Arteriovenous Graft, 369 Advantages of Arteriovenous Graft, 370 Types of Arteriovenous Grafts, 370 Complications of Arteriovenous Grafts, 370 Venous Stenosis, 370 Hemodialysis Reliable Outflow Vascular Access Device, 372 Dialysis Catheters, 373 Catheter Design, 374 Catheter-Associated Problems, 374 Acute Dialysis Catheters, 377
Vascular access is the sine qua non of hemodialysis; it is also the Achilles heel. The process of cleansing the blood of the toxic products of chronic renal failure requires, as its first step, access to the circulation. The importance of the vascular access in the long-term provision of hemodialysis has been apparent from the beginning of the dialysis era. In 1944 Willem Kolff reported, after his first patient had received 12 dialysis treatments over a 26-day period, that all of the veins were “ruined.”1 A surgical cutdown of the radial artery followed but caused severe bleeding during heparinization. Kolff concluded that “we believe to be able to keep patients suffering from uremia and anuria alive so long as blood vessels for puncture are available.”1 It is interesting that more than six decades later we are still in the same position. Fortunately, today we have better alternatives to provide access to the circulation; yet, it is unfortunate that none of these are ideally suited for the purpose. The ideal vascular access should have the basic characteristics listed in Box 23.1. Unfortunately, the ideal vascular access does not exist. There are several choices, which are classified as arteriovenous fistula (AVF), arteriovenous graft (AVG), or central vein catheter. Although each of these has its own set of problems, the characteristics of the AVF make it the preferred choice for most patients.
an AVF is the lowest of the three types of access, and AVFs are associated with lower hospitalization rates than are seen in patients with AVGs (relative risk [RR] = 1.47) or catheters (RR = 2.3).3 Because patients with an AVF have fewer access-related problems, especially infection,4 they have a lower mortality and morbidity compared with patients with either an AVG or a central venous catheter.3 With the exception of transposed fistulas, an AVF can be created with very little patient morbidity associated with the procedure compared with the insertion of a synthetic AVG, and the surgical procedure is relatively simple and is generally quickly accomplished.
ARTERIOVENOUS FISTULA There are a number of benefits associated with an AVF. This type of access is associated with the best primary patency rate, the best cumulative patency rate, and the lowest rate of thrombosis and requires the fewest interventions over the duration of its life cycle.2 Cost of implantation and maintenance of
TYPES OF ARTERIOVENOUS FISTULAS Classification of Fistulas AVF nomenclature incorporates its anatomical location, inflow artery, and outflow vein,5 such as radial-cephalic (the radial artery and the cephalic vein). Although there are standard AVF configurations, an AVF can be created anywhere there is a cannulatable vein (which may require transposition) BOX 23.1 Characteristics of Ideal Dialysis
Easy repetitive access to the circulation Ability to reliably provide blood flow > 500 mL/min Hemostasis at the end of dialysis accomplished easily and quickly Function for the life of the patient Freedom from complication Cosmetically acceptable
SECTION III Dialysis
of sufficient diameter to be attached to an adequate inflow artery. AVF types can be classified into three different categories: simple direct, vein transposition, and vein translocation (Table 23.1). Bioengineered veins have been developed and are currently in phase III clinical trials. The use of these vessels presents a model very similar to a transposition AVF.6
Fistula Types Based on Anatomy Although a variety of different anatomical types of AVF can be surgically created, most AVF creations fall within three TABLE 23.1 Categories of Arteriovenous
Easiest of the AVFs to create. Vein and the artery are used in their normal positions. Distal end of the vein is freed and connected to the adjacent artery. Most difficult to create. Created using vein that is not easily assessable for dialysis use. Proximal end of the vein is left intact. Distal portion of the vein is transposed to an assessable position. Requires creation of a tunnel or pocket for the newly positioned vein. Vessel is removed from one anatomical location and moved to a new site. Requires the creation of both a venous and an arterial anastomosis. Requires the creation of a tunnel for its new location.
basic configurations (Fig. 23.1). There is a separate category of AVFs sometimes referred to as middle-arm or bidirectional fistulas that have been created when neither of the three basic configurations are possible. These are created using the proximal radial artery with either the median antebrachial vein or the median cubital vein.7 The suitability of the median antebrachial vein may be contributed to in part by the fact that the venipuncturist does not commonly access it. According to accepted guidelines,8,9 the order of preference for the creation of permanent vascular access should start distally in the upper extremity and progress proximally to preserve venous anatomy. According to this approach, the radial-cephalic AVF would be considered primary and the brachial-cephalic and brachial-basilic would be considered secondary choices. Some have advocated that the middle-arm AVFs should be considered tertiary.10 If it is not possible to create one of the basic configurations of AVF, then reasonable attempts at creating a transposed AVF should be made before consideration is given to the insertion of AVG; however, it is important to consider patient-specific factors (e.g., comorbid conditions, anticipated longevity) at the time a surgical plan is devised. In the event that an AVG is placed, it should ideally be done with the plan that it will be used for the dual purposes of providing dialysis access during its problem-free life and for the development of the upper arm veins for the later creation of a secondary AVF once its use becomes problematic.
Life Cycle of the Arteriovenous Fistula The life cycle of an AVF can be divided into five distinct clinical phases (Fig. 23.2). The first three phases can be characterized as developmental stages (Fig. 23.3) of the AVF, eventually leading to a clinically functional dialysis access. Although in most successful cases, an AVF progresses through these developmental stages over a period of 4 to 6 weeks, time is
C FIG. 23.1 Fistula types based on anatomy. (A) Radial-cephalic fistula (radial artery and the cephalic vein); (B) brachial-cephalic fistula (brachial artery and cephalic vein); (C) brachial-basilic fistula (brachial artery and basilic vein).
CHAPTER 23 Vascular Access not considered an element of these definitions because it does not exert an influence on whether the defined outcome has been achieved.11
Phase 1: Creation Phase 1 of the AVF’s life cycle corresponds to the first developmental stage of the access—that is, creating an arteriovenous communication. If this is successful, as demonstrated by the presence of blood flow after creation, a patent AVF has been achieved. Phase 2: Maturation The maturation phase corresponds to the second developmental stage of the AVF and is characterized by evolution from AVF patency to a physiologically mature AVF, considered to have the potential for being used as a hemodialysis access. As stated earlier, AVF maturation is characterized by a continuous, progressive, and relatively rapid increase in blood flow and vessel diameter sufficient to permit reproducible clinical usability for hemodialysis. Studies have found that blood flow
alone, or a combination of blood flow and vessel diameter, are reliable indirect indicators for predicting the successful use of an AVF for hemodialysis.12-19 Using these metrics, the physiologically mature AVF is defined as having an internal diameter >0.5 cm (measured without a tourniquet)12,18,19 and a blood flow >500 mL/min.11 A blood flow of 400 to 500 mL/ min (measured from the brachial artery) has been found to have an accuracy of 53% to 93%,14-17 sensitivity of 67% to 96%,14,16-19 and specificity of 65% to 90%14,16,17,19 for predicting clinical AVF maturation. The combination of both AVF blood flow and internal vessel diameter of the vessel (500 mL/ min, 0.5 cm) has been found to have a sensitivity of 84% and a specificity of 93%.19 It has been reported that most AVFs that mature will do so in 4 to 8 weeks.12-19
Phase 3: Clinical Use, Initial This third phase requires that successful clinical use of the AVF be demonstrated. This is the third and final stage of AVF development, referred to as a clinically functional AVF. This definition is necessary to separate from the second stage, AVF
Phase of Life Cycle
Initial Clinical Use
Sustained Clinical Use
Patent AV Access
Physiologically Mature AV Access
Clinically Functional AV Access
Uninterrupted Clinical Use
Direction of Movement Endpoint
Restoration and Preservation of Clinical Use
FIG. 23.2 Five phases of life cycle of an arteriovenous fistula. Clinical Significance
Minimum Stage 1
Non-Patent AV Access
Non-Mature AV Access
Non-Functional AV Access
Patent AV Access
Physiologically Mature AV Access
Clinically Functional AV Access
AV Access Creation Success Diagnostic Criteria Direct
Demonstration of blood flow using imaging modality
Presence of pulse, thrill, or bruit on physical exam
Cannulate with 2 dialysis needles for 75% of dialysis sessions within a 4 week period and achieve the prescribed dialysis AVF Flow - ≥ 500 mL/min and Internal diameter - > 0.5cm AVG Flow - ≥ 600 mL/min
FIG. 23.3 Three stages of arteriovenous fistula development.
SECTION III Dialysis
maturation, because clinical functionality is dependent on individual patient characteristics in addition to physiological changes that occur within the target vessel. It is possible for an AVF to be physiologically mature and have the capacity to provide adequate dialysis access but be unusable because of its location or depth. In addition, predialysis placement of the access will predictably result in a fully mature (physiologically) AVF not being used for a prolonged period and in some cases never being used.20,21 In these cases, proof of functionality is never obtained, or at least is delayed, even though optimal physiological changes may have occurred. A clinically functional AVF is defined as one that can be cannulated with two dialysis needles for at least 75% of dialysis sessions within a 4-week period and achieves the prescribed dialysis.6 This definition, based on less than 100% success at cannulation, takes into account the fact that many patients with newly created AVFs have cannulation-related complications, although the access is destined to have longterm successful use.22
Phase 4: Clinical Use, Sustained Once the clinical functionality of an AVF has been proven, it enters the fourth phase of its life cycle, characterized by continuous, effective, problem-free use for hemodialysis. This is the ultimate criterion for judging success. Unfortunately, most cases will alternate between this phase and phase 5, characterized as dysfunction. The duration of this phase is indeterminate and is limited by the occurrence of problems and complications. Phase 5: Dysfunction This phase is characterized by the occurrence of a problem that interferes with the routine use of the AV access, threatens patency or results in a loss of patency, presents a significant risk for medical complication, or adversely affects the patient’s sense of well-being. Intervention is often required to resolve the problem. If this is successful, the AVF returns to phase 4.
COMPLICATIONS ASSOCIATED WITH ARTERIOVENOUS FISTULAS Although the AVF is associated with fewer complications than are seen with other types of vascular access, they do occur and they should be dealt with effectively. The major complications that occur in conjunction with arteriovenous AVFs can be categorized under the headings of early failure, late failure, excessive flow, ischemia, aneurysm formation, and infection. Both early and late failures have multiple causes.
