Long-term Hemodialysis Access Salvage: Problems and Challenges for Nephrologists and Interventional Radiologists

Editorial

I Long-termHernodialysis Access Salvage:

problems and Challenges for Ne hrologists and Interventional RadiologistsP Gregg M. Gaylord, M D Tim E. Taber, M D

LONG-TERM HEMODIALYSIS is a life-sustaining procedure for over 120,000 patients with end-stage renal disease in the United States. Since the inception of hemodialysis, however, the development and maintenance of adequate arteriovenous (AV)access has proved to be a clinician's "nightmare" (1).Over 20% of patient admissions and in-hospital patient days are accounted for by access problems in this group of patients. The mean length of stay for these problems has been reported at 5.8 days, thus making the minimum cost of hospitalization greater than $2,000 (2). The cost of additional procedures to correct access problems can easily triple this figure. With prolonged survival of a growing population of long-term hemodialysis patients, lack of availability of suitable transplant organs, and possibly the use of genetically engineered erythropoietin to treat the anemia of renal insufficiency, the number of thrombosed grafts seems certain to increase. The development of the Scribner shunt and the Brescia-Cimino (BC) native fistula offered the first potential for relatively permanent AV conduits (3). As these accesses have not proved optimal, the search has continued for superior accesses. This search has led to development of grafts using human umbilical vein, autogenous saphenous vein, synthetic Dacron, bovine carotid artery, and finally now, polytetrafluoroethylene (PTFE) (4-11).

Index terms: Dialysis, shunts, 91.494 rials

Edito-

JVIR 1993; 4:103-107

I From the Department of Radiology, Methodist Hospital, 1701 N Senate Blvd, Indianapolis, IN 46202. Received July 15, 1992; revision requested August 3; revision received September 16; accepted September 27. Address reprint requests to G.M.G.

' SCVIR, 1993

The vast majority of long-term hemodialysis accesses are currently PTFE grafts placed primarily in one of the patient's upper extremities. There are eight conventional sites for access placement in each patient (right and left distal forearm, proximal forearm, brachium, and thigh). A strategy for access placement has evolved, with most surgeons preferring the BC fistula when possible (10%-25% of cases) or the use of the forearm for initial graft placement, saving the larger veins of the upper arm for future fistula creation or PTFE graft placement. Leg grafts are used as a "last resort" when upper body access is no longer possible. When all access sites are lost, the alternatives are long-term ambulatory peritoneal dialysis or, in the fortunate few, renal transplantation. Thus, the preservation of these accesses has become an increasingly important endeavor. In addition, as hemodialysis technology has evolved, the need for quantitation of the dialysis prescription has become evident. Over the last few years, the technique for quantitating dialysis has become widely available. This ability to measure the adequacy of a hemodialysis prescription has allowed clinicians to more widely use improved dialyzer membranes and machines to perform "high-efficiency" dialysis. In addition to requiring this next generation of hemodialysis hardware, more efficient dialysis has allowed higher dialysis blood flow rates while continuing to control ultrafiltration rate. This dependence on higher blood pump speeds once again focuses attention on the need for an adequate and reliable hemodialysis access (12-15). Finally, hemodialysis has, since its inception, remained the most popular dialytic choice of patients requiring renal replacement therapy. This preference, coupled with the potential for a prolonged life expectancy of those patients undergoing hemodialysis, has pushed the number of patients dependent on hemodialysis upward at a

yearly rate of approximately 10% (16). As a consequence, the need to develop and maintain reliable hemodialysis accesses has grown more imperative. All of the above focuses the attention of the dialysis community on the need to develop and maintain adequate hemodialysis access. Commonly encountered complications, however, threaten the survival of angioaccess in these patients. These complications include thrombosis, infection, pseudoaneurysm formation, and subcutaneous infiltration with resultant hematoma. Clinically, hemodialysis access failure is most commonly (60%-90%) related to thrombosis, with as many of 56% of all thromboses due to recurrent thrombosis of a previously clotted graft (11,1719). Causes of thrombosis include venous stenoses, intra-access stenoses, or arterial insufficiency. Reports in the surgical and radiologic literature differ as to the freauencv ., of venous anastomotic stenosis, with rates varying from 34% to 85%,respectively (1,201. The reason for this discrepancy might be explained, in part, by failure to obtain an angiogram of the fistula at the time of surgical thrombectomy. The remainder of thromboses are largely due to excess puncture site compression after dialysis, hypotension, hypercoagulable states, arterial inflow problems, or unknown causes. Unlike the BC fistula, which has a 30-day failure rate reported at 24%, synthetic grafts tend to thrombose several months after implantation. The rate of BC fistula failure is not dependent on access site, but is related to the size and condition of native veins and, to a lesser degree, native arteries. When comparing the overall longevity of BC fistulas and PTFE grafts, there is no significant difference. However, a BC fistula created at a site with adequate vasculature has a significantly greater longevity than a PTFE graft (17). Standard treatment for thrombosed dialysis access grafts due to venous anastomotic stenosis is surgical thrombectomy followed by revision. When

