Management strategies in hemodialysis vascular access
From NIER
By Dr. Joke van der Linden (2006)
Originally published as general introduction to the PhD thesis of Dr. Van der Linden, which she published in 2006 under supervision of her promotor Prof. Dr. W. Weimar and copromotores Dr. M.A. van den Dorpel and Dr. P.J. Blankestijn, at the Erasmus University of Rotterdam, the Netherlands
Contents |
[edit] Abstract
Since the introduction of the arteriovenous fistula (AVF) and the use of interposition graft (AVG) little improvement has been made in the vascular access field. Still, vascular access related complications are one of the most important reasons for hospitalisation, morbidity and mortality. The native arteriovenous fistula is the vascular access of choice because of its low risk of thrombosis and infection. However construction is not always possible, necessitating the use of prosthetic grafts. This review describes the ongoing problems encountered in the vascular access field and describes important pre- and postoperative strategies to improve the care for vascular accesses in hemodialysis.
[edit] Introduction
Gaining proper access to the circulation is a prerequisite for hemodialysis in order to transport blood from the patient to the artificial kidney and back to the patient again. In 1943, Dr. Willem J. Kolff first encountered the problem of gaining access to the bloodstream for hemodialysis (1). After 34 days of puncturing readily accessible blood vessels he failed to find further possibilities to enter the bloodstream. As a consequence his patient died. The chronic hemodialysis era began almost 20 years later, when Quinton and Scribner introduced the first external arterio-venous shunt constructed of Teflon, that allowed repeated access to the vascular system (2). Unfortunately, infection and thrombosis often limited the long-term use of this access type. In 1966 a major breakthrough in vascular access surgery was achieved by the introduction of the first endogenous fistula by Brescia and Cimino (3-5). They created a side-to-side anastomosis between the radial artery and cephalic vein, which ensured function as a vascular access. Later, brachio-cephalic and transposed brachio-basilic fistulae were constructed by Dunlop (6) and Stonebridge (7) respectively. At present the arterio-venous fistula (AVF) is still considered to be the vascular access of choice. After adequate maturation, the AVF has the highest long-term patency rates because of low risk of thrombosis and infection (8,9).
Unfortunately, creation of an AVF is not always possible as a consequence of prior vascular access surgery, or insufficient caliber of forearm vessels. Subsequently, the use of various prosthetic grafts has emerged as an alternative to native fistula. These arterio-venous grafts (AVG) are typically positioned in the forearm, in a looped or straight configuration. Nowadays, polytetrafluoroethylene (PTFE) is the most used graft-material. Unfortunately, AVG appear to be associated with a significantly higher risk of thrombosis and infection as compared with AVF (10-13).
Since the introduction of the AVF and the PTFE AVG, little improvement has been made in the vascular access field. Still, vascular access related complications are one of the most important reasons for patient hospitalisation, morbidity and even mortality (13,14). In the United States access complications are estimated to cost about to $1 billion per annum, and are responsible for 17-30% of all hospital admissions in dialysis patients (15-17). Interestingly, the cost of vascular access related care was found to be more than fivefold higher for patients with AVG compared with patients with a functioning AVF (18). In an attempt to improve overall patency rates and reduce access related costs, the NFK-DOQI committee currently recommends that in any dialysis center the majority of new dialysis patients should have a primary AVF constructed (19).
Despite these recommendations large variations in vascular access practice patterns are found. Fistula use still is much lower in the United States than in Europe (9). AVF use was found to be actually 0% in some facilities in the United States (9). These differences are frequently attributed to unfavourable patient characteristics such as diabetes, peripheral vascular disease, and older age of patients (9,20,21). However, the observed differences persist after adjustment for these patient characteristics. Facility’s preferences and approaches to vascular access practice still seem to be major determinants of vascular access use (22).
[edit] Endothelial function in chronic renal disease
Cardiovascular complications are a major cause of death and morbidity of ESRD patients (23). Early studies suggested that uremia is associated with accelerated atherosclerosis (24,25). Over the last decade endothelial dysfunction has been identified as an important mediator in this process. Nitric oxide (NO) is one of the main factors involved in the anti-atherosclerotic effects of the endothelium, and chronic renal failure has been associated with impaired NO bioavailability (26,27).