Failure to Mature As stated earlier, an AVF is superior to an AVG; however, data on which AVFs’ superiority has been established are based on AVFs that successfully mature and become clinically functional and generally exclude AVFs that failed to mature. Were data from all AVFs (nonmaturing and maturing) to be considered, more than a year would elapse before the superiority
of the AVF became apparent.23 This difference is due primarily to early failure. Failure to mature, also referred to as early or primary failure, is defined as an AVF that is never usable for dialysis or that fails within 3 months of use, and failure rates ranging from 20% to 60% have been reported.14,24-27 According to US Renal Data System data, 36% of AVFs created in 2014 failed and the average time between AVF creation and first use was 133 days.28 Although many AVFs can be salvaged,29,30 those that are often require more than one procedure to become clinically usable31 and have a shortened primary patency rate, making repetitive interventions necessary for continued clinical use.32,33 Reasons for the high incidence of early AVF failure are not totally clear. However, one must realize that the dialysis practice and population at risk for end-stage renal disease (ESRD) have changed over time. When the radial-cephalic AVF first was described in 1966 by Brescia et al.,34 nearly all patients had chronic glomerulonephritis, the average patient age was 43 years, and blood flows used for dialysis were 250 to 300 mL/min. The early AVF failure rate was 11%. Today’s dialysis patients are different—they are much older (many >70 years), and three-quarters of them have five or more comorbidities, with 90% having cardiovascular disease and 50% having diabetes.35,36 In addition, the average blood pump speed is much higher: 350 to 450 mL/min. Therefore it is not surprising that achieving functional AVFs in today’s ESRD population is often a challenge. Additional risk factors for poorer AVF development include female sex, African American race, older age, greater body mass index (>35 kg/m2),37 and history of diabetes, peripheral vascular disease, or coronary artery disease.26,27 The three most commonly created AVFs, the radialcephalic, the brachial-cephalic, and the brachial-basilic transposition, have differing rates of early failure. The early failure rate for the brachial-basilic transposed AVF is reported to be the lowest, followed by the brachial-cephalic and then the radial cephalic, which has the highest failure rate.38-40 The early failure rate for brachial-basilic transposition AVFs it is reported to be between 0% to 21% in various series.38-40 Compared with brachial-cephalic AVFs in the same series, brachial-basilic transpositions have an early failure rate of 0% versus 27%, 21% versus 32%, and 18% versus 38%.39,41 Radial-cephalic AVF failure rates of more than 60% have been reported.42 Most investigators agree that nonmaturing AVFs have an associated anatomical problem.30,43,44 With the exception of thrombosed AVFs, three important principles have been established related to early failure: (1) A distinct lesion or lesions can generally be identified as the underlying cause of failure; (2) the problem can generally be identified by physical examination and confirmed by imaging; and (3) the lesions can be corrected with a high expectation of success (except for certain preexisting lesions, which should have been avoided by quality vascular mapping). Although several problems commonly exist when an AVF fails to mature,30,43 the most common lesion observed in these cases is juxta-anastomotic stenosis.45 This is defined
CHAPTER 23 Vascular Access
B FIG. 23.4 Lesions associated with AVF nonmaturation. (A) Juxta-anastomotic stenosis in radialcephalic fistula (black arrow, lesion; white arrow, fistula); (B) accessory vein (black arrows, accessory vein; white arrow, fistula).
as stenosis occurring within the first 3 to 4 cm of the AVF, immediately adjacent to the arterial anastomosis (Fig. 23.4A). The anastomosis may also be involved, resulting in luminal narrowing, decreased AVF blood flow leading to problems of maturation, and early thrombosis. In some instances, the problem is poor preoperative vessel selection. The cause of failure to mature may be related to lesions that should have been recognized before the creation of the access. In reported cases, preexisting proximal venous stenosis has been documented as present in 4% to 59% of cases and central venous stenosis in 2.6% to 9% of cases.30,31,43,46-49 Small arteries or arteries with stenotic lesions may be present and contribute to AVF nonmaturation with an incidence ranging between 4% to 6%.46,48 When an AVF is created, the inflow artery generally dilates in parallel with dilatation and increasing blood flow in the AVF. If this fails to occur, the AVF will likely not mature. Another type of preexisting problem that can affect AVF development and maturation is the presence of accessory veins.30,31,43,47,50-52 These are side branches of the forearm veins used for the construction of an AVF (Fig. 23.4B). Most accessory veins are not problematic; however, because AVF maturation is dependent on blood flow, a large accessory vein that diverts a major portion of the flow away from the target vessel can result in failure of maturation.
Late Arteriovenous Fistula Failure Late AVF failure is defined as failure that occurs after a period of normal use. The primary causes of late failure are venous stenosis and acquired arterial lesions (Fig. 23.5). These lesions are manifest as a pathophysiological change in the AVF resulting from increasing resistance, leading to a decline in blood flow, followed by inadequate dialysis and eventually thrombosis. The same types of lesions that are seen in association
with early failure may be also seen here. Whether present initially and clinically unimportant or whether they developed (or progressed) over time during AVF use is not clear.52 The most common cause of late AVF failure is venous stenosis.46,53 The site of the relevant lesion varies with the site of the AVF arteriovenous anastomosis. In distal radial-cephalic AVFs, virtually all stenoses are found in the inflow region (anastomotic and juxta-anastomotic), whereas outflow lesions are found almost exclusively in midforearm and elbow/upper arm AVF.54-56 Venous stenosis associated with an AVF generally develops at areas of vein bifurcation, at swing points, and in association with venous valves.45,52,57 The development of collateral veins is common, often extensive, and tends to preserve flow in the access (Fig. 23.6). Stenosis of the inflow artery has been reported as a cause of late AVF failure in 6% to 18% of cases.46,53 These lesions can also lead to decreased blood flow in the access, resulting in inadequate dialysis and eventually thrombosis. In general, 100% of all thrombosed AVFs have either venous or arterial-associated pathological anatomy.46 Thrombosis is the endpoint of late AVF failure, and it occurs at a rate that is approximately one-sixth of that for an AVG.58
Excessive Flow After the early, rapid increase in dialysis access blood flow (Qa) after AVF creation, there is a tendency for Qa to continue to slowly, yet progressively increase for the life of the access. Although this is generally tolerated and in some cases enhances the dialysis functionality of the AVF, it can also lead to problems, the most clinically relevant of which is high-output heart failure (HOHF). HOHF is a particularly serious problem considering the fact that cardiovascular disease is the leading cause of death in the ESRD population.59 Currently, there is no generally accepted definition of excess
SECTION III Dialysis
Qa. It has been suggested that the ratio of Qa to cardiac output (Qa/CO), referred to as cardiopulmonary recirculation (CPR), be used as a gauge. Normal values for this ratio are generally considered to be in the range of 20% to 25%. Patients with levels greater than this, or with Qa in excess of 2 L/min (Fig. 23.7), should be considered at higher risk for the development of HOHF.60 The risk for HOHF is directly proportional to the Qa and inversely proportional to the patient’s preexisting cardiac status.61 Many patients can tolerate a high Qa associated with an elevated CPR; however, even levels considered to be
within the normal range can be excessive for the impaired heart because compromised cardiac function may limit the increase in CO that is required. For this reason, it has been suggested that the cardiac index may be a better gauge for the establishment of HOHF because it is more individualized. Moreover, it has been suggested that patients with symptoms of heart failure (dyspnea either at rest or with varying degrees of exertion; orthopnea; paroxysmal dyspnea; and edema, pulmonary and/or peripheral) that are resistant to medical management and occur in association with a cardiac index >4.0 L/min/m2 should be considered as having HOHF.62
B FIG. 23.5 Lesions associated with the late AVF failure. (A) Venous stenosis with pseudo aneurysms upstream from the lesion (black arrow, the lesion); (B) arterial stenosis (black arrow, lesion; white arrow, fistula).
68 M / 02-Nov-1946 Vascular Access 51.65
FIG. 23.6 Collateral veins upstream from the stenotic
lesion (black arrows, collateral veins; white arrow, site of stenosis).
120 Lt Prox Fistula FV 3476.07 ml/min TAMV 38.07 cm/s Diam 13.92 mm 90 60 30 0 -30 -60 -90 -120
FIG. 23.7 AVF blood flow measured from the radial
artery (flow value is indicated by arrow).
CHAPTER 23 Vascular Access Hand Ischemia: Dialysis Access Steal Syndrome When an arteriovenous access is placed in an extremity, a unique physiological state is established, because blood flow to the hand must now also supply the access. This hand/vascular access complex consists of a proximal artery feeding into two competing circuits connected in series—the arteriovenous access and the peripheral vascular bed on which perfusion of the hand is dependent. The former is a low-resistance pathway and is located proximally. The latter is downstream and is characterized by high resistance. Collateral arteries that bypass the access circuit to feed the periphery directly also contribute to this complex. Most patients tolerate this abnormal physiological state because of compensatory mechanisms. However, in some instances, there is a failure of these mechanisms and hand ischemia, referred to as dialysis access steal syndrome (DASS), occurs. DASS can occur with either an AVG or an AVF; however, it is more common with the latter. Two distinct clinical variants of hand ischemia are recognized as associated with the placement of a dialysis access: ischemic monomelic neuropathy (IMN), where changes are confined to the nerves of the hand, and DASS, in which ischemic changes affect all tissues of the hand to a varying degree of severity.63 DASS is reported to occur in 1.6% to 8% of cases with an arteriovenous access.64-69 Major predisposing risk factors include the use of the brachial artery as the inflow, diabetes, BOX 23.2 Stages of Dialysis Access Steal
Stage I: Pale/livid hand and/or cool hand without pain Stage II: Pain during exercise and/or during dialysis Stage III: Rest pain or loss of motor function Stage IV: Tissue loss
female sex, age >60 years, peripheral artery disease, and multiple previous access procedures.68,70-72 Of these, the use of the brachial artery appears to create the greatest risk for this condition. In addition, DASS is reported to occur more readily in patients with AVFs with large anastomoses and Qa.69 Based on patient-specific clinical signs and symptoms, DASS is categorized into four stages reflecting increasing clinical severity (Box 23.2, Fig. 23.8). These four stages guide treatment choices for DASS. DASS varies in its time of onset and may be acute, subacute, or chronic.73,74 Acute DASS is defined as the onset of signs and symptoms that appear immediately or within hours of the time of the surgical procedure. Acute DASS is most commonly associated with the placement of an AVG. DASS that occurs later, but within 1 month of access placement, is defined as subacute. Those cases occurring after this period are classified as chronic. These latter two groups are more commonly seen in association with AVFs and more specifically with brachial artery–based AVFs, although either an AVF or an AVG can be involved at any the three periods. It is important to differentiate DASS from IMN. IMN is a distinct clinical entity associated with interference of a major limb artery resulting in multiple distal, axonal-loss mononeuro pathies.75 The attributable causal factor is believed to be occlusion of the brachial artery during the AV access surgical procedure. The syndrome develops quickly, typically within minutes to hours of AVF creation. The pathognomic feature is the presence of diffuse neurological dysfunction, usually in the absence of significant ischemic changes in the tissues of the hand and fingers, which differentiates it from DASS. Attributable neuropathic symptoms include pain, paresthesias, and numbness in the distribution of all three forearm nerves along with diffuse motor weakness or paralysis. Involvement of fewer than all three forearm nerves should bring the diagnosis into serious question.76 Typically the hand is warm, capillary refill is preserved,
B FIG. 23.8 Stages of DASS. (A) Early DASS with no tissue loss; (B) stage IV DASS with tissue loss at the fingertips.
SECTION III Dialysis
A B FIG. 23.9 Ischemic monomelic neuropathy with hand deformity and primary median nerve palsy; however, all three forearm nerves were involved. (A) Lateral view; (B) dorsal view. and a palpable radial or ulnar pulse or audible Doppler signal is present.76 The motor deficits resulting from the IMN nerve damage cause severe disability to the involved hand (Fig. 23.9). The exact incidence of IMN is not known, because most of the literature is based on case reports, but it is not believed to be a common occurrence. IMN occurs exclusively in association with an arteriovenous access that is brachial artery based.76 There are no reports of IMN precipitated by a distal forearm procedure. Although there are case reports to the contrary,77 the condition occurs almost exclusively in diabetic hemodialysis patients.78,79
0.2% per year thereafter.84 This is considerably less than that of AVGs and catheters.4,76 AVF-associated infection can take the form of cellulitis, an abscess, bacteremia, septic emboli, and sepsis.71,85,86 AVF infections occurring during the immediate postoperative period are generally related to a problem with aseptic technique during surgery, whereas those occurring later are most often related to contamination during cannulation. Late AVF infection has been attributed to the buttonhole cannulation technique.87
Aneurysm Formation Most of the bulges that are noted in association with an AVF are true aneurysms; that is, they contain all layers of the vessel wall. Although there is no universally accepted definition for an aneurysmal AVF, it is commonly defined as an AVF that is three times the diameter of the adjacent normal vein or a minimum of 2 cm.80 These pathological lesions represent degenerative changes in the vein wall and are relatively common.81 The features that characterize an aneurysm typically result from the combination of repeated dialysis needle punctures and hemodynamic factors, such as downstream peripheral or central venous stenosis.82,83 As an aneurysm develops and expands, it can lead to complications such as pain, objectionable cosmetic appearance, difficult cannulation, risk for bleeding, and problems with access blood flow.82 Aneurysms can be fusiform, ectatic, or spherical (Fig. 23.10). The fusiform type of aneurysm is commonly seen in association with segmental overuse—that is, repetitive cannulation in a localized area leading to weakening of the vessel wall. With increased pressure, progressive ballooning of the vessel wall develops, generally at the arterial and venous cannulation sites, and have a fusiform appearance. The ectatic type of aneurysm represents a relatively diffuse enlargement of the entire AVF related to downstream stenosis. If allowed to progress, it eventually achieves an appearance that has been referred to as a megafistula. The spherical aneurysm is related to a localized defect in the wall of the AVF. At times, this anomaly appears acutely in association with a problematic cannulation and may be a pseudoaneurysm, rather than a true aneurysm.
