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| Journal of Vascular Access 2005; 6: 64 - 71 |
| Hemodialysis arteriovenous fistulas: A nineteenth century view of a twenty first century problem |
J.L. Ross1
1Department of Nephrology, Ochsner Clinic Foundation, New Orleans, Louisiana - USA
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ABSTRACT
This is a literature review which approaches the problem of successful use of arteriovenous fistulas for dialysis within the construct of Virchow’s triad. By organizing the literature with regard to Virchow’s concepts of blood flow, vascular injury, and thrombophilia an improved understanding arteriovenous fistula
placement, maintenance and repair can be obtained. This process is designed to increase understanding and options for treatment by looking at this problem and using scientific knowledge gained in cardiology, oncology and vascular surgery medicine. Future approaches to fistulas will hopefully be a multifaceted and based in
cellular pathophysiology as well as surgical and radiologic interventions and repairs.
Key Words. Arteriovenous fistulas, Hemodialysis, Stenosis, Thrombosis
INTRODUCTION
Hemodialysis is the most widely used mode of treatment of renal failure in the United States and Europe. Vascular access for hemodialysis is one of the most influential components determining the success or failure of dialytic therapy. Intra-dialytic blood flow is a major determinant of effective clearance and thereby effective treatment. A vascular access that can deliver a high blood flow reliably, causes few complications, and needs little maintenance would be the ideal in every patient. The closest choice available which meets those criteria is the arteriovenous fistula (AVF) (1, 2). While we, as Nephrologists, intend to create fistulas in all our patients, in many we have problems in either the creation, use and/or maintenance of AVFs as a chronic dialysis access. In the United States, we have lagged behind many other industrialized nations in our use of AVFs for hemodialysis. In 1997 the Kidney/Dialysis Outcomes Quality Initiative (K/DOQI) was formed in an effort to improve renal care and develop a unified consensus and method to do so. The recommendation that came from the vascular access section of the second meeting of K/DOQI in 2000 was that 50% of the incident patients and 40% of the prevalent patients should be receiving hemodialysis via an arteriovenous fistula. This statement is based on overwhelming evidence that the AVF had a longer life expectancy and required less intervention to deliver an adequate dose of hemodialysis (1-3). There are approximately 300,000 adult dialysis patients in the United States. In-center hemodialysis is the method of care for 89% of that patient population (1). The cost of administering such a program is about 15 billion dollars. At least 10% of the costs are directly related to vascular access care (3). This number alone made the Center for Medicare and Medicaid Services (CMS) consider the “Fistula First” Continuing Quality improvement project of vital importance. The purpose of this national project is to achieve and even exceed the K/DOQI recommendations (4). The thinking is that the dialysis population will benefit from increased use of AVFs by improved delivery of dialytic treatment via a superior vascular access. In addition, CMS savings will be significant based on the need for less intervention. The AVF is the hemodialysis access of the present and future. The pressure to increase the use of the AVF as the primary method of delivery of hemodialysis has been building since the first K/DOQI recommendations in 1997. Much of the developed world has better fistula rates than the United States (5) (Fig. 1).
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FIG. 1
Percent of incident patients starting hemodialysis with
ateriovenous fistulas.Data from article references 1,5,and 6. |
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While the desire to increase the rate of fistula placement as described in the 2003 annual report of the ESRD Clinical Performance Measures project is clearly evident, we have been very slow to change and have even fallen short of our own expectations (1, 6). The delay in transitioning to the AVF can be attributed to multiple problems in the planning, placement, positioning and use of this type of access. This article will look at the problems in successful arteriovenous fistula placement and use through the construct developed by Rudolph Virchow in 1856 (7). In the Nineteenth century, this German physician developed the theory which states that vascular clotting occurs because of one or all of three factors. These are blood flow, vascular injury and prothrombotic tendencies. The process of narrowing or stenosis in the hemodialysis access leading to thrombosis and clot becomes clearer when looked at through the eyes of Virchow. If we apply this nineteenth century view to our AVF problems in the twenty first century, we can gain some new insight which will lead to better approaches to patient care in this area.