The ability to adjust to high blood flow and proper vasodilatation, needed after creation of AVF, could be strongly influenced by endothelial function of the forearm vessels. Endothelium-dependent vasodilatation of forearm capacitance vessels is affected by many diseases, among which several are known to cause renal failure, like diabetes and hypertension (28). Local infusion of vasodilators causes a less pronounced increase of forearm flow in hypertensive patients as compared to normotensive controls (29-35). Also, the hyperaemic response after temporary arterial occlusion is reduced in hypertensive patients (29-34). Similar results are found in patients with diabetes and congestive heart failure (36,37). In addition, uraemia or so-called uraemic factors like homocysteine or endogenous inhibitors of NO-synthase (ADMA) could be directly toxic to the vascular endothelium (38,39).
In addition to the impaired vasodilatation of capacitance vessels due to endothelial dysfunction, several authors demonstrated reduced venous forearm distensibility in patients with hypertension, diabetes, chronic heart failure and end stage renal disease (40-43). Vein wall distensibility is controlled by collagen, elastin and smooth muscle. Wali et al. demonstrated accumulation of collagen fibres in place of smooth muscle cells in pre-access cephalic veins, which would cause a decrease in the elasticity of the vein wall (44). These functional properties of the forearm vasculature could interfere with proper maturation of the AVF.
Increasing the placement of AVF and an aggressive policy for vascular access monitoring could improve quality of life and overall outcomes for hemodialysis patients significantly.
[edit] Choice of access: preoperative testing
With the recognition of the superiority of the AVF and the increasing comorbidity of the hemodialysis population, efforts are made to evaluate the vasculature of the arm of the patient prior to access surgery. This would help the surgeon to choose the access site and type with the highest likelihood of success in the individual patient. The NKF-DOQI guidelines provide recommendations concerning preoperative evaluation in addition to obtaining careful patient history and physical examination of the patient’s venous venous, arterial, and cardiopulmonary systems (10). In patients who meet specified criteria such as edema of the extremity, collateral vein development, or previous subclavian catheter placement, venography is indicated. In compare to Doppler studies, venography has the advantage of accurate evaluation of central vein structures. However, patients with reduced kidney function in whom contrast agents are undesirable, Doppler ultrasound or magnetic resonance imaging may be preferred.
[edit] Preoperative Doppler ultrasound
Doppler ultrasound has been the most extensively studied and widely used test to guide access creation (45-51). Several authors demonstrated that vessel size and blood flow are of predictive value for AVF outcome. AVF creation with a cephalic vein and/or radial artery smaller than 1,5-2,0 mm is likely to fail and may indicate brachio-cephalic or transposed brachio-basilic AVF or insertion of a graft (45,52,53). A pre-operative brachial artery flow of at least 40 mL/min and a flow of 400 mL/min or more in the subclavian vein are associated with better primary patency rates and fistula function (47). Also, the use of a standardized program of preoperative arterial en venous mapping with ultrasonography could increase the use of AVF and reduce early failure rates (48,50,54).
[edit] Forearm strain-gauge plethysmography
Venous occlusion strain-gauge plethysmography is a frequently used technique for measurement of forearm blood flow and venous compliance (55). Throughout the years the method has been standardized and computerized, resulting in a reasonably simple and reliable technique (56-58). It works on the principle that during short-term occlusion of venous return, the rate of distension of the forearm is proportional to the rate of arterial inflow into the forearm. Provided that the arterial blood pressure remains constant, changes in flow reflect changes in smooth muscle tone in small arteries and arterioles. A venous occlusion upper arm cuff is rapidly inflated to 60 mmHg during 4 heartbeats and deflated during 3 heartbeats. Distension of the arm is detected by a length transducer - specifically, a fine rubber tube containing mercury - placed around the maximal circumference of the forearm. The influence of the circulation of the hand on the measurements of forearm blood flow (FBF) is only small, which makes the use of a wrist cuff unnecessary (55). Subjects lay in supine position with the arm supported above heart level.
FBF can be measured at rest and after arterial infusion of drugs. FBF is expressed as mL blood flow/min/100ml forearm. Incremental infusions of acetylcholine, metacholine or serotonine are frequently used drugs to examine endothelium-dependent vasodilatation. Sodium nitroprusside (SNP) is the most frequent used drug to examine endothelium-independent vasodilatation.
Venous compliance is the change in blood volume for a given change in pressure produced by a cuff around the arms or legs. The cuff pressure restricts blood flow from the tissues and causes the blood to pool. The upper arm cuff is inflated to a cuff pressure of 20 mmHg and is kept inflated during 3 minutes for stabilization of arm volume and venous pressure values. The cuff is deflated for 2 minutes to minimize accumulation of interstitial fluid due to capillary filtration. After repeating the same procedure during cuff pressures of 30, 40, 50 and 60, the obtained volume/pressure ratios are used in a linear regression analysis to obtain the volume-pressure relationship as an estimate of venous compliance.