Secondary AVFs (SAVF) are important to the hemodialysis vascular access strategy of all nephrologists. A SAVF is defined as an AVF that is created after an AV access, usually an AVG, using the outflow veins of that access. In general, this is a forearm access and the AVF is created using an upper arm draining vein. Because of the forearm access, the veins of the upper arm undergo the same process of maturation as is seen with AVF development and for the same reasons.88-92 In most cases this involves the creation of either a brachial-cephalic or a brachial-basilic AVF. Even when one of these veins is not suitable, there may be an adequate vein in the forearm that can be used as a bidirectional, middle-arm SAVF.93 When an AV graft is placed in a patient, it should be done with a dual purpose in mind—first, to provide an access for hemodialysis, and second, as a means of maturing veins in the upper arm for a SAVF. The National Vascular Access Improvement Initiative (Fistula First)94 recommended that every patient receiving dialysis via an AVG be viewed as a potential candidate for a SAVF. To identify a suitable patient for an SAVF, visualizing the veins of the upper arm is necessary and is most easily accomplished by simply having patients roll up their sleeve (Fig. 23.11). With any type of procedure to treat AVG dysfunction, the angiographic studies that are performed can be used to identify optimal candidates for a SAVF if the operator is alert to the issue. In a study of the angiograms that were performed as part of either an angioplasty or a thrombectomy procedure, 75% of the patients with lower-arm grafts were found to have one or both upper-arm superficial veins that were optimal for SAVF conversion.89 The success with SAVF creation has been very good, particularly considering that many of these patients were not initially suitable for AVF creation, and they often have a history of prior procedures. The 1-year primary and cumulative
Infection Infections in AVF are uncommon and are reported to occur in less than 0.4% of cases in the postoperative period and
Secondary Arteriovenous Fistulas
CHAPTER 23 Vascular Access
C FIG. 23.10 AVF aneurysms. (A) Fusiform aneurysm. (B) Ectatic aneurysm. (C) Spherical aneurysm.
FIG. 23.11 Good candidate for secondary fistula (forearm loop AVG; black arrow, upper arm cephalic vein is an excellent candidate for secondary fistula [white arrow]).
patency rates for SAVFs have been reported in the range of 71% to 82.5% and 92.5% to 100%, respectively.95,96
ARTERIOVENOUS GRAFT Although the AVF was introduced by Brescia and coworkers in 1966,34 an AVF was not possible in many patients. After that innovation, vascular access evolved through the use of
saphenous vein translocation,97,98 bovine carotid artery graft,99 and the Dacron velour vascular graft,100 but still there were major short-term and chronic problems with these access types. In 1976 the problem of vascular access was solved, or so it was thought, through the use of expanded polytetrafluoroethylene (ePTFE).101 The AVG was initially considered only as a substitute access in patients in whom an AVF was not possible; however, this philosophy soon became lost and it became the access of choice in the United States, a practice that led to major problems and one that has been very difficult to reverse. In 1997, the first iteration of National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI) Clinical Practice Guidelines for Vascular Access was published and stressed the need to decrease the reliance on AVGs.102 However, in 1998, 58% of patients on dialysis for 2 or more years were still using an AVG.103 The National Vascular Access Improvement Initiative, which came to be referred to as Fistula First, was launched in January 2003.94 This was a Medicare initiative designed to decrease AVG reliance and increase AVF use in the United States. Since that time there has been a slow but progressive decline in the prevalence of AVG use, declining to a level of 18.3% in 2014.104 It is important to note that there remains a population of patients for whom an AVG represents the best choice for a dialysis vascular access. In general, these patients fall into two categories: (1) patients with vascular anatomy that is not favorable for the creation of an AVF as determined by vascular mapping;
SECTION III Dialysis
(2) patients with comorbidities that increase the risk for short life expectancy and the time required for an AVF maturation and for whom the high risk for primary failure makes AVF creation imprudent. Elderly patients also fall within this latter group. In a study using Medicare-derived data,105 dialysis survival was tabulated and four age groups were evaluated: 65 to 79, 80 to 84, 85 to 89, and >90. At 6 months after dialysis initiation, the mortality was 20%, 30%, 40%, and 45%, respectively; in accordance with these results,106 it was found that an AVF was not associated with better survival compared with an AVG used as the first predialysis access among patients older than 80 years.
Advantages of Arteriovenous Graft Although considered more problematic than AVFs, AVGs have several advantages. They are comparatively easy to insert and repair, can be used at multiple anatomical sites, can be created in a variety of shapes and configurations, have a short maturation time, are technically easy to cannulate, and offer a large area for cannulation. Although there is a higher infection rate compared with an AVF, their primary disadvantage relates to the development of stenosis from neointimal hyperplasia, which tends to shorten their patency. Reported primary patency rates for AVGs range from 40% to 60% at 1 year,107 yet with aggressive management of thrombosis, secondary patency rates as high as 90% at 1 year can be achieved.108
Types of Arteriovenous Grafts Unfortunately, a large proportion of patients start dialysis with a central venous catheter, which creates an inordinate risk to the patient. Using the standard ePTFE graft shortens the time required to develop a clinically functional AVF; however, traditional dialysis programs wait 2 to 3 weeks before the use of a newly placed AVG, so a central venous catheter is still required for dialysis access. Data from the Dialysis Outcomes and Practice Patterns Study (DOPPS) was used to examine the average time of AVG cannulation.109 Investigators found that the relative risk for graft failure (reference group = first cannulation at 2 to 3 weeks) was 0.84 with first cannulation at <2 weeks (P = 0.11), 0.94 with first cannulation at 3 to 4 weeks (P = 0.48), and 0.93 with first cannulation at >4 weeks (P = 0.48), suggesting that earlier cannulation was not associated with AVG failure. Moreover, multilayered early cannulation grafts have been developed that can be cannulated within 24 hours of placement and have no increase in complication rates compared with traditional ePTFE.110 An AVG can be placed in a number of different sites and configurations, as long as the cannulation segment is accessible and there is blood return to the right atrium. However, the most common AVG sites are the forearm, the upper arm, and the thigh. Although it is distinctly unusual to see anything other than a loop graft in the thigh, either straight, curved, or loop grafts may be placed in the upper extremity locations.
COMPLICATIONS OF ARTERIOVENOUS GRAFTS Complications occur much more commonly with AVGs than with AVFs. The major complications are venous stenosis (including the venous anastomosis), arterial stenosis
(including the arterial anastomosis) thrombosis, infection, pseudoaneurysm formation, and hand ischemia.111
Venous Stenosis The most common complications associated with an AVG are venous stenosis, arterial stenosis, and thrombosis. In most cases the problems of stenosis and thrombosis share the relationship of disease and symptom. The histological characteristics of venous and arterial stenosis are well characterized as aggressive neointimal hyperplasia.112 The net result of this process is a progressively expanding lesion that encroaches on the lumen of the vessel, causing a progressive increase in resistance and a decrease in flow, often resulting in eventual thrombosis. Venous stenosis occurs most often at the venous anastomosis but may occur anywhere within the access conduit, composed of the arterial anastomosis, AVG, the venous anastomosis, and its peripheral and central draining veins. In a review of 2300 cases of venous stenosis,113 the following distribution of lesions was found: venous anastomosis 60%, peripheral vein 37%, within the graft 38%, central veins 3.2%, and multiple locations 31% (Fig. 23.12). Percutaneous angioplasty is the treatment of choice for venous stenosis. Among a pooled cohort of 2166 cases from 15 published studies, AVG-related peripheral vein stenosis treated with angioplasty was associated with a primary patency of 62% and a cumulative patency of 85% at 6 months.114-117 In metaanalysis based on 34 relevant studies, the primary and cumulative patency rate for AVGs at 6 and 18 months was 58% and 33% and 76% and 55%, respectively.118 The dialysis vascular access should be thought of as a complete circuit starting and ending with the heart. The venous side represents only one-half of the circuit, whereas the other half is arterial. Arterial lesions adversely affect access inflow, and a hemodynamically significant lesion can develop anywhere in the arterial tree from the ascending aorta to the arterial anastomosis. Reports of inflow stenosis in dysfunctional AVGs range between 14% to 42%.44,54 These lesions are generally treatable with angioplasty.54 Over time, progressive stenosis can result in thrombosis. The frequency of AVG thrombosis is approximately 1 to 1.5 per patient per year.119 Approximately 85% to 90% of all cases of graft thrombosis are associated with an underlying anatomical lesion.119
Infection Infection (Fig. 23.13) is a common cause of AVG loss120,121 and a prominent cause of patient mortality.122,123 In one report, infection was reported to occur at a frequency of 1.3 episodes per 100 dialysis months and was associated with bacteremia at a rate of 0.7 cases per 100 dialysis months.124 In a prospective Canadian study in which surveillance for hemodialysis-related bloodstream infections was performed in 11 centers during a 6-month period, it was found that the relative risk for bloodstream infection with an AVG access was 2.5 per 1000 dialysis procedures. This was compared with a rate of 0.2 in patients receiving dialysis via an AVF.125
CHAPTER 23 Vascular Access
C FIG. 23.12 Venous stenosis in AVG. (A) Venous anastomosis stenosis (arrow); (B) draining vein stenosis (arrow); (C) central vein (brachiocephalic vein) stenosis (arrow).
FIG. 23.13 AVG infection at multiple sites (arrows).
The hospitalization rate for dialysis patients is double that of the general population, and infection is the attributable cause in 20% of cases.56 The development of dialysis access sepsis is associated with a higher incidence of myocardial infarction, congestive heart failure, cerebral stroke, and peripheral artery ischemic disease in the subsequent years.126 Not only does AVG infection result in significant morbidity, it results in AVG loss in a proportion of affected patients.127 A number of risk factors for AVG infection have been recognized, including cannulation technique, AVG location, and duration of use. Patient personal hygiene appears to be the most important risk factor for the development of access-related infection128; however, episodes of infection have been traced to individual dialysis facility staff and can be related to poor needle insertion technique.129,130 This underscores the importance of staff training in infection control measures.
SECTION III Dialysis
B FIG. 23.14 AVG pseudoaneurysms. (A) Ectatic pseudoaneurysm (arrow); (B) spherical pseudoaneurysm (arrow).
Femoral AVGs are often placed when all upper limb access sites have been used. These AVGs are at higher risk for infection.131 The incidence of graft infection increases with the duration of AVG use,64,132,133 suggesting another reason to evaluate AVG patients for a SAVF. AVG infections are generally attributable to common skin microorganisms represented by gram-positive bacteria. In most cases, the causative organism of the AVG infection is Staphylococcus aureus or other gram-positive pathogens, such as coagulase-negative staphylococci. S. aureus is identified in nearly 68% cases of AVG infection,128 followed by Staphylococcus epidermitis.134 Gram-negative bacteria are less commonly the cause of infection, and some episodes are polymicrobial.135
Pseudoaneurysm Formation A pseudoaneurysm (“false aneurysm”) is characterized by actual disruption of the layers of the AVG leading to a bulging anatomical defect (Fig. 23.14). Pseudoaneurysm deformities are common and have been reported to have an incidence as high as 60%.81 Two concurrent events are typically required for the appearance of the dilatation characterizing a pseudoaneurysm. First, the dialysis needle has a thin wall and is very sharp. When it punctures the wall of the AVG, it acts like a cookie cutter, either removing a small plug or creating a flap. Other types of needles, even those of large gauge, make a slit when they puncture the graft. Repetitive cannulation in a localized area eventually results in a defect. Second, increased pressure within the AVG develops as a result of downstream venous stenosis. With the increased pressure, bulging occurs and tends to be progressive. This occurs earlier and is more accentuated if puncture sites are not rotated.136,137 However, even with site rotation, structural damage to the AVG over a prolonged period will result in a defect. With long-term AVG use, this defect can be quite extensive. The seriousness of a pseudoaneurysm lies in its associated complications. In addition to the objectionable cosmetic appearance and difficulty with cannulation of the access, pseudoaneurysms can result in pain and an increased risk
for thrombosis and infection. The most serious complication, however, is thinning of the skin overlying the defect in the graft. Histological study of the pseudoaneurysm has shown that it consists of only a perigraft fibrous tissue capsule directly overlying the area of the defect.136 As the enlargement progresses, the skin over the AVG can become scarred, thinned, and avascular. In some cases, this can lead to ulceration and spontaneous bleeding, which can be life threatening.