BLOOD FLOW
The major components of blood flow through the potential fistula are: cardiac output, mean arterial blood pressure, functional diameter of the feeding artery and the venous pressure of the draining vein. There is evidence that the minimum blood flow in a fistula must be at least 300 cc/min at the time of surgery to become functional (8). However, as the fistula develops it must have 600 to 800 cc/min flow to maintain patency. This figure of 600 cc/min is a common flow in forearm radial artery fistulas while upper arm fistulas usually have a flow of over 1200 to 1400 cc/min (8). The usual increase in cardiac output to accommodate the additional flow through a fistula may be from 8 to 13% and may even increase over time (9, 10). The initial response to creation of a fistula is to increase stroke volume and heart rate. Ultimately, the patient must increase total plasma volume to accommodate the enlarged vascular bed (10, 11). The cardiac output in many dialysis patients may not be normal prior to placing an AVF. Therefore it is common that renal patents not be able to achieve this augmentation in cardiac function and will ultimately decrease their blood pressure in response to fistula placement. The systolic blood pressure needed to maintain fistula function has been found to be 85 mmHg (12). Patients with poor cardiac function may either go into high output cardiac failure or develop hypotension which can ultimately clot the fistula itself (13). The early placement of fistulas has been shown to be a factor in increased probability of successful fistula development (14). This has been attributed to the fact that a patient’s cardiac compliance is better when they are not in a uremic state. The consensus is from K/DOQI that a patient should be referred for fistula placement as soon as possible after the patient has a creatinine clearance of less than 25 cc/min (4, 6). Choosing a site for fistula placement is a key element in success. Ultrasound vascular mapping has become standard to choose both the best vein and artery. The minimum artery diameter by ultrasound is 1.6 to 2 mm and the vein should be at least 3 mm by ultrasound (15). In addition to the external diameter of the artery, it is important to note the internal diameter of the artery and any proximal stenosis and the viability of collateral flow to the limb involved. Evidence of the poor function of fistulas with intimal arterial disease is an example of the need to look at more than external arterial diameter when evaluating arteries for fistula. The fact that this level of arterial disease exists in many of our patients may reveal how much co morbid disease may be influencing fistula development (16). The size of the vessels to start with is important but the ability to enlarge as a response to the shear stress of a fistula is vital to the development of a usable access. Mapping studies which test for augmentation or enlargement of the vessel have excellent predictive value with regard to fistula development (17). The designated vein must be preserved for fistula use early. Peripheral intravenous access, blood draws, blood pressures, central lines and especially peripherally introduced central catheters (PICC) should be avoided if at all possible in the chosen vessel (18). Thus early referral for ultrasound evaluation would be the best way to identify and preserve the needed vessels for vascular access. After selection of the artery and vein for a potential fistula, the decision of the anastomosis must be analyzed by the vascular surgeon placing the access. The choices are an end to side, side to side or end to end anastomosis. Each type has its advantages and disadvantages. When the fistula is made there is an increase in flow and shear forces in the artery immediately. Subsequently flow within the fistula will increase by 50 to 100% from the intra-operative level within the first several weeks (13). For a radial fistula this means going from about 300 cc/min at the time of surgery to over 600 cc/min. When discussing upper arm fistulas, the initial figure is closer to 700 cc/min and increase also by 50 to 100% of initial rate as the vessels dilate (19). As the flow increase from the proximal artery to the draining vein, the flow from to the distal artery is decreased. This is compensated for to some degree by arterial collateral circulation. However under many circumstances the decrease resistance in the distal artery can promote increase flow from collateral circulation into the distal artery and result in retrograde or reversed flow towards the anastomosis
(13)
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FIG. 2
The flow patterns in a longstanding arteriovenous fistula.
Data from reference 13. |
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(Fig. 2). Reversed flow in the distal artery supports the idea of an end to side or end to end artery to vein construction in forearm fistulas and at the same time ligating the distal artery. Since it is not always possible to ligate the distal artery, it is important to optimize flow in the fistula itself and minimize steal from the distal limb. The length of a side to side anastomosis has been shown to be optimal at just slightly less than 75% of the diameter of the artery. Any increase of the anastomosis over 75% of the diameter of the artery does not significantly enhance the flow through the fistula. By keeping the anastomotic length at this level there is preservation of flow within the distal artery to enough of a degree to prevent significant steal or reversed flow from the distal limb (20) (Fig. 3).
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FIG. 3
Relationship between arterial flow and anastomotic
length as a percent of the diameter of the artery.Data from refer-
ence 13. |
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The venous limb can seriously effect the development of an arteriovenous fistula. If the valves of a distal vein in a side to side anastomosis become incompetent then flow can proceed down the distal vein away from the AVF. This may limit flow towards the heart via the proximal or draining vein (13). If multiple collateral or feeder veins develop along with the primary vein, the fistula itself does not develop with a single enlarged useable vein. The treatment for this has been to ligate the veins that are considered feeder or collateral veins. Evidence has shown that there is an excellent salvage rate of poorly developing fistulas using this method (21).