So far, the value of forearm venous compliance and blood flow prior to AVF creation has never been evaluated. This thesis presents two studies that focus on this subject.
[edit] Preoperative magnetic resonance venography
Preoperative use of magnetic resonance (MR) venography and its advantage over conventional contrast-enhanced venography was documented by Menegazzo et al (59). Although it is considered non-invasive and safe, the quality of the basilic and central veins cannot be assessed, which is a major drawback of the MR venography (60). Furthermore, the cost-effectiveness of MR venography is questionable.
[edit] Prevention of vascular access thrombosis
In AVG, most thrombotic events result from one or more progressive stenoses in the venous outflow tract, typically at the venous anastomosis (61-64). These stenoses are caused by intimal and fibromuscular hyperplasia (65,66). Any obstruction to the outflow from the graft will result in an increase in venous pressure in the dialysis circuit with an accompanying decrease in blood flow (67). Stenoses in AVF tend to occur more centrally at vein bifurcations and venous valves, rather than close to the venous outlet. Stenoses in AVF frequently result in development of collateral veins draining the AVF. As a result, a venous stenosis will cause a reduction in blood flow but often without the increase in venous pressure. Arterial inflow stenoses account for less than 5% of lesions in accesses (67).
Prospective surveillance of vascular accesses for hemodynamically significant stenoses, and subsequent referring for percutaneous transluminal angioplasty (PTA) or surgical revision, improves patency rates and decreases the incidence of thrombosis (Kanterman 1995, Besarab 1995, Beathard 1995, Windus 62,64,68,69). At present, access flow (Qa) and venous pressure measurements are preferred techniques that can be used in surveillance of both AVG and AVF (10).
[edit] Access flow
Several methods are available for measuring access flow (Qa). The most widely used and validated method is the ultrasound dilution technique, first introduced by Krivitski (70-73). It is based on the Fick-principle: dilution of blood in the extracorporeal circuit is measured by ultrasound. (70).
Although it is known that low-flow circumstances provoke thrombosis, the optimal threshold level for intervention has not been definitively determined. A limited number of studies using serial access flow measurements, suggest that grafts showing a flow between 500 and 800 ml/min are at risk for thrombosis (74-76). This has led to the general recommendation that intervention should be considered in patients with flows less than 600 ml/min (10). A trend of decreasing access flow could be more predictive of venous stenosis than a single access flow measurement, however studies on this subject show conflicting results (77,78). Paulson et al. demonstrated that a decrease in flow had a sensitivity of 80%, but had a false-positive rate of 30% (78). This may lead to unnecessary interventions. Still, the NKF-K/DOQI committee recommends referral for angiography in patients with access flows less than 1000 ml/min, who show a decrease of more than 25% over 4 months time (10). Much less evidence is available on the value of flow measurements in AVF. Flow measurement in AVF is unreliable when needles are placed in collateral veins, and the optimal threshold for predicting failure of AVF has not been determined. More important, the incidence or thrombosis in fully matured AVF is very low, which makes it very difficult to evaluate the effect of flow-based monitoring strategies on reducing thrombosis of AVF. However, a flow-based surveillance program with prophylactic PTA of stenoses was shown to effectively reduce thrombosis rates and access-related morbidity in a prospective controlled trial (79).
[edit] Venous pressure
Dynamic and static venous pressure measurements are used for access surveillance. Schwab et al. introduced the dynamic venous pressure measurement: venous drip chamber pressure was measured at a pump flow rate of 200-225 mL/min (80). Persistently elevated venous pressure predicted the presence of significant venous stenosis (80). A reduction of thrombotic rate from 0.49 to 0.20 was demonstrated with graft surveillance using dynamic venous pressure monitoring and elective repair when compared to historical controls (80,81). Schwab et el. also included AVF.
However, dynamic venous pressure is importantly influenced by pump flow, needle gauge, blood tubing and blood pressure (82). This problem can be overcome by measuring static venous pressure. Besarab et al. developed a method to measure venous pressure at zero pump flow, corrected for mean arterial blood pressure (VP0/MAP). Referral for angiography and subsequent intevention of significant stenoses in patients with VP0/MAP ³ 0.50, resulted in a decrease in thrombosis rate from 57 to 17 per 100 patient years (68). Again, AVF and AVG were included.