Hand Ischemia: Dialysis Access Steal Syndrome DASS is primarily a problem with AVFs; however, it can also occur with an AVG. DASS varies in its time of onset and may be acute, subacute, or chronic. As stated earlier, an AVG patient may develop hand ischemia at any of these times; however, they are primarily acute—that is, immediately after or within hours of the time of the surgical procedure.73,74
HEMODIALYSIS RELIABLE OUTFLOW VASCULAR ACCESS DEVICE Over the years, the average life expectancy of a patient on hemodialysis has improved. Yet an unfortunate consequence of this increased longevity is the potential for recurrent vascular access problems and exhaustion of arteriovenous access options. In the past, there were only two available alternatives that would allow for continuing dialysis treatment in patients with no upper-extremity option—a central venous catheter or a lower-extremity arteriovenous access. Unfortunately, both expose the patient to an increased risk for infection. The development of a hybrid device, the Hemodialysis Reliable Outflow (HeRO) has provided a third alternative in these cases, as long as central venous patency is established for the insertion of a central venous catheter. The HeRO is a long-term, fully subcutaneous dialysis access that, instead of a venous anastomosis, uses an outflow catheter that is placed percutaneously into the right atrium through the subclavian or internal jugular vein and into the superior vena cava. This outflow component bypasses central
CHAPTER 23 Vascular Access vein stenosis by positioning the tip of the outflow component beyond it, in the right atrium.138 This device, classified as an AVG, consists of two parts—the arterial limb and the venous limb. The arterial limb consists of a 6-mm (internal diameter) AVG that is attached to a peripheral artery at one end and a titanium connector at the other end (Fig. 23.15). This arterial anastomosis and its orientation within the patient’s upper arm is like that of a traditional AVG. The titanium connector attaches to the venous limb, a 19F silicone catheter that is reinforced with a nitinol braid that prevents kinking. As with the traditional ePTFE grafts, the HeRO is cannulated by inserting dialysis needles once the graft is tissue incorporated.139 Relative contraindications to implantation of the HeRO device include a cardiac ejection fraction <20%, systolic blood pressure <100 mmHg, and the presence of infection.138 In a systematic review of the literature,140 the 1-year primary and cumulative pooled patency rates for 409 patients were found to be 21.9% (9.6% to 37.2%) and 59.4% (39.4% to 78%). The range of HeRO-related bacteremia was 0.13 to 0.7 events per 1000 days, and the rate of DASS was 6.3% (1.0 to 14.7%).
Compared with an AVF or AVG, the HeRO graft patency rate is not as good; however, the patient using this device has already had multiple arteriovenous accesses fail. Moreover, the rate of infection is comparable to that of an AVG. When comparing rates of patency and infection of the upper-extremity HeRO with lower-extremity AVG, results vary most likely because of cohort differences. However, one study concluded that lower-extremity AVGs are preferable because they have better patency rates compared with the HeRO device in the upper extremity.141 Conversely, compared with a catheter, the infection rate associated with the HeRO was much lower140 and a cost analysis revealed it to be considerably more economical.142,143 The average number of interventions required to maintain HeRO patency ranges from 1.5 to 3 procedures per year. The great majority of these are for the treatment of stenosis commonly associated with thrombosis. In general, the outcomes of these procedures are the same as the treatment of an AVG.144
DIALYSIS CATHETERS The development of a dual-lumen catheter for removing and returning blood has played and continues to play an important role in hemodialysis.145 Unfortunately, its vantages have been mirrored by serious disadvantages. Catheter use is associated with significant morbidity and mortality risk to the hemodialysis patient, in large part because of their abuse. According to the US Renal Data System, 18.9% of all new hemodialysis patients started dialysis with a catheter in 1996.146 In 2014 that number was in excess of 80%.147 Even in patients who had seen a nephrologist before the initiation of dialysis, the majority initiated dialysis with a catheter. There are two types of dialysis catheter—the acute dialysis catheter (ADC) and the tunneled dialysis catheter (TDC). As the name suggests, the TDC is placed into a central vein through a subcutaneous tunnel (Fig. 23.16). The TDC plays
FIG. 23.15 HeRO graft. AVG segment (double arrow)
connected by titanium connector to outflow catheter (single arrow).
FIG. 23.16 Tunneled dialysis catheter. (A) Appearance of catheter; (B) catheter in place (1, wings of catheter to be secured with suture; 2, catheter in subcutaneous tunnel).
SECTION III Dialysis
BOX 23.3 Advantages and Disadvantages
of Tunneled Dialysis Catheter
Advantages Universally applicable Ability to insert into multiple sites Maturation time not required Venipuncture not required for dialysis No hemodynamic consequences No cardiopulmonary recirculation Ease and low cost of placement and replacement Ability to provide access over a period of months Ease of correcting thrombotic complications Disadvantages High morbidity as a result of: Thrombosis Infection Inflammation Risk of permanent central venous stenosis or occlusion Discomfort and cosmetic disadvantage of external appliance Shorter expected life span than other access types
an important role in the management of the hemodialysis patient, being used for a variety of purposes. Although the AVF is the best solution for hemodialysis access, for some patients with comorbidities, a fistula is impractical because of the short life expectancy of the patient. In addition, they are used for emergent dialysis, for short-term treatment, and as a bridge backup for a dysfunctional arteriovenous access. TDCs have many advantages as a hemodialysis access. Unfortunately, they also have many disadvantages (Box 23.3). Although their advantages are important, they are outweighed by their disadvantages, especially those that create a risk for morbidity and mortality from catheter-associated infection and central venous stenosis and occlusion. The cardiac effects of an arteriovenous access are not found with a TDC. This makes it the preferred vascular access for the ESRD patient with severe cardiac insufficiency. In addition, CPR observed with an arteriovenous access does not occur with the TDC, resulting in an improved dialysis efficiency.148
Catheter Design In the 1980s the TDC concept was introduced via two different types of catheters: the Quinton PermCath (Quinton Instrument Co., Seattle, Washington) and the Canaud catheter, produced in France. The Quinton PermCath was a single oval-shaped catheter with two circular lumens constructed of silicone rubber. It came in 28-, 33-, 36-, and 40-cm lengths and had a Dacron cuff to anchor the catheter in the subcutaneous tissue. The external end was split into a Y configuration that had external connectors with Luer locks and permanently attached clamps. The catheter-tipped lumen for blood outflow (referred to as the arterial lumen) terminated 2.5 cm proximal to the inflow lumen (referred to as the venous lumen). It was thought that the Dacron cuff would limit the incidence of infection by presenting a barrier to bacterial migration from the exit site down the catheter tunnel once it was incorporated.
Initially, these TDCs were placed (and removed) surgically in the operating room. Today placement using a peel-away sheath or simply over a guidewire is routine. Most TDCs are produced with side holes at the tip. The original intent of these holes was to preserve catheter flow if the arterial lumen became occluded by being pressed against the vessel wall; however, this design has the disadvantage of allowing the anticoagulant lock to leak from the tip of the catheter. Since the TDC was first introduced, there have been numerous modifications, especially to the catheter tip design,149 that are intended to reduce potential problems that can occur with use of the TDC. There have been tip designs to improve catheter blood flow, minimize recirculation, and inhibit the formation of a fibrin sheath that affects all central venous catheters and is the major cause of dysfunction. The catheters that we have today are generally classified as twin catheters, step-tipped, split-tipped, symmetrical-tipped, and self-centering catheters (Fig. 23.17).
Catheter-Associated Problems Problems associated with the use of a TDC can be grouped under four headings: (1) adequacy of dialysis, (2) problems associated with placement, (3) catheter dysfunction, and (4) catheter-related infection.
Adequacy of Dialysis A number of factors influence the adequacy of dialysis; however, the vascular access contribution is generally related to inadequate blood flow. NKF KDOQI defines sufficient blood flow through a catheter as 300 mL/min32; however, this should be regarded as the minimum criterion, not the ideal level.150 Optimally, if a tunneled catheter is to be used for hemodialysis therapy of more than 2 to 3 weeks, it should be capable of delivering no less than the prescribed pump speed blood flow, generally 400 mL/min or greater. The primary determinant of catheter blood flow is its dimensions. As with the flow of any fluid through any tubular structure, blood flow in a catheter follows Poiseuille’s law. Interpolation of this law to apply to a dialysis catheter results in a more practical formula, which states that flow = pressure/ resistance.148 Pressure is applied by the blood pump and resistance is determined by catheter dimensions, the major determinant for resistance being diameter. Resistance decreases in proportion to an increase in radius raised to the fourth power (r4). This relationship dictates that relatively small increases in catheter diameter will result in major changes in resistance and the potential for flow. Going from a 10F catheter to a 12F (3F = 1 mm), a change of only 26% in diameter, will result in a 60% drop in resistance. Conversely, there is only a direct relationship between resistance and catheter length, making it less important as a determinant to blood flow than the catheter radius. In fact, increasing the catheter radius by only 19% can compensate for a doubling of length.148 The higher the resistance, the greater the pressure required to achieve a desired level of blood flow. When a graph is created by plotting pressure against flow in a group of patients, as shown in Fig. 23.18, the slope of the line represents hydraulic
CHAPTER 23 Vascular Access
FIG. 23.17 Variations in tunneled dialysis catheter tips.
For 14 F Catheter
200 250 mL/min
For 15 gauge Needle
200 250 mL/min
FIG. 23.18 Hydraulic resistance of 14F tunneled dialysis catheter versus 15-gauge dialysis needle. The slope of the
line represents hydraulic resistance.
resistance. For a dialysis catheter, hydraulic resistance is a measure of the ease (or difficulty) of passing blood through the catheter or needle. The venous pressure recorded by the dialysis machine is essentially the pressure drop of the catheter lumen and is a reflection of hydraulic resistance—that is, the pressure required to achieve the indicated blood flow. The same is true for the arterial pressure, except that the numbers will be negative. It has been reported that a TDC has approximately the same hydraulic resistance as a standard 15-gauge dialysis needle at comparable flow rates.151 Comparison of comparably sized split catheters, step-tipped catheters, and twin catheters have found no significant difference in hydraulic resistance.152 The roller pump flow meter on the dialysis machine blood pump is not truly volumetric; it is a revolutions-per-minute (rpm) meter. The displayed volume flow is an interpolated value that is based on the assumption that each revolution of the roller pump delivers a constant, known volume of blood (i.e., the volume of the pump segment of the blood tubing). However, if the pump segment volume varies, then actual blood flow will also vary to a proportional degree. This variance often happens and it does so under two circumstances. First, the pump relies on the elasticity of the pump segment to expand and refill as the rollers turn. However, because of elastic hysteresis (failure to return to original size on the rebound), there is some flattening of the pump segment during dialysis
as the tubing warms. This results in a slight decrease in blood flow late in the dialysis treatment.153 Second, the pump segment can be partially collapsed if the prepump pressure is excessive. Because there is a potential for prepump pressure to become more negative with increasing flow demands, problems can occur at high blood flow rate settings, because refilling of the pump segment of the dialysis tubing is less complete as prepump pressure becomes more negative. As the blood pump rpm meter progressively increases, its reflection of true volumetric flow becomes progressively more inaccurate.154 To prevent errors caused by excessive negative pressure, it is recommended that the prepump pressure be monitored and that alarms be set to detect when it drops to less than –240 to –260 mmHg.148 Another issue related to TDCs and dialysis adequacy is that of recirculation. Recirculation occurs when blood returning from the dialyzer returns to the dialyzer rather than mixing with the systemic blood, resulting in a decrease in the efficiency of the dialysis treatment. This is of greater concern with a catheter than with an arteriovenous access. A common strategy for dealing with catheter dysfunction is to reverse the dialysis bloodlines and withdraw blood from the distal venous port and return blood from the proximal arterial port, yet this can increase recirculation. None of the commonly used TDCs have significant recirculation when connected correctly, but recirculation increases as much as
SECTION III Dialysis
30% when the lines are reversed.155 An exception to this is the symmetrical-tipped catheter, which has less than 1% recirculation regardless of how the bloodlines are connected.103 It has been found that increasing dialysis blood flow to compensate for problems and improve dialysis efficiency does not increase recirculation significantly.104
the TDC.164-167 The transfemoral route to the inferior vena cava has been used163,168; however, this site should be used only in cases in which the status of the central veins of the thorax precludes TDC placement or the patient has been reduced to a single upper-extremity vein that needs to be preserved for a future arteriovenous access.