VASCULAR INJURY
It is important to realize that the arteries and veins of uremic patients are not normal, when evaluating the patient’s potential for fistula placement. The uremic state is clearly associated with increased risk of atherosclerotic disease. In addition, there is decreased wall distensibility of large arteries. This results in less compliance of the vessels (22). There is some interest in looking at intima media thickness as a numerical gauge of arterial disease. There is no clear cut recommendation at this time with regard to the use of this measure in assessing the degree of arterial disease in renal failure (22, 23). However, when examining the arteries used in creating radiocephalic fistulas, the degree of pre-exist-ing arterial intimal hyperplasia was associated directly with early failure of the access (24). Veins of renal failure patients are not normal either. In addition to localized trauma of intravenous access associated with renal failure and its co-mor-bidities, there is evidence that the histology of the veins in these patients is not normal. When compared with normal controls, it was noted that selected cephalic veins had abnormal fibrous infiltration of the intima and media as well as variable degrees of smooth muscle degenerative changes. The smooth muscle cells themselves did not have the normal fusiform shape and there were increased extracellular collagen fibers separating the muscles cells themselves (25). This suggests that the compliance of both arteries and veins is poor in renal failure. It also may support the early creation of fistulas recommended by K/DOQI before the deleterious of uremia become more pronounced (18). Once the artery and vein are selected and the fistula is formed, the local environment of these vessels is changed drastically. The increased flow and shear stress have been shown to change both the artery and the vein. The increased arterial wall trauma due to shear stress acts on the endothelium and alters cell function (26). Animal evidence suggests increased venous proinflammatory gene expression and intimal hyperplasia (27). As the fistula develops, the diameter of the vein is increased due to the increase in flow. The increased diameter of the draining vein decreases the venous pressure returning it towards normal (28). These changes, however, result in alteration in the cellular composition of the vessel. The inflammatory changes seen in a native arteriovenous fistula should even be more accentuated in an arteriovenous graft which contains exogenous material. The primary rate of patency or the time till first stenosis or thrombosis is about one half to one third the rate in fistulas versus grafts (18, 29). This might be due to the difference in inflammatory qualities of the two different types of vascular access. The location of the lesions was about 80% in the venous anastamosis or venous outlet in grafts and about 44% in the venous outlet in fistulas (29). These lesions are clearly the result of hyperplasia and inflammation at those sites (26, 30). Once the initial stenosis or thrombosis occurs an angiographic intervention is the usual first mode of treatment (18). The secondary patency rate or time until the next intervention is required becomes virtually identical in fistulas and grafts. The primary and secondary stenotic lesions are composed of hyperplastic neointimal tissues (31). The rate of restenosis seemed to be correlated to the degree of inflammatory response as a result of angioplasty (31). Some studies have tried to identify the exact site of “up” regulation of genes associated with this inflammation (32). This type of study has led to exploration of various anti-inflammatory and or immunosuppressive treatments to mitigate the effects of the inflammatory reactions in these vessels. This type of research is still early in its evolution. Brachytherapy, or irradiation, seems to offer some positive animal and mixed human results to date (33, 34). The least investigated and most consistent trauma is the use of metal needles in the vascular access three times a week for hemodialysis. The evidence is very clear that repeated “needling” of the same sites will result in aneurysms (35). Poor cannulation technique can result in hematomas, prolonged external compression and even laceration of the access, all of which will shorten the life of the access. While some alternatives are available which recognize the potential trauma, little research is available in this area. There is much interest in the button hole technique which limits trauma by creating a track into the fistula and uses blunt needles once it is developed (36). The records of the United States patent department in 1978 reveal a type of needle that would leave a compliant flexible material in the vessel instead of metal (37). Such needles are just being trialed in Canada and Japan and have not yet been introduced in the United States.