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these methods are used successfullv. the results are the equivalent of pl&ing a new graft. Each revision, however, uses additional proximal native vein. Also, prospective evaluation of the venous system is a reliable way of excluding unsatisfactory access sites, with a resulting potential threefold improvement in thrombosis rates and fistula patency (21,221. These two factors, combined with the increased longevity of patients with chronic renal failure, has led to increased interest in graft salvage by interventional radiologists. One problem that persists in the dialysis literature is the definition of "failed access." In one highly regarded surgical report, failure is defined as "re~lacementof a failed access bv a new one" (17). In a review paper of vascular access preservation by Windus and Delmez, they define failure as a functional problem when "flow is insufficient to support the needs of dialysis" (23).The former definition emphasizes the preservation of a particular access site, while the latter specifies the functional status of the graft as the prime determinant of vascular access. Both definitions have merit, and each should be considered a factor in determining outcomes of interventions. Also, noninvasive methods for screening of functional abnormalities must be developed that consistently differentiate functional from anatomic problems if screening methods are to prove valuable.

Access Graft Monitoring and Pharmacologic Interventions: Tools of the Nephrologist From a primary care clinicianlnephrologist's standpoint, the care of the hemodialysis patient's access has become a team approach. It is the nephrologist's task to provide ongoing evaluation of the access and to avoid the complications outlined above as long as possible. Unfortunately, outpatient "bedside" noninvasive evaluation is not widely available on a daily basis. The most commonly used bedside parameter to evaluate a functioning access is measurement of recirculation. Recirculation is a phenomenon that occurs when venous outflow resistance (usually due to venous stenosis) pre-

vents dialysed blood from returning directly into the venous system. Proximal resistance or obstruction causes blood to flow retrograde in the graft, thus re-entering the arterial needle. The percentage of blood that is "recirculated" % R in this fashion can be quantitated using the following formula:

P-A %R=x 100, P - v where P = serum blood urea nitrogen (BUN) level from a systemic venous sample, usually measured in the opposite arm; A = serum BUN level from the dialyzer inlet; and V = serum BUN level from the dialyzer outlet. Recirculation rates are also dependent on dialyzer pump speeds (blood flow rates) and placement site of access. When recirculation rates exceed 15%20%, venous outflow obstruction should be suspected. While other methods have been suggested to improve the accuracy of this measurement, this method remains the easiest to quantitate in the outpatient setting (24,251. Other noninvasive maneuvers for evaluating access adequacy include evaluating hemodialysis machine venous pressure as an indirect measurement of distal access stenoses. While this can be helpful, it too may vary with blood pump speed and cannot qualitatively or quantitatively help evaluate access stenoses (26,271. Finally, physical examination of an AV graft has been purported to provide valuable evidence in the evaluation of potential stenoses (28).An attempt to quantitate functional stenosis of an access by auscultation of the bruit or palpation of the thrill, and measurement of pulse was suggested by Dr Beathard. Evidence of access stenosis included discontinuous bruitlthrill, thrill confined to one area of the graft, or poor pulsation. Of these parameters, the auscultation of a continuous midgraft bruit in our hands has proved to be the most helpful in the screening of functioning accesses. This final exercise, the physical examination of the access remains one of the most important but overlooked methods of noninvasive hemodialysis access strategies available to the clinical nephrologist.

All of these methods, however, can provide only the grossest of screens in the search for hemodialysis access dysfunction. Radiologic techniques provide complementary and, in many cases, relatively definitive means of evaluating these AV conduits. A laundry list of invasive and noninvasive techniques to evaluate and preserve hemodialysis accesses, however, may miss the point. If we assume that the most common cause of graft failure is thrombosis and that most of these thromboses are at least associated with venous anastomotic stenoses caused by neointimal hyperplasia, our efforts should rightly be focused on avoiding these stenoses (29,301. Toward this end, multiple techniques have been tried on animals and humans with mixed results. These techniques have ranged from mechanical treatments, outlined elsewhere in this article, to the use of pre- and postoperative medications. These medications include glucocorticoids, azathioprine, dipyridamole, fish oil, calcium channel blockers, angiotensin converting enzyme inhibitors, colchicine, lipid-lowering agents, aspirin, and heparin, to name only a few. Ongoing research at many institutions continues to try to discover this "magic bullet," but so far to no avail (31-46).