Problems Related to Catheter Placement When choosing a site for the placement of a TDC, there are two issues to consider: (1) The catheter must be placed into a location capable of providing the blood flow necessary for hemodialysis, and (2) care must be taken to minimize the chances of inducing central vein stenosis. To achieve the blood flow levels demanded by the dialysis prescription, the tip of the TDC must be placed in a location that is capable of delivering a large volume of blood. This requires that it be placed in the vena cava or atrium. If the catheter is in the brachiocephalic vein, blood flow levels are often inadequate. The primary contributor of central venous occlusive disease (CVO) in the dialysis patient is the central venous catheter. Preservation of the central veins is critical to vascular access selection and outcomes; therefore CVO is a very serious problem. Vein selection for catheter insertion plays an important role in central vein preservation. CVO results from chronic mechanical irritation to the endothelium of the vessel.156 Although this injury occurs regardless of the target vessel, the degree to which it occurs appears to be related to the anatomy of the vessel—that is, whether the catheter has a straight path to the vena cava and atrium or whether there are curves. When the catheter is in place, there is constant motion because of the movement of the mediastinal structures created by respiration and the beating of the heart. Mechanical irritation is augmented if the catheter follows a curved pathway to its target location. A catheter placed in the right internal jugular vein with its straight descending course to the atrium permits the least amount of contact between the catheter and the vessel wall and therefore the least amount of irritation. Although the incidence of central venous stenosis is in the range of 10%145,157-160 when the right internal jugular is used, it is by far the best choice for TDC placement. The number of patients with limited venous access options has increased as the dialysis population has grown and patients on dialysis experience greater longevity, creating a need for alternate sites for TDC placement. Although the incidence of CVO is significantly higher with the left compared with the right internal jugular vein,145,157-159 it represents the second choice for TDC placement if the right internal jugular is not available. The incidence of CVO resulting from TDC placement in the subclavian vein is reported to be in the range of 30% to 50%.160-162 Because of this, it has been suggested that this vein never be used for TDC placement unless it is known with certainty that the patient will never need a peripheral arteriovenous dialysis access.37,163 With loss of the internal jugular veins, other central veins are often enlarged, such as the external and anterior jugular veins, and have been used successfully for the placement of
Catheter Dysfunction The most common complication associated with a TDC is catheter dysfunction secondary to poor blood flow.169 This is defined as failure to attain and maintain an extracorporeal blood flow sufficient to perform hemodialysis without significantly lengthening the hemodialysis treatment. In general, this is considered to be a blood flow less than 300 mL/min (at a negative pressure ≤–250).170 Catheter dysfunction may be classified as early or late.171 Early catheter failure is defined as that which occurs immediately after placement, whereas late dysfunction is defined as a catheter that initially functioned in an optimal fashion but then became dysfunctional. In general, the problems that result in early dysfunction are related to catheter position or technical problems with placement. Under the heading of improper positioning are catheter tip malorientation, tip malposition, and placement into the wrong vessel. Technical problems that can result in early failure include a kinked catheter and sutures that are constrictive. All these problems should be recognized and corrected at the time of catheter placement. Late catheter dysfunction is generally the result of either partial or total thrombosis and is classified as either extrinsic or intrinsic.171 An extrinsic thrombus is one that forms outside of the catheter and is not attached to it. Examples of extrinsic thrombosis include (1) thrombosis of the vessel in which the catheter has been placed; (2) mural thrombus, in which thrombus forms and is attached to the wall of the vein or the atrium at the point of contact with the catheter; and (3) catheter-related atrial thrombus, in which the thrombus presents as a mass within the right atrium and is attached to the catheter. An intrinsic thrombus is one that either forms within the catheter or surrounds it as a sleeve or sheath. Although thrombus may form within the lumen of the catheter, often attached to side holes, the most common cause of delayed catheter dysfunction is a fibrin sheath. Fibrin sheath formation has been identified in up to 76% of dialysis catheters by pull-back venography.172-174 Sheathing of the catheter starts as early as 24 hours after catheter insertion and eventually extends to the catheter tip.175,176 Animal studies have found that the structural components of the fibrin sheath evolve over time as the fibrin sheath becomes organized and is eventually converted into fibroepithelial tissue.176,177 When the sheath covers the arterial port of the catheter, it acts as a flap valve, often resulting in an inability to aspirate blood from the port, resulting in limited blood flow and abnormal arterial pressures. The reported incidence of catheter dysfunction secondary to this problem ranges between 13% to 57%.178 In addition to catheter dysfunction, the fibrin sheath has been reported to be associated with additional thrombus formation and subsequent infection.179,180
CHAPTER 23 Vascular Access Catheter-Related Infection Infection associated with TDCs can be classified into three categories: exit site infection, tunnel infection, and catheterrelated bloodstream infection (CRBSI). An exit site infection is defined as culture-positive inflammation external to the cuff, localized to the exit site, and not extending above the cuff.181 A tunnel infection is defined as culture-positive inflammation within the catheter tunnel internal to the Dacron cuff with a negative blood culture.181 Isolated tunnel infections (negative blood culture) are not a common occurrence but when present are generally associated with CRBSI and should be treated in accordance with the more serious CRBSI classification. CRBSI is defined as bacteremia in a patient with a catheter and no other explanation for the positive blood culture. Much of the morbidity and mortality related to these infections is due to metastatic infection, which has been reported to range in frequency from 3.2% to 50%, depending somewhat on the type of organism involved,182-185 with the risk increased in the setting of S. aureus infection.184 Metastatic complications such as septic arthritis, osteomyelitis, endocarditis, and epidural abscess can occur, and although the incidence of these complications is relatively low,186 they have significant gravity because of their dire consequences. CRBSI is a biofilm infection. This means that more than 99.9% of bacteria grow as aggregated “sessile” communities attached to the surface of the catheter, rather than as “planktonic” or free-floating cells in the circulation.187 The biofilm develops when the attached cells excrete polymers that facilitate adhesion, matrix formation, and alteration of the organism’s phenotype with respect to growth rate and gene transcription.94,188 The hallmark of biofilm-related infections is marked resistance to antimicrobials and to host defenses, necessitating infected TDC removal or catheter exchange for optimal eradication of the infection.
ACUTE DIALYSIS CATHETERS An ADC, also referred to as a noncuffed dialysis catheter (Fig. 23.19), is defined as a catheter designed for short-term use as a vascular access in the dialysis patient. Its use should be restricted to acute dialysis and for limited duration in hospitalized patients. Noncuffed femoral catheters should only be used in bedbound patients.170 The ADCs differ from the TDC in several ways: (1) They are more rigid and are designed to be placed over a guidewire without the use of dilators; (2) most designs are somewhat pointed at the tip; (3) they do not possess a cuff; and (4) they are not placed using a tunnel but rather by a direct insertion into the target vein. A comparison of ADC and TDC usage is difficult because they are generally used in different patients and for different conditions. One study189 analyzed the outcome of 37 TDCs and 235 ADCs (149 patients, 11,612 catheter-days) during a 3-year period in an attempt to compare the two. Infection rates were 2.9 per 1000 catheter-days for TDCs, 15.6 for acute catheters (internal jugular), and 20.2 for acute catheters (femoral). They found that within 2 weeks both actuarial and infection-free survival were superior for TDCs (P < 0.05 vs. all separate groups).
B FIG. 23.19 Acute dialysis catheters. (A) Precurved
catheter; (B) straight catheter.
From a practical viewpoint, the ADC represents a device that has utility; however, when the choice is between an ADC and a TDC, the decision should always favor the latter. Although the ADC is often inserted at the bedside and often believed to be more easily placed than a TDC, when one considers the risk for placement, time required, and skill necessary for catheter insertion, the ADC has no attribute to recommend it over the use of a TDC. Adequate dialysis can be achieved using an ADC because most of ADCs are capable of delivering 400 mL/min or greater blood flow. If the catheter is placed properly and is of the appropriate length, recirculation rates are generally within acceptable limits. It is important to note that catheter length is critical because an ADC greater than 15 cm increases the risk for atrial perforation when inserted through the right internal jugular vein. The tips of catheters placed in the neck should reside in the superior vena cava, and those inserted through the groin should be reach the inferior vena cava. Tip placement in a smaller vein increases the risk for significant recirculation. In general, 15-cm catheters should be used in the right internal jugular, 20-cm catheters in the left internal jugular, and 20-cm or 24-cm catheters in the femoral vein.190 One study191 looked at recirculation rates for ADCs that were of different links and placed in different veins. Recirculation rates for ADCs have been examined based on catheter length and vessel insertion site. Reported rates were 4%, 5%, and 10% for the 12.5 cm in the internal jugular vein, the 20 cm in the subclavian, and 24 cm in the femoral vein, respectively. Complications from ADCs include thrombosis, infection, central vein stenosis, and vessel and cardiac perforation. Thrombosis leading to catheter dysfunction is a common problem with all catheters, and although the incidence of dysfunction with the ADC is approximately the same as with the TDC, the risk for infection is considerably higher.192 The risk for CRBSI from an ADC increases over time in an exponential fashion at both the femoral and internal jugular site; however, the risk for infection at the femoral site is greater. In addition, if an exit site infection occurs and the ADC is left in place, the risk for bacteremia rises dramatically.193 Central venous catheters, particularly subclavian catheters, are the major cause of central venous stenosis in the hemodialysis patient.194-197 The incidence of subclavian stenosis after ADC placement has been reported to be in the range of 42%
SECTION III Dialysis
to 50%. In contrast, the rate of brachiocephalic stenosis after use of the internal jugular vein has been reported to be 0% to 10%.160,161 For this reason, subclavian ADCs should be avoided if at all possible. Some nephrologists feel that acute catheter use is better reserved for the femoral vein only. When an acute catheter is left in place for a prolonged period, progressive vascular erosion can occur and lead to perforation. This is related to the length and relative rigidity of these devices. Improper catheter positioning or migration of the tip out of the proximal superior vena cava increases the
risk for this occurrence. This can result in a hemothorax or atrial perforation and pericardial tamponade.198 A full list of references is available at www.expertconsult.com.