THROMBOPHILIA OR PROTHROMBOTIC TENDENCIES
There are uremic alterations in platelet adherence and subsequent bleeding that are associated with poor platelet aggregation. This type of adherence problem virtually disappears in the dialyzed renal failure patient. Therefore, the well dialyzed renal failure patient is left vulnerable to clotting. Clotting is a complex interaction between the vascular endothelium, platelets, and a balance of prothrombotic and thrombolytic factors. Evidence clearly shows that abnormal tissue factors due to inflammatory cytokines in patients with either arteriovenous fistulas or grafts create a prothrombotic state. These endothelial factors and platelet activation increase thrombosis in vascular access. Comparing renal failure patients with both grafts and fistulas there are clear differences in platelet activation and prothrombotic tissue factors in those patients who clot their vascular access frequently versus those who do not (38, 39).Taking advantage of this information several studies have been designed to monitor clotting in those patients who have had the inflammatory or tissue reaction blocked or mitigated. In a moderately sized study of grafts only, the use of ACE inhibitors have been associated with prolonged access survival (40). Another much smaller study demonstrated that 4,000 mg of fish oil daily, which inhibits cyclooxygenase and prostaglandin production, prevented graft thrombosis in both fistulas and grafts (41). Anti-platelet agents such as aspirin, dipyridamole, and clopidogrel have been studied and the results these agents to increase risk of bleeding without much benefit in vascular access thrombosis prevention (41, 42). The “foreign” quality of grafts has been demonstrated to promote the development of Anti-cari-olipin and Lupus anti-coagulants in renal failure patients who are not diagnosed with Systemic Lupus Erythematous. Those same patients have an increased risk of vascular access clotting through the interference of those antibodies with the action of Protein C (43). Elevations in homocysteine have been clearly demonstrated in renal failure patients. Homocysteine is known to increase the generation of oxygen radicals and impair endothelial derived nitric oxide and thus increase the inflammatory response of the endothelium. This elevation has been associated with increased risk of cardiovascular events. Some evidence has been shown that treatment of elevated homocysteine levels with high dose folic acid improves the cardiovascular prognosis (44). Studies of the association of elevated homocysteine levels in vascular access thrombosis have not clarified the relationship with clotting. The largest prospective study does suggest an association between elevated homocysteine levels and vascular access clotting. This is true regardless of whether the access was a graft or fistula (45). At this time, no randomized prospective trial of treatment has been done with regard to elevated homocysteine levels and vascular access thrombosis. Few studies exist with regard to changes in the blood prothrombotic and thrombolytic factors in hemodialysis patients. Alterations in Protein C, Protein S, anti-thrombin III, D-dimer, fibrinogen, fibrinopeptide A, and von Willenbrand factor have been demonstrated in renal failure (46). Calciphilaxis has been associated with Protein C deficiency and subsequent thromboembolism (47). Thus previously held concepts that renal failure patients have less than normal risk for thromboembolism are being challenged. Autopsies and case reviews suggest that the risk of venous thromboembolism in hospitalized renal failure patients is closer to the general hospitalized population than previously thought (48). One other intriguing study demonstrates alterations in clotting factors in longtime hemodialysis patients which were corrected in these same patients after transplantation (49) (Fig. 4).
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FIG. 4
Levels of Protein C (PC),Protein S (PS),and Anti-
Thrombin III (ATIII).Pre-and Post-transplant as a percent of
normal.Data from reference 49. |
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Significantly, hypoalbuminemia has been consistently a strong predictor of thromboembolism. Decreased oncotic pressure is thought to result in decreased intravascular volume and subsequent higher concentration of thrombophilic factors (50). All of this information would support both the early placement of hemodialysis access and the initiation of dialysis prior to uremic symptoms developing as recommended by K/DOQI (18).
CONCLUSIONS
It is important in our quest to have the majority of our patients dialyzed via an arteriovenous fistula, that we create long lasting functional accesses for our patients. Some of the surgical literature reviews various surgical techniques favoring lower versus upper arm fistulas (51-53). Other articles purport that certain types surgical techniques including vessel handling, clips, clamps and sutures will improve fistula outcomes (12-14). It has also become evident that, while we can create more fistulas, our rate of maturation and utility has suffered as we attempt to reach the goals set by K/DOQI (54). When the vascular access is allowed to proceed from maximal flow to stenosis or thrombosis our ability to successfully prolong the functionality of the access by either surgical or radiological means is limited (55, 56). There is a consensus that monitoring of the in-tra-dialytic blood flow is useful in predicting stenosis or thrombosis (1, 6, 18, 57). Many different dilutional or ultrasound methods have been used to assess the flow through the access and compare this with the gold standard of angiogram (58-60). However there is a growing awareness that early diagnosis and intervention for stenosis with angioplasty doesn’t alter the life expectancy of the access (61). Thus, more intervention may increase costs but not the useful duration of any given access. It is, therefore, incumbent on our nephrology community to review our methods in evaluation, placement, use and repair and compare them in all aspects to other civilized countries whose fistula success rate is much higher than ours (62). Review of the success or failure of maturation (primary patency rate) and the time of access survival till the first intervention (secondary patency rate) need to be apart of our future evaluations of any access program. It is the only way that the goal of a long lasting functional access can be achieved. The analysis of this problem as one of flow, vascular injury and coagulation is not unique (63). The use of Vir-chow’s triad in guiding research in hemodialysis vascular access would be the most logical and scientific way in which to proceed. The construct of this nineteenth century physician may be the very view that assists us in solving our twenty-first century problem.
Address for correspondence:
Jamie L. Ross, MD
Ochsner Clinic Foundation
1514 Jefferson Highway
New Orleans, LA 70121 - USA
jross@ochsner.org
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