Percutaneous Diagnosis and Intervention: Tools of the Interventional Radiologist Many of the percutaneous interventions applied by interventional radiologists in the peripheral circulation have been used for dialysis graft management. The graft angiogram, is the most effective means of evaluating vascular access and should be routinely employed preoperatively and for evaluation of failing grafts (18). Despite the lack of functional information provided by graft angiograms, it remains the best method for evaluation of not only the access site, but of the entire arterial inflow and venous outflow system. Recent reports of dialysis graft evaluation with transcutaneous color Doppler flow imaging have suggested a possible screening technique for detection of access stenoses (47). The effect a screening program would have on preservation of access remains to be determined.

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Percutaneous treatment of thrombosed angioaccess with urokinase has generated a great deal of interest. Rapid, low-dose techniques can restore patency within an hour of initiation (48,491,at a cost comparable to that of surgical thrombectomy. The use of urokinase is still contraindicated in patients at risk for anticoagulation or fibrinolytic therapy (ie, in patients with recent stroke, central nervous system malignancy, history of major gastrointestinal bleeding, active hemorrhage, recent major surgery). Fortunately, only a few patients are excluded with use of these criteria. A recent surgical thrombectomy or the uncomplicated placement of a central venous dialysis access catheter is not a contraindication to fibrinolytic therapy when we have used a rapid pulse-spray technique. In our experience, conventional drip infusion techniques required an average time more than twice that of a modified pulse-spray technique (99 minutes 5 27 vs 48 minutes k 131, though each required doses of approximately 600,000-750,000 U of urokinase. Given the efficacy of rapid techniques, conventional drip infusion methods for dialysis graft thrombolysis are not recommended (50). More recently, mechanical methods of clot dissolution have been successfully applied in dialysis access grafts (51-53). Thus, the primacy of surgical thrombectomy for rapid restoration of graft patency is being challenged. A variety of reports on the efficacy of percutaneous transluminal angioplasty (PTA) of venous outflow, arterial inflow, or anastomotic graft strictures indicate a relative lack of efficacy compared to surgical revision, with mean functioning graft rates of 4-6 months after single PTA compared to 14-18 months or more after surgical revision (17,541. PTA, unlike surgical revision, does not require use of new vein sites, is repeatable, and is less expensive than surgical alternatives. With a strategy of multiple PTA procedures, functioning access may be extended for up to 18 months with a total of one to five treatments (55). The challenge to the interventional radiologist and nephrologist is knowing when to quit. A cost comparison alone does not yield the answer,

since preservation of access site may be the ultimate determining factor in the total cost. Newer techniques for treatment of stenoses in dialysis patients include directional atherectomy (56,571and placement of metallic stents. Atherectomy shows promise for improved longterm graft function compared with PTA, and is superior to PTA for intragraft strictures and for cases in which PTA balloons are unable to expand in the tough, dense material that often forms at or adjacent to anastomotic sites (58). Preliminary work with stents at anastomotic sites and proximal veins is encouraging, but larger series are needed to ascertain their ultimate utility (59). There have been case reports of successful treatment of pseudoaneurysms of access sites with balloon occlusion devices (60). Other complications of dialysis grafts, including embolization of distal arteries of the forearm and leg, can occasionally be managed with transcatheter thrombolysis. Infected grafts, as demonstrated by local swelling with positive blood cultures or aspiration of purulent material from the local site of involvement, should not be treated with percutaneous interventional methods.