REFERENCES 1. Kolff WJ, Berk HTJ. Artificial kidney; dialyzer with great area. Acta med scand. 1944;117:121–134. 2. Perera GB, Mueller MP, Kubaska SM, et al. Superiority of autogenous arteriovenous hemodialysis access: maintenance of function with fewer secondary interventions. Ann Vasc Surg. 2004;18:66–73. 3. Dhingra RK, Young EW, Hulbert-Shearon TE, et al. Type of vascular access and mortality in U.S. hemodialysis patients. Kidney Int. 2001;60:1443–1451. 4. Anel RL, Yevzlin AS, Ivanovich P. Vascular access and patient outcomes in hemodialysis: questions answered in recent literature. Artif Organs. 2003;27:237–241. 5. Sidawy AN, Gray R, Besarab A, et al. Recommended standards for reports dealing with arteriovenous hemodialysis accesses. J Vasc Surg. 2002;35:603–610. 6. Lawson JH, Glickman MH, Ilzecki M, et al. Bioengineered human acellular vessels for dialysis access in patients with end-stage renal disease: two phase 2 single-arm trials. Lancet. 2016;387:2026–2034. 7. Bonforte G, Rossi E, Auricchio S, et al. The middle-arm fistula as a valuable surgical approach in patients with end-stage renal disease. J Vasc Surg. 2010;52:1551–1556. 8. NKF-K/DOQI Clinical practice guidelines for hemodialysis adequacy, update 2006. Am J Kidney Dis. 2006;48(Suppl 1):S2–S90. 9. Sidawy AN, Spergel LM, Besarab A, et al. The society for vascular surgery: clinical practice guidelines for the surgical placement and maintenance of arteriovenous hemodialysis access. J Vasc Surg. 2008;48:S2–S25. 10. Holtmann B, Anderson CB. Carpal tunnel syndrome following vascular shunts for hemodialysis. Arch Surg. 1977;112:65–66. 11. Beathard GA, Lok CE, Glickman MH, et al. Definitions and end points for interventional studies for arteriovenous dialysis access. Clin J Am Soc Nephrol. 2018;13:501–512. 12. Wong V, Ward R, Taylor J, et al. Factors associated with early failure of arteriovenous fistulae for haemodialysis access. Eur J Vasc Endovasc Surg. 1996;12:207–213. 13. Lin SL, Huang CH, Chen HS, et al. Effects of age and diabetes on blood flow rate and primary outcome of newly created hemodialysis arteriovenous fistulas. Am J Nephrol. 1998;18:96– 100. 14. Robbin ML, Chamberlain NE, Lockhart ME, et al. Hemodialysis arteriovenous fistula maturity: US evaluation. Radiology. 2002;225:59–64. 15. Malovrh M. Native arteriovenous fistula: preoperative evaluation. Am J Kidney Dis. 2002;39:1218–1225. 16. Ives CL, Akoh JA, George J, et al. Pre-operative vessel mapping and early post-operative surveillance duplex scanning of arteriovenous fistulae. J Vasc Access. 2009;10:37–42. 17. Back MR, Maynard M, Winkler A, et al. Expected flow parameters within hemodialysis access and selection for remedial intervention of nonmaturing conduits. Vasc Endovascular Surg. 2008;42:150–158. 18. Ferring M, Henderson J, Wilmink T. Accuracy of early postoperative clinical and ultrasound examination of arteriovenous fistulae to predict dialysis use. J Vasc Access. 2014;15:291–297. 19. Zhu YL, Ding H, Fan PL, et al. Predicting the maturity of haemodialysis arteriovenous fistulas with colour Doppler ultrasound: a single-centre study from China. Clin Radiol. 2016;71:576–582.
20. Al-Jaishi AA, Oliver MJ, Thomas SM, et al. Patency rates of the arteriovenous fistula for hemodialysis: a systematic review and meta-analysis. Am J Kidney Dis. 2014;63:464–478. 21. Lee T, Thamer M, Zhang Y, et al. Outcomes of elderly patients after predialysis vascular access creation. J Am Soc Nephrol. 2015;26:3133–3140. 22. van Loon MM, Kessels AG, van der Sande FM, et al. Cannulation practice patterns in haemodialysis vascular access: predictors for unsuccessful cannulation. J Ren Care. 2009;35:82–89. 23. Allon M, Lok CE. Dialysis fistula or graft: the role for randomized clinical trials. Clin J Am Soc Nephrol. 2010;5:2348–2354. 24. Dember LM, Beck GJ, Allon M, et al. Effect of clopidogrel on early failure of arteriovenous fistulas for hemodialysis: a randomized controlled trial. JAMA. 2008;299:2164–2171. 25. Ascher E, Gade P, Hingorani A, et al. Changes in the practice of angioaccess surgery: impact of dialysis outcome and quality initiative recommendations. J Vasc Surg. 2000;31:84–92. 26. Ernandez T, Saudan P, Berney T, et al. Risk factors for early failure of native arteriovenous fistulas. Nephron Clin Pract. 2005;101:c39–c44. 27. Lok CE, Allon M, Moist L, et al. Risk equation determining unsuccessful cannulation events and failure to maturation in arteriovenous fistulas (REDUCE FTM I). J Am Soc Nephrol. 2006;17:3204–3212. 28. U.S. Renal Data System, USRDS. Annual Data Report, National Institutes of Health. Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases. 2016. 29. Asif A, Roy-Chaudhury P, Beathard GA. Early arteriovenous fistula failure: a logical proposal for when and how to intervene. Clin J Am Soc Nephrol. 2006;1:332–339. 30. Beathard GA, Arnold P, Jackson J, et al. Aggressive treatment of early fistula failure. Kidney Int. 2003;64:1487–1494. 31. Falk A. Maintenance and salvage of arteriovenous fistulas. J Vasc Interv Radiol. 2006;17:807–813. 32. Lee T, Tindni A, Roy-Chaudhury P. Improved cumulative survival in fistulas requiring surgical interventions to promote fistula maturation compared with endovascular interventions. Semin Dial. 2013;26:85–89. 33. Harms J, Rangarajan S, Young C, et al. Outcomes of arteriovenous fistulas and grafts with or without intervention before successful use. J Vasc Surg. 2016;64:155–162. 34. Brescia MJ, Cimino JE, Appel K, et al. Chronic hemodialysis using venipuncture and a surgically created arteriovenous fistula. N Engl J Med. 1966;275:1089–1092. 35. Mendelssohn DC, Ethier J, Elder SJ, et al. Haemodialysis vascular access problems in Canada: results from the Dialysis Outcomes and Practice Patterns Study (DOPPS II). Nephrol Dial Transplant. 2006;21:721–728. 36. Woods JD, Turenne MN, Strawderman RL, et al. Vascular access survival among incident hemodialysis patients in the United States. Am J Kidney Dis. 1997;30:50–57. 37. Chan MR, Young HN, Becker YT, et al. Obesity as a predictor of vascular access outcomes: analysis of the USRDS DMMS Wave II study. Semi Dial. 2008;21:274–279. 38. Chemla ES, Morsy MA. Is basilic vein transposition a real alternative to an arteriovenous bypass graft? A prospective study. Semi Dial. 2008;21:352–356. 39. Maya ID, O’Neal JC, Young CJ, et al. Outcomes of brachiocephalic fistulas, transposed brachiobasilic fistulas, and upper arm grafts. Clin J Am Soc Nephrol. 2009;4:86–92. 40. Moossavi S, Tuttle AB, Vachharajani TJ, et al. Long-term outcomes of transposed basilic vein arteriovenous fistulae. Hemodial Int. 2008;12:80–84.
41. Hakaim AG, Nalbandian M, Scott T. Superior maturation and patency of primary brachiocephalic and transposed basilic vein arteriovenous fistulae in patients with diabetes. J Vasc Surg. 1998;27:154–157. 42. Moncef G. Surgical revision of failing or thrombosed native arteriovenous fistulas: a single center experience. Saudi J Kidney Dis Transpl. 2010;21:258–261. 43. Nassar GM, Nguyen B, Rhee E, et al. Endovascular treatment of the “failing to mature” arteriovenous fistula. Clin J Am Soc Nephrol. 2006;1:275–280. 44. Duijm LE, Liem YS, van der Rijt RH, et al. Inflow stenoses in dysfunctional hemodialysis access fistulae and grafts. Am J Kidney Dis. 2006;48:98–105. 45. Badero OJ, Salifu MO, Wasse H, et al. Frequency of swing-segment stenosis in referred dialysis patients with angiographically documented lesions. Am J Kidney Dis. 2008;51:93–98. 46. Turmel-Rodrigues L, Mouton A, Birmele B, et al. Salvage of immature forearm fistulas for haemodialysis by interventional radiology. Nephrol Dial Transplant. 2001;16:2365–2371. 47. Clark TW, Cohen RA, Kwak A, et al. Salvage of nonmaturing native fistulas by using angioplasty. Radiology. 2007;242:286–292. 48. Manninen HI, Kaukanen E, Makinen K, et al. Endovascular salvage of nonmaturing autogenous hemodialysis fistulas: comparison with endovascular therapy of failing mature fistulas. J Vasc Interv Radiol. 2008;19:870–876. 49. Shin SW, Do YS, Choo SW, et al. Salvage of immature arteriovenous fistulas with percutaneous transluminal angioplasty. Cardiovasc Intervent Radiol. 2005;28:434–438. 50. Faiyaz R, Abreo K, Zaman F, et al. Salvage of poorly developed arteriovenous fistulae with percutaneous ligation of accessory veins. Am J Kidney Dis. 2002;39:824–827. 51. Planken RN, Duijm LE, Kessels AG, et al. Accessory veins and radial-cephalic arteriovenous fistula non-maturation: a prospective analysis using contrast-enhanced magnetic resonance angiography. J Vasc Access. 2007;8:281–286. 52. Beathard GA, Settle SM, Shields MW. Salvage of the nonfunctioning arteriovenous fistula. Am J Kidney Dis. 1999;33:910– 916. 53. Romero A, Polo JR, Garcia Morato E, et al. Salvage of angioaccess after late thrombosis of radiocephalic fistulas for hemodialysis. Int Surg. 1986;71:122–124. 54. Asif A, Gadalean FN, Merrill D, et al. Inflow stenosis in arteriovenous fistulas and grafts: a multicenter, prospective study. Kidney Int. 2005;67:1986–1992. 55. Bakran A, Mickley V, Passlick-Deetjen J. Management of the Renal Patient: Clinical Algorithms On Vascular Access For Hemodialysis. Lengerich, Berlin, Bremen, Miami, Riga, Viernheim, Vienna, Zagreb: Pabst Science Publishers. 2003. 56. Schwarz C, Mitterbauer C, Boczula M, et al. Flow monitoring: performance characteristics of ultrasound dilution versus color Doppler ultrasound compared with fistulography. Am J Kidney Dis. 2003;42:539–545. 57. Falk A, Teodorescu V, Lou WY, et al. Treatment of “swing point stenoses” in hemodialysis arteriovenous fistulae. Clin Nephrol. 2003;60:35–41. 58. Beathard G. Complications of vascular access. In: Lameire N, Mehta R, eds. Complications of Dialysis – Recognition and Management. New York: Marcel Dekker, Inc.; 2000:1–27. 59. U.S. Renal Data System, USRDS. Annual Data Report, National Institutes of Health. Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases. 2016.