An increased thrombotic tendency is an important cause of complications in patients on chronic hemodialysis. Still, the relationship between hypercoagulability and vascular access thrombosis is largely unknown. At present, no evidence-based consensus has been established regarding pharmacological prevention of access prevention. The coagulability abnormalities leading to thrombotic tendency in chronic hemodialysis patients will be discussed in this thesis.
[edit] Treatment of vascular access stenosis and thrombosis
Access stenosis and thrombosis are treated either radiologically or surgically. Prior to the introduction of access surveillance programs the most common clinical presentation of access failure was thrombosis. Traditionally, surgical thrombectomy with or without revision was utilized for dialysis access salvation. Surgical therapy has the advantage of elimination of the lesion. However, this has the great disadvantage of loss of potential access puncture sites. Considering the recurrent nature of venous stenosis, this may cause vascular access problems over time. Although literature reports slightly better patency rates after surgical correction of stenosis (83), general opinions are in favour of percutaneous treatment, because of the previously mentioned disadvantage together with the need for hospitalization.
Nowadays, patients often present with access stenosis, which is primarily treated with percutaneous transluminal angioplasty (PTA). Angioplasty is a safe outpatient procedure, which can be successfully repeated if necessary (84). Compared with surgery, PTA has the advantage of preserving access sites. Also, even centrally located stenoses are accessible. Initial success rates of PTA range from 80 to 94% (62,85,86). The highest rate of technical failure is associated with central lesions (84). Primary patency rates at 6 months after PTA range from 43 to 77% (61,62,84,87), again with poorest long-term success in central lesions (nearly 25% at 6 months, 84). Results after vascular access thrombosis are generally worse, with a reported patency rate of only 19% in one study (88). Additive placement of self-expanding stents should be considered only in a selected group of patients, with central -elastic- lesions not responsive to PTA, or recurrence within 3 months after successful PTA, and patients with vein rupture after PTA (89). Lesions that cannot be dilated with angioplasty should not be treated with stent placement.
[edit] References
1. Kolff WJ, Berk HTh: The artificial kidney: a dialyzer with a great area. Acta Med Scand 1944; 117:121-34
2. Quinton WE, Dillard D, Scribner BH: Cannulation of blood vessels for prolonged hemodialysis. Trans Am Soc Artif Intern Organs 1960; 104-13
3. Brescia MJ, Cimino JE, Appel K, Hurwich BJ: Chronic hemodialysis using venipuncture and surgically created arteriovenous fistula. N Eng J Med 1966; 275:1089-92
4. Cimino JE, Brescia MJ: The early development of the arteriovenous fistula needle technique for hemodialysis. ASAIO J 1994; 923-7
5. Kapoian T, Sherman RA: A brief history of vascular access for hemodialysis: an unfinished story. Sem Nephrol 1997; 17:239-45
6. Dunlop MG, Mackinlay JY, Jenkins AM: Vascular access: experience with the brachiocephalic fistula. Ann R Coll Surg Engl 1986; 68:203-6
7. Stonebridge PA, Edington D, Jenkins AM: ‘Brachial/basilic vein’ transposition for vascular access. J R Coll Surg Edinb 1995; 40:219-20
8. Churchill DN, Taylor W, Cook RJ, LaPlante P, Barre P, Cartier P, Fay WP, Goldstein MB, Jindal K, Mandin H, McKenzie JK, Muirhead N, Parfrey PS, Posen GA, Slaughter D, Ulan RA, Werb R: Canadian hemodialysis morbidity study. Am J Kidney Dis 1992; 14:214-34
9. Pisoni RL, Young EW, Dykstra DM, Greenwood RN, Hecking E, Gillispie B, Wolfe RA, Goodkin DA, Held PJ: Vascular access use in Europe and the United States: results from the DOPPS. Kidney Int 2002; 61:305-16