The Challenge It is clear from the discussion presented here that hemodialysis access preservation and salvage are formidable problems. The challenge is so daunting that maintainance of adequate access has evolved into a team approach. Hemodialysis patients have become dependent on, not only a primary healthcare giverlnephrologist but also the services of the radiologist and the access surgeon. What then do we as clinicians do about the problem of hemodialysis access failure? As nephrologists and primary care physicians participating in the daily treatment of the hemodialysis population, we physically examine these accesses and remain ever vigilant for signs of impending catastrophe. As radiologists, we image potential areas of concern, employ thrombolysis when necessary, and perform angioplasty and atherectomy in stenotic areas. As ac-

cess surgeons, we surgically place new accesses and repair and replace poorly functioning accesses. Finally, as researchers, we all continue our relentless search for the perfect AV hemodialysis access knowing that lives depend on our continuing diligence. Ref erences 1. Owen WF J r , Williams WW Jr. A patient with recurrent thrombosis in polytetrafluoroethylene dialysis grafts. Semin Dial 1990; 3:127-131. 2. Besarab A, Dorrell S, Moritz M, Sullivan K, Michael H. Preserving vascular access. Semin Dial 1991; 4:155-156. 3. Johnson JM, Anderson JM. Reasonable expectations for PTFE grafts in hemodialysis access. Dial Transplant 1983; 12:238-240. 4. Dardik H, Ibrahim IK, Dardik I. Arteriovenous fistulas constructed with modified human umbilical cord vein graft. Arch Surg 1976; 111:60-62. 5. Jenkins AMcL, Buist TAS, Glover SD. Medium-term follow-up of forty autogenous vein and forty PTFE (GoreTex) grafts for vascular access. Surgery 1980; 88:667-672. 6. May J , Tiller D, Johnson J , et al. Saphenous-vein arteriovenous fistula in regular dialysis treatment. N Engl J Med 1969; 280:770. 7. Szilagyi DE, Smith RF, Elliot JP, Allen HM. Long-term behavior of a Dacron arterial substitute: clinical roentgenologic and histologic correlations. Ann Surg 1965; 162:453-477. 8. Hurt AV, Batello-Cruz M, Skipper BJ, et al. Bovine carotid artery heterograft versus polytetrafluoroethylene grafts. Am J Surg 1983; 146:844-847. 9. Butler HG, Baker LD, Johnson JM. Vascular access for chronic hemodialysis: PTFE versus bovine heterograft. Am J Surg 1977; 134:791-793. 10. Morgan AP, Dammin GJ, Lazarus JM. Failure modes in secondary vascular access for hemodialysis. ASAIO Trans 1978; 1:44-49. 11. Raju S. Polytetrafluoroethylene grafts for hemodialysis access. Ann Surg 1987; 206:666-673. 12. Lindsay RM, Henderson LW. Adequacy of dialysis. Kidney Int Suppl 1988; 33(suppl24):92-99. 13. Gotch FA. Dialysis of the future. Kidney Int Suppl1988; 33(suppl24): S100-104. 14. Collins AJ, Keshaviah P. Are there limitations to shortening dialysis treatment? ASAIO Trans 1988; 34:l-5. 15. Schwab S, Lambert M, Collins D, Mid-

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Chervu A, Moore WS. An overview of intimal hyperplasia. Gynecol Obstet 1990; 171:433-447. Ney AL, Odland MD, Andersen RC. Causes and evaluation of incipient vascular access failure in chronic hemodialysis. Semin Dial 1992; 4:174-178. Snow AD, Bolender RP, Wight TN, Clowes AW. Heparin modulates the composition of the extracellular matrix domain surrounding arterial smooth muscle cells. Am J Path01 1990; 137: 313-330. Colyvas N, Rapp JH, Phillips NR, et al. Relation of plasma lipid and apoprotein levels to progressive intimal hyperplasia after arterial endarterectomy. Circulation 1992; 85:1286-1292. Sahni R, Maniet AR, Voci G, Banka VS. Prevention of restenosis by lovastatin (abstr). Circulation 1989;80(suppl II):65. Shoenfeld NA, Eldrup-Jorgensen J, Connolly R, et al. The effect of low molecular weight dextran on platelet deposition onto prosthetic materials. J Vasc Surg 1987; 5:76-82. MacDonald RG, Panush RS, Pepine CJ. Rationale for use of glucocorticoids in modification of restenosis after percutaneous transluminal coronary angioplasty. Am J Cardiol 1987; 60: 56B-60B. Rutherford RB, Jones DN, Bergentz SE. et al. The efficacv of dextran 40 in preventing early postoperative thrombosis following difficult lower extremity c 1984; 1:765-773. bypass. J ~ a s surg DeCampli WM, Kosek JC, Mitchell RS, Handen CE, Miller DC. Effects of aspirin, dipyridamole, and cod liver oil on accelerated myointimal proliferation in canine veno-arterial allografts. Ann Surg 1988; 208:746-754. Chervu A, Moore WS, QuinonesBaldrich WJ, Henderson T. Efficacy of corticosteroids in suppression of intimal hyperplasia. J Vasc Surg 1989; 10: 129-134. Landymore RW, Karmazyn M, Macaulay MA, Sheridan B, Cameron CA. Correlation between the effects of aspirin and dipyridamole on platelet function and prevention of intimal hyperplasia in autologous vein grafts. Can J Cardiol 1988; 4:56-59. Dryjski M, Mikat E, Bjornsson TD. Inhibition of intimal hyperplasia after arterial injury by heparins and heparinoid. J Vasc Surg 1988; 8:623-633. Quinones-Baldrich WJ, Ziomek S, Henderson T, Moore WS. Patency and intimal hyperplasia: the effect of aspirin on small arterial anastomosis. Ann Vasc Surg 1988; 2:50-56.