60. Basile C, Lomonte C, Vernaglione L, et al. The relationship between the flow of arteriovenous fistula and cardiac output in haemodialysis patients. Nephrol Dial Transplant. 2008;23:282–287. 61. Amerling R, Ronco C, Kuhlman M, et al. Arteriovenous fistula toxicity. Blood Purif. 2011;31:113–120. 62. Wasse H, Singapuri MS. High-output heart failure: how to define it, when to treat it, and how to treat it. Semi Nephrol. 2012;32:551–557. 63. Beathard GA, Spergel LM. Hand ischemia associated with dialysis vascular access: an individualized access flow-based approach to therapy. Semi Dial. 2013;26:287–314. 64. Raju S. PTFE grafts for hemodialysis access. Techniques for insertion and management of complications. Ann Surg. 1987;206:666–673. 65. Zibari GB, Rohr MS, Landreneau MD, et al. Complications from permanent hemodialysis vascular access. Surgery. 1988;104:681–686. 66. Odland MD, Kelly PH, Ney AL, et al. Management of dialysis-associated steal syndrome complicating upper extremity arteriovenous fistulas: use of intraoperative digital photoplethysmography. Surgery. 1991;110:664–669; discussion 669–670. 67. West JC, Evans RD, Kelley SE, et al. Arterial insufficiency in hemodialysis access procedures: reconstruction by an interposition polytetrafluoroethylene graft conduit. Am J Surg. 1987;153:300–301. 68. Davidson D, Louridas G, Guzman R, et al. Steal syndrome complicating upper extremity hemoaccess procedures: incidence and risk factors. Can J Surg. 2003;46:408–412. 69. Tordoir JH, Dammers R, van der Sande FM. Upper extremity ischemia and hemodialysis vascular access. Eur J Vasc Endovasc Surg. 2004;27:1–5. 70. Goff CD, Sato DT, Bloch PH, et al. Steal syndrome complicating hemodialysis access procedures: can it be predicted? Ann Vasc Surg. 2000;14:138–144. 71. Spergel LM, Ravani P, Roy-Chaudhury P, et al. Surgical salvage of the autogenous arteriovenous fistula (AVF). J Nephrol. 2007;20:388–398. 72. Wixon CL, Hughes JD, Mills JL. Understanding strategies for the treatment of ischemic steal syndrome after hemodialysis access. J Am Coll Surg. 2000;191:301–310. 73. Scheltinga MR, van Hoek F, Bruijninckx CM. Time of onset in haemodialysis access-induced distal ischaemia (HAIDI) is related to the access type. Nephrol Dial Transplant. 2009;24:3198–3204. 74. Lazarides MK, Staramos DN, Kopadis G, et al. Onset of arterial ‘steal’ following proximal angioaccess: immediate and delayed types. Nephrol Dial Transplant. 2003;18:2387–2390. 75. Wilbourn AJ, Furlan AJ, Hulley W, et al. Ischemic monomelic neuropathy. Neurology. 1983;33:447–451. 76. Miles AM. Vascular steal syndrome and ischaemic monomelic neuropathy: two variants of upper limb ischaemia after haemodialysis vascular access surgery. Nephrol Dial Transplant. 1999;14:297–300. 77. Rogers NM, Lawton PD. Ischaemic monomelic neuropathy in a non-diabetic patient following creation of an upper limb arteriovenous fistula. Nephrol Dial Transplant. 2007;22:933–935. 78. Riggs JE, Moss AH, Labosky DA, et al. Upper extremity ischemic monomelic neuropathy: a complication of vascular access procedures in uremic diabetic patients. Neurology. 1989;39:997–998.
REFERENCES 79. Rivers SP, Scher LA, Veith FJ. Correction of steal syndrome secondary to hemodialysis access fistulas: a simplified quantitative technique. Surgery. 1992;112:593–597. 80. Pasklinsky G, Meisner RJ, Labropoulos N, et al. Management of true aneurysms of hemodialysis access fistulas. J Vasc Surg. 2011;53:1291–1297. 81. Salahi H, Fazelzadeh A, Mehdizadeh A, et al. Complications of arteriovenous fistula in dialysis patients. Transplant Proc. 2006;38:1261–1264. 82. Balaz P, Bjorck M. True aneurysm in autologous hemodialysis fistulae: definitions, classification and indications for treatment. J Vasc Access. 2015;16:446–453. 83. Rajput A, Rajan DK, Simons ME, et al. Venous aneurysms in autogenous hemodialysis fistulas: is there an association with venous outflow stenosis. J Vasc Access. 2013;14:126–130. 84. Taylor B, Sigley RD, May KJ. Fate of infected and eroded hemodialysis grafts and autogenous fistulas. Am J Surg. 1993;165:632–636. 85. Fong IW, Capellan JM, Simbul M, et al. Infection of arterio-venous fistulas created for chronic haemodialysis. Scand J Infect Dis. 1993;25:215–220. 86. Churchill DN, Taylor DW, Cook RJ, et al. Canadian hemodialysis morbidity study. Am J Kidney Dis. 1992;19:214–234. 87. Muir CA, Kotwal SS, Hawley CM, et al. Buttonhole cannulation and clinical outcomes in a home hemodialysis cohort and systematic review. Clin J Am Soc Nephrol. 2014;9:110–119. 88. Beathard GA. Strategy for maximizing the use of arteriovenous fistulae. Semi Dial. 2000;13:291–296. 89. Beathard GA. Interventionalist’s role in identifying candidates for secondary fistulas. Semi Dial. 2004;17:233–236. 90. Nguyen VD, Treat L, Griffith C, et al. Creation of secondary AV fistulas from failed hemodialysis grafts: the role of routine vein mapping. J Vasc Access. 2007;8:91–96. 91. Work J. How can the use of arteriovenous fistulas be increased? Semi Dial. 2003;16:220–221. 92. Asif A, Unger SW, Briones P, et al. Creation of secondary arteriovenous fistulas: maximizing fistulas in prevalent hemodialysis patients. Semi Dial. 2005;18:420–424. 93. Jennings WC. Creating arteriovenous fistulas in 132 consecutive patients: exploiting the proximal radial artery arteriovenous fistula: reliable, safe, and simple forearm and upper arm hemodialysis access. Arch Surg. 2006;141:27–32; discussion 32. 94. Donlan RM. Biofilm formation: a clinically relevant microbiological process. Clin Infect Dis. 2001;33:1387–1392. 95. Slayden GC, Spergel L, Jennings WC. Secondary arteriovenous fistulas: converting prosthetic AV grafts to autogenous dialysis access. Semi Dial. 2008;21:474–482. 96. Salman L, Alex M, Unger SW, et al. Secondary autogenous arteriovenous fistulas in the “fistula first” era: results of a longterm prospective study. J Am Coll Surg. 2009;209:100–105. 97. Flores Izquierdo G, Ronces Vivero R, Exaire E, et al. [Venous autologous graft for hemodialysis (original technic). Preliminary report]. Arch Inst Cardiol Mex. 1969;39:259–266. 98. May J, Tiller D, Johnson J, et al. Saphenous-vein arteriovenous fistula in regular dialysis treatment. N Engl J Med. 1969;280:770. 99. Rosenberg N, Henderson J, Lord GH, et al. An arterial prosthesis of heterologous vascular origin. JAMA. 1964;187:741–743. 100. Dunn I, Frumkin E, Forte R, et al. Dacron velour vascular prosthesis for hemodialysis. Proc Clin Dial Transplant Forum. 1972;2:85.
101. Baker Jr LD, Johnson JM, Goldfarb D. Expanded polytetrafluoroethylene (PTFE) subcutaneous arteriovenous conduit: an improved vascular access for chronic hemodialysis. Trans Am Soc Artif Intern Organs. 1976;22:382–387. 102. NKF-DOQI clinical practice guidelines for vascular access. National Kidney Foundation-Dialysis Outcomes Quality Initiative. Am J Kidney Dis. 1997;30:S150–S191. 103. Tal MG. Comparison of recirculation percentage of the palindrome catheter and standard hemodialysis catheters in a swine model. J Vasc Interv Radiol. 2005;16:1237–1240. 104. Carson RC, Kiaii M, MacRae JM. Urea clearance in dysfunctional catheters is improved by reversing the line position despite increased access recirculation. Am J Kidney Dis. 2005;45:883–890. 105. Kurella M, Covinsky KE, Collins AJ, et al. Octogenarians and nonagenarians starting dialysis in the United States. Ann Intern Med. 2007;146:177–183. 106. DeSilva R, Patibandla B, Vin Y, et al. Fistula first is not always the best strategy for the elderly. J Am Soc Nephrol. 2013:24. 107. Schild AF. Maintaining vascular access: the management of hemodialysis arteriovenous grafts. J Vasc Access. 2010;11: 92–99. 108. Akoh JA. Prosthetic arteriovenous grafts for hemodialysis. J Vasc Access. 2009;10:137–147. 109. 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;19:2334–2340. 110. Glickman MH, Burgess J, Cull D, et al. Prospective multicenter study with a 1-year analysis of a new vascular graft used for early cannulation in patients undergoing hemodialysis. J Vasc Surg. 2015;62:434–441. 111. Beathard G. Complications of Vascular Access. New York: Marcel Dekker, Inc.; 2000. 112. Roy-Chaudhury P, Arend L, Zhang J, et al. Neointimal hyperplasia in early arteriovenous fistula failure. Am J Kidney Dis. 2007;50:782–790. 113. Beathard GA. Angioplasty for arteriovenous grafts and fistulae. Semi Nephrol. 2002;22:202–210. 114. Beathard GA, Litchfield T. Physician operators forum of rms lifeline I. effectiveness and safety of dialysis vascular access procedures performed by interventional nephrologists. Kidney Int. 2004;66:1622–1632. 115. Rajan DK, Bunston S, Misra S, et al. Dysfunctional autogenous hemodialysis fistulas: outcomes after angioplasty—are there clinical predictors of patency? Radiology. 2004;232:508–515. 116. Maeda K, Furukawa A, Yamasaki M, et al. Percutaneous transluminal angioplasty for Brescia-Cimino hemodialysis fistula dysfunction: technical success rate, patency rate and factors that influence the results. Eur J Radiol. 2005;54:426– 430. 117. Yang TY, Cheng HW, Weng HH, et al. Percutaneous transluminal angioplasty for radial-cephalic fistulae with stenosis at the arteriovenous junction. Am J Med Sci. 2012;343:435–439. 118. Huber TS, Carter JW, Carter RL, et al. Patency of autogenous and polytetrafluoroethylene upper extremity arteriovenous hemodialysis accesses: a systematic review. J Vasc Surg. 2003;38:1005–1011. 119. Beathard G. Complications of Vascular Access. New York: Marcel Dekker, Inc.; 2000.
120. Cull JD, Cull DL, Taylor SM, et al. Prosthetic thigh arteriovenous access: outcome with SVS/AAVS reporting standards. J Vasc Surg. 2004;39:381–386. 121. Schutte WP, Helmer SD, Salazar L, et al. Surgical treatment of infected prosthetic dialysis arteriovenous grafts: total versus partial graft excision. Am J Surg. 2007;193:385–388; discussion 388. 122. Sarnak MJ, Jaber BL. Mortality caused by sepsis in patients with end-stage renal disease compared with the general population. Kidney Int. 2000;58:1758–1764. 123. Lafrance JP, Rahme E, Lelorier J, et al. Vascular access-related infections: definitions, incidence rates, and risk factors. Am J Kidney Dis. 2008;52:982–993. 124. Kaplowitz LG, Comstock JA, Landwehr DM, et al. A prospective study of infections in hemodialysis patients: patient hygiene and other risk factors for infection. Infect Control Hosp Epidemiol. 1988;9:534–541. 125. Taylor G, Gravel D, Johnston L, et al. Prospective surveillance for primary bloodstream infections occurring in Canadian hemodialysis units. Infect Control Hosp Epidemiol. 2002;23:716–720. 126. Foley RN, Guo H, Snyder JJ, et al. Septicemia in the United States dialysis population, 1991 to 1999. J Am Soc Nephrol. 2004;15:1038–1045. 127. Akoh JA, Patel N. Infection of hemodialysis arteriovenous grafts. J Vasc Access. 2010;11:155–158. 128. Kaplowitz LG, Comstock JA, Landwehr DM, et al. Prospective study of microbial colonization of the nose and skin and infection of the vascular access site in hemodialysis patients. J Clin Microbiol. 1988;26:1257–1262. 129. Fan PY, Schwab SJ. Vascular access: concepts for the 1990s. J Am Soc Nephrol. 1992;3:1–11. 130. Kessler M, Hoen B, Mayeux D, et al. Bacteremia in patients on chronic hemodialysis. A multicenter prospective survey. Nephron. 1993;64:95–100. 131. Geenen IL, Nyilas L, Stephen MS, et al. Prosthetic lower extremity hemodialysis access grafts have satisfactory patency despite a high incidence of infection. J Vasc Surg. 2010;52:1546–1550. 132. Minga TE, Flanagan KH, Allon M. Clinical consequences of infected arteriovenous grafts in hemodialysis patients. Am J Kidney Dis. 2001;38:975–978. 133. Allon M, Depner TA, Radeva M, et al. Impact of dialysis dose and membrane on infection-related hospitalization and death: results of the HEMO Study. J Am Soc Nephrol. 2003;14:1863– 1870. 134. Ryan SV, Calligaro KD, Scharff J, et al. Management of infected prosthetic dialysis arteriovenous grafts. J Vasc Surg. 2004;39:73–78. 135. Lentino JR, Baddour LM, Wray M, et al. Staphylococcus aureus and other bacteremias in hemodialysis patients: antibiotic therapy and surgical removal of access site. Infection. 2000;28:355–360. 136. Delorme JM, Guidoin R, Canizales S, et al. Vascular access for hemodialysis: pathologic features of surgically excised ePTFE grafts. Ann Vasc Surg. 1992;6:517–524. 137. Charara JGR, Gill F, Guzman R. Morphologic assessment of ePTFE graft wall damage following hemodialysis needle punctures. J Appl Biomater. 1990;1:279–287. 138. Schwab SJ, Beathard G. The hemodialysis catheter conundrum: hate living with them, but can’t live without them. Kidney Int. 1999;56:1–17.