10. National Kidney Foundation. K/DOQI clinical practice guidelines for vascular access. Am J Kidney Dis 2001; 37 (Suppl 1):S137-S181
11. Cayco AV, Abu-Alfa AK, Mahnensmith RL, Perazella MA: Reduction in arteriovenous graft impairment: results of a vascular access surveillance protocol. Am J Kidney Dis 1998; 32:302-8
12. Sands JJ, Jabyac PA, Miranda CL, Kapsick BJ: Intervention based on monthly monitoring decreases hemodialysis access thrombosis. ASAIO J 1999; 45:147-50
13. Powe NR, Jaar B, Furth SL, Hermann J, Briggs W: Septicaemia in dialysis patients: incidence, risk factors and prognosis. Kidney Int 1999; 55: 1081-90
14. Schwab SJ, Beathard G: The hemodialysis catheter conundrum: hate living with them, but can’t live without them. Kidney Int 1999; 56: 1-17
15. U.S. Renal Data System. The economic cost of ESRD, vascular access procedures, and Medicare spending for alternative modalities of treatment. Am J Kidney Dis 1997; 30 (Suppl.1):S160-S177
16. Feldman HI, Kobrin S, Wasserstein A: Hemodialysis Vascular Access Morbidity. J Am Soc Nephrol 1996; 7:523-35
17. Chazan JA, London MR, Pono L: The impact of diagnosis-related groups on the cost of hospitalisation for end-stage renal disease patients at Rhode Island Hospital from 1987 to 1990. Am J Kidney Dis 1992; 6:523-5
18. Lee H, Manns B, Taub K, Ghali WA, Dean S, Johnson D, Donaldson C: Cost analysis of ongoing care of patients with end-stage renal disease: the impact of dialysis modality and dialysis access. Am J Kidney Dis 2002; 40:611-22
19. National Kidney Foundation. NKF-DOQI clinical practice guidelines for vascular access. Am J Kidney Dis 1997; 30 (Suppl 3): S152-S191
20. Allon M, Ornt DB, Schwab SJ, Rasmussen C, Delmez JA, Greene T, Kusek JW, Martin AA, Minda S: Factors associated with the prevalence of arteriovenous fistulas in hemodialysis patients in the HEMO study. Kidney Int 2000; 58:2178-85
21. Hirth RA, Turenne MN, Woods JD, Young EW, Port FK, Pauly MV, Held PJ: Predictors of type of vascular access in hemodialysis patients. JAMA 1996; 276:1303-7
22. Young EW, Dykstra DM, Goodkin DA, Mapes DL, Wolfe RA, Held PJ: Hemodialysis vascular access preferences and outcomes in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Kidney Int 2002; 61:2266-71
23. Amann K, Tyralla K, Gross ML, Eifert T, Adamczak M, Ritz E: Special characteristics of atherosclerosis in chronic renal failure. Clin Nephrol 2003; 60 (Suppl.1):S13-21
24. Lindner A, Charra B, Sherrard DJ, Scribner BH: Accelerated atherosclerosis in prolonged maintenance hemodialysis. N Engl J Med 1974; 28:697-701
25. Rostand SG, Gretes JC, Kirk KA, Rutsky EA, Andreoli TE: Ischemic heart disease in patients with uremia undergoing maintenance hemodialysis. Kidney Int 1979; 16:600-11
26. Wever R, Boer P, Hijmering M, Stroes E, Verhaar M, Kastelein J, Versluis K, Lagerwerf F, van Rijn H, Koomans H, Rabelink T: Nitric oxide production is reduced in patients with chronic renal failure. Arterioscler Thromb Vasc Biol 1999; 19:1168-72
27. Stroes ES, Joles JA, Chang PC, Koomans HA, Rabelink TJ: Impaired endothelial function in patients with nephrotic range proteinuria. Kidney Int 1995; 48:544-50
28. Anderson TJ: Assessment and treatment of endothelial dysfunction in humans. J Am Coll Cardiology 1999; 34:631-8
29. Pedrinelli R, Spessot M, Salvetti A: Reactive hyperemia during short-term blood flow and pressure changes in the hypertensive forearm. J Hypertens 1990; 8:467-71
30. Pedrinelli R, Dell’omo G, Gimelli A, Di Bello V, Talarico L, Corchia A, Sambuceti G, Neglia D, Parodi O: Myocardial and forearm blood flow reserve in mild-moderate essential hypertensive patients. J Hypertens 1997; 15:667-73