O'Keefe JH, Giorgi LV, Hartzler GO, et al. Effects of diltiazem on complications and restenosis after coronary angioplasty. Am J Cardiol1991; 67:373-376. Brozovich FV, Morganroth J , Gottlieb NB, Gottlieb RS. Effect of angiotensin converting enzyme inhibition on the incidence of restenosis after percutaneous transluminal coronary angioplasty. Cathet Cardiovasc Diagn 1991; 23:263-267. Powell JS, Clozel J , Muller RK, et al. Inhibitors of angiotensin-converting enzyme prevent myointimal proliferation after vascular injury. Science 1989; 245:186-188. Clowes AW, Reidy MA. Prevention of stenosis after vascular reconstruction: pharmacologic control of intimal hyperplasia-a review. J Vasc Surg 1991; 13:885-891. Muller DWM, Ellis SG, Topol EJ. Colchicine and antineoplastic therapy for the prevention of restenosis after percutaneous coronary interventions. J A m Coll Cardiol 1991; 17:126B131B. Dousset V, Grenier N, Douws C, et al. Hemodialysis grafts: color Doppler flow imaging correlated with digital subtraction angiography and functional status. Radiology 1991; 181:89-94. Valji K, Bookstein J J , Roberts AC, Davis GB. Pharmacomechanical thrombolysis and angioplasty in the management of clotted hemodialysis grafts: early and late clinical results. Radiology 1991; 178:243-247. Brunner MC, Matalon TS, Pate1 SK, McDonald V, Jensik SC. Ultrarapid urokinase in hemodialysis access occlusion. JVIR 1991; 2:503-506. Gaylord GM. Rapid thrombolysis of dialysis access grafts (abstr).JVIR 1991; 2:44. Trerotola SO, Lund GB, Savader SJ, Venbrux AC, Osterman FA. New device for mechanical thrombectomy of dialysis access grafts (abstr). JVIR 1992; 3:25. Schmitz-Rode T, Gunther RW. Percutaneous mechanical thrombolysis: a comparative study of various rotational catheter systems. Invest Radio1 1991; 26:557-563. Gaylord GM, Ehrman KO. TracWright catheter for mechanical thrombolysis of occluded dialysis access grafts (abstr). JVIR 1992; 3:24. Brooks JL, Sigley RD, May KJ, Mack RM. Transluminal angioplasty versus surgical repair for stenosis of hemodialysis grafts. Am J Surg 1987; 153:530-531.

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55. Gmelin E, Winterhoff R, Rinast E. Insufficient hemodialysis access fistulas: late results of treatment with percutaneous balloon angioplasty. Radiology 1989; 171:657-660. 56. Vorwerk D, Gunther RW. Removal of intimal hyperplasia in vascular endoprosthesis by atherectomy and balloon dilatation. AJR 1990; 154:617-618. 57. Zemel G, Katzen BT, Benenati JF,

Dake MD, Lempert TE. Directional atherectomy of dialysis access fistula stenosis. JVIR 1990; 1:35-38. 58. Gaylord GM. Balloon angioplasty versus Simpson atherectomy for treatment of dialysis access grafts: work in progress (abstr). JVIR 1991; 2:25. 59. Giinther RW, Vorwerk D, Bohndorf K, et al. Venous stenoses in dialysis shunts: treatment with self-expanding

metallic stents. Radiology 1989; 170: 401-405. 60. Selby J B Jr, Pruett TL, Westervelt FB Jr, Tegtmeyer CJ. Treatment of hemodialysis fistula pseudoaneurysms with detachable balloons: technique and preliminary results (abstr). JVIR 1991; 2:24.