139. Excerpts from the USRDS 1997 Annual Report. IV. The USRDS dialysis morbidity and mortality study: Wave 2. Am J Kidney Dis. 1997;30(suppl 1):S67–S85. 140. U.S. Renal Data System, USRDS. Annual Data Report, National Institutes of Health. Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases; 2016. 141. Depner TA. Catheter performance. Semi Dial. 2001;14:425– 431. 142. Ash SR. Advances in tunneled central venous catheters for dialysis: design and performance. Semi Dial. 2008;21:504–515. 143. Besarab A, Pandey R. Catheter management in hemodialysis patients: delivering adequate flow. Clin J Am Soc Nephrol. 2011;6:227–234. 144. Twardowski Z. Blood flow, negative pressure and hemolysis during hemodialysis. Home Hemodial Int. 1999;3:45–50. 145. Mankus RA, Ash SR, Sutton JM. Comparison of blood flow rates and hydraulic resistance between the mahurkar catheter, the tesio twin catheter, and the ash split cath. ASAIO J. 1998;44:M532–M534. 146. Schmidt DF, Schniepp BJ, Kurtz SB, et al. Inaccurate blood flow rate during rapid hemodialysis. Am J Kidney Dis. 1991;17:34–37. 147. Depner TA, Rizwan S, Cheer AY, et al. High venous urea concentrations in the opposite arm. A consequence of hemodialysis-induced compartment disequilibrium. ASAIO Trans. 1991;37:M141–M143. 148. Vesely TM, Ravenscroft A. Hemodialysis catheter tip design: observations on fluid flow and recirculation. J Vasc Access. 2016;17:29–39. 149. Forauer AR, Theoharis C. Histologic changes in the human vein wall adjacent to indwelling central venous catheters. J Vasc Interven Radiol. 2003;14:1163–1168. 150. Lin BS, Kong CW, Tarng DC, et al. Anatomical variation of the internal jugular vein and its impact on temporary haemodialysis vascular access: an ultrasonographic survey in uraemic patients. Nephrol Dial Transplant. 1998;13:134–138. 151. Wivell W, Bettmann MA, Baxter B, et al. Outcomes and performance of the tesio twin catheter system placed for hemodialysis access. Radiology. 2001;221:697–703. 152. Salgado OJ, Urdaneta B, Colmenares B, et al. Right versus left internal jugular vein catheterization for hemodialysis: complications and impact on ipsilateral access creation. Artif Organs. 2004;28:728–733. 153. Schillinger F, Schillinger D, Montagnac R, et al. Post catheterisation vein stenosis in haemodialysis: comparative angiographic study of 50 subclavian and 50 internal jugular accesses. Nephrol Dial Transplant. 1991;6:722–724. 154. Cimochowski GE, Worley E, Rutherford WE, et al. Superiority of the internal jugular over the subclavian access for temporary dialysis. Nephron. 1990;54:154–161. 155. Hernandez D, Diaz F, Rufino M, et al. Subclavian vascular access stenosis in dialysis patients: natural history and risk factors. J Am Soc Nephrol. 1998;9:1507–1510. 156. Zaleski GX, Funaki B, Lorenz JM, et al. Experience with tunneled femoral hemodialysis catheters. AJR Am J Roentgenol. 1999;172:493–496. 157. Forauer AR, Brenner B, Haddad LF, et al. Placement of hemodialysis catheters through dilated external jugular and collateral veins in patients with internal jugular vein occlusions. AJR Am J Roentgenol. 2000;174:361–362.
REFERENCES 158. Pittiruti M, Malerba M, Carriero C, et al. Which is the easiest and safest technique for central venous access? A retrospective survey of more than 5,400 cases. J Vasc Access. 2000;1:100–107. 159. Skandalos IK, Amvrosiadis DM, Christodoulou A, et al. Catheterization of the external jugular vein for hemodialysis. Khirurgiia (Mosk). 2005:47–50. 160. Yevzlin AS, Chan MR, Wolff MR. Percutaneous, non-surgical placement of tunneled, cuffed, external jugular hemodialysis catheters: a case report. J Vasc Access. 2007;8:126–128. 161. Page B, Legendre C, Souissi M, et al. [Tunneled double femoral catheters: emergency vascular access for hemodialysis]. Nephrologie. 1994;15:83–85. 162. Little MA, O’Riordan A, Lucey B, et al. A prospective study of complications associated with cuffed, tunnelled haemodialysis catheters. Nephrol Dial Transplant. 2001;16:2194–2200. 163. NKF-K/DOQI Clinical practice guidelines for hemodialysis adequacy, update 2006. Am J Kidney Dis. 2006;48(suppl 1):S2–S90. 164. Beathard GA. Catheter thrombosis. Semi Dial. 2001;14: 441–445. 165. Alomari AI, Falk A. The natural history of tunneled hemodialysis catheters removed or exchanged: a single-institution experience. J Vasc Interven Radiol. 2007;18:227–235. 166. Oguzkurt L, Tercan F, Torun D, et al. Impact of short-term hemodialysis catheters on the central veins: a catheter venographic study. Eur J Radiol. 2004;52:293–299. 167. Gray RJ, Levitin A, Buck D, et al. Percutaneous fibrin sheath stripping versus transcatheter urokinase infusion for malfunctioning well-positioned tunneled central venous dialysis catheters: a prospective, randomized trial. J Vasc Interv Radiol. 2000;11:1121–1129. 168. Hoshal Jr VL, Ause RG, Hoskins PA. Fibrin sleeve formation on indwelling subclavian central venous catheters. Arch Surg. 1971;102:353–358. 169. Xiang DZ, Verbeken EK, Van Lommel AT, et al. Composition and formation of the sleeve enveloping a central venous catheter. J Vasc Surg. 1998;28:260–271. 170. O’Farrell L, Griffith JW, Lang CM. Histologic development of the sheath that forms around long-term implanted central venous catheters. JPEN J Parenter Enteral Nutr. 1996;20:156–158. 171. Suhocki PV, Conlon Jr PJ, Knelson MH, et al. Silastic cuffed catheters for hemodialysis vascular access: thrombolytic and mechanical correction of malfunction. Am J Kidney Dis. 1996;28:379–386. 172. Raad II , Luna M, Khalil SA, et al. The relationship between the thrombotic and infectious complications of central venous catheters. JAMA. 1994;271:1014–1016. 173. Timsit JF, Farkas JC, Boyer JM, et al. Central vein catheter-related thrombosis in intensive care patients: incidence, risks factors, and relationship with catheter-related sepsis. Chest. 1998;114:207–213. 174. Schwab SJ, Beathard G. The hemodialysis catheter conundrum: hate living with them, but can’t live without them. Kidney Int. 1999;56:1–17. 175. Kessler M, Hoen B, Mayeux D, et al. Bacteremia in patients on chronic hemodialysis. Nephron. 1993;64:95. 176. Kovalik EC, Raymond JR, Albers FJ, et al. A clustering of epidural abscesses in chronic hemodialysis patients: risks of salvaging access catheters in cases of infection. J Am Soc Nephrol. 1996;7:2264–2267. 177. Marr KA, Sexton DJ, Conlon PJ, et al. Catheter-related bacteremia and outcome of attempted catheter salvage in patients undergoing hemodialysis. Ann Intern Med. 1997;127:275–280.
178. Beathard GA. Management of bacteremia associated with tunneled-cuffed hemodialysis catheters. J Am Soc Nephrol. 1999;10:1045. 179. Sadd TF. Central venous dialysis catheters: catheter associated infection. Semi Dial. 2001;14:446–451. 180. Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: a common cause of persistent infections. Science. 1999;284:1318–1322. 181. Murga R, Miller JM, Donlan RM. Biofilm formation by gram-negative bacteria on central venous catheter connectors: effect of conditioning films in a laboratory model. J Clin Microbiol. 2001;39:2294–2297. 182. Weijmer MC, Vervloet MG, ter Wee PM. Compared to tunnelled cuffed haemodialysis catheters, temporary untunnelled catheters are associated with more complications already within 2 weeks of use. Nephrol Dial Transplant. 2004;19:670–677. 183. Oliver MJ. Acute dialysis catheters. Semi Dial. 2001;14:432– 435. 184. Kelber J, Delmez JA, Windus DW. Factors affecting delivery of high-efficiency dialysis using temporary vascular access. Am J Kidney Dis. 1993;22:24–29. 185. Oliver MJ, Mendelssohn DC, Quinn RR, et al. Catheter patency and function after catheter sheath disruption: a pilot study. Clin J Am Soc Nephrol. 2007;2:1201–1206. 186. Oliver MJ, Callery SM, Thorpe KE, et al. Risk of bacteremia from temporary hemodialysis catheters by site of insertion and duration of use: a prospective study. Kidney Int. 2000;58:2543–2545. 187. Vanherweghem JL, Yassine T, Goldman M, et al. Subclavian vein thrombosis: a frequent complication of subclavian vein cannulation for hemodialysis. Clin Nephrol. 1986;26:235–238. 188. Schwab SJ, Quarles LD, Middleton JP, et al. Hemodialysisassociated subclavian vein stenosis. Kidney Int. 1988;33: 1156–1159. 189. Clark DD, Albina JE, Chazan JA. Subclavian vein stenosis and thrombosis: a potential serious complication in chronic hemodialysis patients. Am J Kidney Dis. 1990;15:265–268. 190. Barrett N, Spencer S, McIvor J, et al. Subclavian stenosis: a major complication of subclavian dialysis catheters. Nephrol Dial Transplant. 1988;3:423–425. 191. Fan PY. Acute vascular access: new advances. Adv Ren Replace Ther. 1994;1:90–98. 192. Oliver MJ, Mendelssohn DC, Quinn RR, et al. Catheter patency and function after catheter sheath disruption: a pilot study. Clin J Am Soc Nephrol. 2007;2:1201. 193. Oliver MJ, Callery SM, Thorpe KE, et al. Risk of bacteremia from temporary hemodialysis catheters by site of insertion and duration of use: a prospective study. Kidney Int. 2000;58:2543. 194. Vanherweghem JL, Yassine T, Goldman M, et al. Subclavian vein thrombosis: a frequent complication of subclavian vein cannulation for hemodialysis. Clin Nephrol. 1986;26:235. 195. Schwab SJ, Quarles LD, Middleton JP, et al. Hemodialysisassociated subclavian vein stenosis. Kidney Int. 1988;33:1156. 196. Clark DD, Albina JE, Chazan JA. Subclavian vein stenosis and thrombosis: a potential serious complication in chronic hemodialysis patients. Am J Kidney Dis. 1990;15:265. 197. Barrett N, Spencer S, McIvor J, Brown EA. Subclavian stenosis: a major complication of subclavian dialysis catheters. Nephrol Dial Transplant. 1988;3:423. 198. Fan PY. Acute vascular access: new advances. Adv Ren Replace Ther. 1994;1:90.