31. Taddei S, Virdis A, Mattei P, Arzilli F, Salvetti A: Endothelium-dependent forearm vasodilatation is reduced in normotensive subjects with familial history of hypertension. J Cardiovasc Pharmocol1992; 20(s12):s193-s195
32. Panza JA, Quyyumi AA, Brush JE, Epstein SE: Abnormal endothelium-dependent vascular relaxation in patients with essential hypertension. N Eng J Med 1990; 323:22-7
33. Schulte KL, Braun J, Meyer-Sabellek W, Wegscheider K, Gotzen R, Distler A: Functional versus structural changes of forearm vascular resistance in hypertension. Hypertension 1988; 11:320-5
34. Schulte KL, Braun J, Meyer-Sabellek W, Wegscheider K, Gotzen R, Distler A: Effects of reactive hyperemia and nifedipine on forearm vascular resistance in essential hypertension: evidence for functional abnormality. J Cardiovasc Pharmacol 1987; 10(s10):s134-s135
35. Rossi M, Taddei S, Fabbri A, Tintori G, Credidio L, Virdis A, Ghiadoni L, Salvetti A, Giusti C: Cutaneous vasodilatation to acetylcholine in patients with essential hypertension. J Cardiovasc Pharmacol 1997; 29:406-11
36. Schobel HP, Schmieder RE: Vasodilatory capacity of forearm resistance vessels is augmented in hypercholesterolemic patients after treatment with fluvastatin. Angiology 1998; 49(9):743-8
37. Hirooka Y, Imaizumi T, Harada S, Masaki H, Momohara M, Tagawa T, Takeshita A: Endothelium-dependent forearm vasodilatation to acetylcholine but not to substance P is impaired in patients with heart failure. J Cardiovasc Pharmacol 1992; 20(s12):s221-s225
38. Morris STW, McMurray JJV, Rodger RSC, Jardine AG:Impaired endothelium-dependent vasodilatation in uraemia. Nephrol Dial Transplant 2000; 15:1194-200
39. Pannier B, Guerin AP, Marchais SJ, Metivier F, Safar M, London GM: Postischemic vasodilatation, endothelial activation, and cardiovascular remodeling in end-stage renal disease. Kidney Int 2000; 57: 1091-9
40. Widgren BR, Berglund G, Wikstrand J, Andersson OK: Reduced venous compliance in normotensive men with positive family histories of hypertension. J Hypertens 1992; 10:459-65
41. Ogilvie R, Nadeau J, Lutterodt A: Vasodilator capacity of forearm vessels in hypertension. Clin Exp Hypertens 1982; 4:1391-407
42. Bell D, Collier A, Nicoll JJ, Jackson M, Millar AM, Clarke BF, Muir AL: Reduced venous compliance and increased transcapillary escape of protein in insulin-dependent diabetic patients. Diabet Med 1988; 5:454-8
43. Kooman JP, Wijnen JA, Draaijer P, van Bortel LM, Gladziwa U, Peltenburg HG, Struyker-Boudier HA, van Hooff JP, Leunissen KM: Compliance and reactivity of the peripheral venous system in chronic intermittent hemodialysis. Kidney Int 1992; 41:1041-8
44. Wali MA, Eid RA, Al-Homrany MA: Smooth muscle changes in the cephalic vein of renal failure patients before use as an arteriovenous fistula (AVF). J Smooth Muscle Res 2002; 38: 75-85
45. Wong V, Ward R, Taylor J, Selvakumar S, How TV, Bakran A: Factors associated with early failure of arteriovenous fistulae for haemodialysis access. Eur J Endovasc Surg 1996; 12:207-13
46. Malovrh M: Native arteriovenous fistula: preoperative evaluation. Am J Kidney Dis 2002; 39: 1218-25
47. Yerdel MA, Kesenci M, Yazicioglu KM, Döşeyen Z, Türkçapar AG, Anadol E: Effect of haemodynamic variables on surgically created arteriovenous fistula flow. Nephrol Dial Transplant 1997; 12:1684-88
48. Silva MB, Hobson RW, Pappas PJ, Jamil Z, Araki T, Goldberg MC, Gwertzman G, Padberg FT: A strategy for increasing use of autogenous hemodialysis access procedures: impact of preoperative non-invasive evaluation. J Vasc Surg 1998; 27:302-8
49. Mendes RR, Farber MA, Marston WA, Dinwiddie LC, Keagy BA, Burnham SJ: Prediction of wrist arteriovenous fistula maturation with preoperative vein mapping with ultrasonography. J Vasc Surg 2002; 36: 460-3
50. Ascher E, Gade P, Hingorani A, Mazzariol F, Gunduz Y, Fodera M, Yorkovich W: Changes in the practice of angioaccess surgery: impact of dialysis outcome and quality initiative recommendations. J Vasc Surg 2000; 31:84-92
51. Robbin ML, Gallichio MH, Deierhoi MH, Young CJ, Weber TM, Allon M: US: vascular mapping before hemodialysis access placement. Radiology 2000; 217:83-88
52. Malovrh M: Non-invasive evaluation of vessels by duplex sonography prior to construction of arteriovenous fistulas for hemodialysis. Nephrol Dial Transplant 1998; 13:125-29
53. Brimble KS, Rabbat CG, Treleaven DJ, Ingram AJ: Utility of ultrasonographic venous assessment prior to forearm arteriovenous fistula creation. Clin Nephrol 2002; 58:122-8
54. Parmley MC, Broughan TA, Jennings WC: Vascular ultrasonography prior to dialysis access surgery. Am J Surg 2002; 184:568-72
55. Lind L, Sarabi M, Millgård J: Methodological aspects of the evaluation of endothelium-dependent vasodilatation in the human forearm. Clin Physiol 1998; 18:81-7
56. Petrie JR, Ueda S, Morris AD, Murray LS, Elliot HL, Connell JMC: How reproducible is bilateral forearm plethysmography? Br J Clin Pharmocol 1998; 45:131-9
57. Chang PC, Van Brummelen P: Calibration and variability of forearm blood flow measured by strain gauge plethysmography. J Cardiovasc Pharmocol 1987; 10: S123-125
58. Chang PC, Verlinde R, Bruning TA, Van Brummelen P: A micro-computer-based, R-wave triggered system for hemodynamic measurements in the forearm. Comput Biol Med 1988; 18: 157-63
59. Menegazzo D, Laissy JP, Durrbach A, Debray MP, Messin B, Delm V, Mignon F, Schouman-Claeys E: Hemodialysis access fistula creation: preoperative assessment with MR venography and comparison with conventional venography. Radiology 1998; 209: 723-8
60. Turmel-Rodriques L, Bourquelot P, Paynaud A, Beyssen B, Sapoval M: Hemodialysis fistula: preoperative MR venography – a promising but partial view. Radiology 2000; 214:302-3
61. Safa AA, Valji K, Roberts AC, Ziegler TW, Hye RJ, Oglevie SB: Detection and treatment of dysfunctional hemodialysis access grafts: effect of a surveillance program on graft patency and the incidence of thrombosis. Radiology 1996; 199:653-7
62. Kanterman RY, Vesely TM, Pilgram TK, Guy BW, Windus DW, Picus D: Dialysis access grafts: anatomic location of venous stenosis and results of angioplasty. Radiology 1995; 195:135-9
63. Roberts AB, Kahn MB, Bradford S, Lee J, Ahmed Z, Fitzsimmons J, Ball D: Graft surveillance and angioplasty prolongs dialysis graft patency. J Am Coll Surg 1996; 183:486-92
64. Beathard GA: Thrombolysis versus surgery for the treatment of thrombosed dialysis access grafts. J Am Soc Nephrol 1995; 6:1619-24
65. Swedberg SH, Brown BG, Sigley R, Wight TN, Gordon D, Nicholls SC: Intimal fibromuscular hyperplasia at the venous anastomosis of PTFE grafts in hemodialysis patients. Clinical, immunocytochemical, light and electron microscopic assessment. Circulation 1989; 80:1726-36
66. Hofstra L: Intimal hyperplasia in human vascular grafts. A study in peripheral bypasses and arteriovenous fistulas. Thesis Rijksuniversiteit Limburg Maastricht 1995, ISBN 90-5278-190-7
67. Sullivan KL, Besarab A, Bonn J, Shapiro MJ, Gardiner GA, Moritz MJ: Hemodynamics of failing dialysis grafts. Radiology 1993; 186:867-872
68. Besarab A, Sullivan KL, Ross RP, Moritz MJ: Utility of intra-access pressure monitoring in detecting and correcting venous outlet stenoses prior to thrombosis. Kidney Int 1995; 47:1364-73
69. Windus DW, Audrain J, Vanderson R, Jendrasak MD, Picus D, Delmez JA: Optimalization of high-efficiency hemodialysis by detection and correction of fistula dysfunction. Kidney Int 1990;38: 337-41
70. Krivitski NM: Theory and validation of access flow measurement by dilution technique during hemodialysis. Kidney Int 1995; 48:244-50
71. Depner TA, Krivitski NM: Clinical measurement of blood flow in hemodialysis access fistulae and grafts by ultrasound dilution. ASAIO J 1995; 41: M745-9
72. Sands J, Glidden D, Miranda C: Hemodialysis access flow measurement. Comparison of ultrasound dilution and duplex ultrasonography. ASAIO J 1996; 42: M899-901
73. Bosman PJ, Boereboom FT, Bakker CJ, Mali WP, Eikelboom BC, Blankestijn PJ, Koomans HA: Access flow measurements in hemodialysis patients: in vivo validation of an ultrasound dilution technique. J Am Soc Nephrol 1996; 7:966-9
74. Shackleton CR, Taylor DC, Buckley AR, Rowley VA, Cooperberg PL, Fry PD: Predicting failure in polytetrafluoroethylene vascular access grafts for hemodialysis: a pilot study. Can J Surg 1987; 30:442-4
75. Sands J, Young S, Miranda C: The effect of Doppler flow screening studies and elective revisions on dialysis access failure. ASAIO J 1992;38:M524-7
76. Besarab A, Lubkowski T, Frinak S, Ramanathan S, Escobar F: Detecting vascular access dysfunction. ASAIO J 1997; 43:M539-43
77. Neyra NR, Ikizler TA, May RA,E, Himmelfarb J, Schulman G, Shyr Y, Hakim RM: Change in access blood flow over time predicts vascular access trombosis. Kidney Int 1998; 54:1714-9
78. Paulson WD, Ram SJ, Birk CG, Zapczynski M, Martín SR, Work J: Accuracy of decrease in blood flow in predicting hemodiálisis graft trombosis. Am J Kidney Dis 2000; 35:1089-95
79. Tessitore N, Mansueto G, Bedogna V, Lipari G, Poli A, Gammaro L, Baggio E, Morana G, Loschiavo C, Laudon A, Oldrizzi L, Maschio G: A prospective controlled trial on effect of percutaneous transluminal angioplasty on functioning arteriovenous fistulae survival. J Am Soc Nephrol 2003; 14:1623-7
80. Schwab SJ, Raymond JR, Saeed M, Newman GE, Dennis PA, Bollinger RR: Prevention of hemodialysis fistula thrombosis. Early detection of venous stenoses. Kidney Int 1989; 36: 707-11
81. Cayco AV, Abu-Alfa AK, Mahnensmith RL, Perazella MA: Reduction in arteriovenous graft impairment: results of a vascular access surveillance protocol. Am J Kidney Dis 1998; 32:302-8
82. Besarab A, Dorrell S, Moritz M: Determinants of measured dialysis venous pressure and its relationship to true intra-access venous pressure. ASAIO Trans 1991; 37:M270-M1
83. Dougherty MJ, Caliigaro KD, Schindler N, Raviola CA, Ntoso A: Endovascular versus surgical treatment for thrombosed hemodialysis grafts: a prospective randomized study. J Vasc Surg 1999; 30:1016-23
84. Beathard GA: Percutaneous transvenous angioplasty in the treatment of vascular access stenosis. Kidney Int 1992; 42: 1390-7
85. Saeed M, Newman GE, McCann RL, Sussman SK, Braun SD, Dunnick ND: Stenoses in dialysis fistulas: treatment with percutanous angioplasty. Radiology 1987; 164: 693-7
86. Lumsden AB, MacDonald MJ, Kikeri D, Cotsonis GA, Harker LA, Martin LG: Prophylactic balloon angioplasty fails to prolong the patency of expanded polytetrafluoroethylene arteriovenous grafts: results of a prospective randomized study. J Vasc Surg 1997; 26: 382-90
87. Lay LPY, Ashleigh RJ, Tranconi L, Ackrill P: Result of angioplasty of Brescio-Cimino haemodialysis fistulae: medium-term follow-up. Clinical Radiology 1998; 53: 608-11
88. Lilly RZ, Carlton D, Barker J, Saddekni S, Hamrick K, Oser R, Westfall AO, Allon M: Predictors of arteriovenous graft patency after radiologic intervention in hemodialysis patients. Am J Kidney Dis 2001; 5: 945-53
89. Aruny JE, Lewis CA, Cardella JF, Cole PE, Davis A, Drooz AT, Grassi CJ, Gray RJ, Husted JW, Jones MT, McCowan TC, Meranze SG, Van Moore A, Neithamer CD, Oglevie SB, Omary RA, Patel NH, Rholl KS, Roberts AC, Sacks D, Sanchez O, Silverstein MI, Singh H, Swan TL, Towbin RB: Quality improvement guidelines for percutaneous management of the thrombosed or dysfunctional dialysis access. Standards of Practice Committee of the Society of Cardiovascular & Interventional Radiology. J Vasc Interv Radiol 1999; 10:491-8
