Volume 51, Issue 4, Pages 702-708 (April 2008)

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Vascular Access: Core Curriculum 2008

published online 04 March 2008.

Article Outline

• History

• Epidemiology

• Preoperative Vascular Mapping

• Vascular Access Monitoring and Surveillance

• Pathogenesis of Access Stenosis

• AV Fistulas

• AV Grafts

• Hemodialysis Catheters

• Catheter-Related Bacteremia (CRB)

• Acknowledgment

• Additional Readings

• Copyright

More than 90% of dialysis patients in the United States are on hemodialysis therapy. These patients require a reliable vascular access to deliver dialysis treatment thrice weekly. The ideal access would be: (1) easy to place, (2) ready for immediate use, (3) able to deliver sufficient blood flow to achieve adequate dialysis, (4) have a long patency, and (5) have a low rate of complications. None of the 3 types of vascular access (arteriovenous [AV] fistulas, AV grafts, and tunneled dialysis catheters) fulfill all these requirements (Table 1). Fistulas have the longest patency and require the fewest interventions after they are cannulated successfully for dialysis. However, they have the greatest primary failure rate and require the longest time for maturation (6 to 12 weeks). Grafts have a lower primary failure rate than fistulas and can be cannulated fairly quickly (within 2 to 3 weeks). However, they are prone to recurrent stenosis and thrombosis and have a greater frequency of salvage procedures (angioplasty, thrombectomy, and surgical revision) to maintain their long-term patency for dialysis. Finally, catheters are easily placed and can be used for dialysis immediately. However, they deliver lower blood flows, predispose to central vein stenosis, and have the greatest rates of thrombosis and infection. The Kidney Disease Outcomes Quality Initiative (KDOQI) Vascular Access guidelines promote an increase in fistula use for dialysis. An unintentional byproduct of increased fistula placement has been the concurrent increase in use of dialysis catheters. Optimizing vascular access outcomes requires advanced planning; close collaboration among nephrologists, access surgeons, radiologists, and dialysis staff; close monitoring and intervention for complications; and maintenance of prospective computerized access databases. Achieving this goal can be expedited by having dedicated access coordinators.

Table 1.

Comparison of Vascular Access Types


Feature	Fistula	Graft	Catheter
Primary failure rate (%)	20-50	10-20	<5
Time to first use (wk)	6-12	2-3	Immediate
Frequency of intervention	Very low	Moderate	High
Dialysis blood flow	Excellent	Excellent	Moderate
Frequency of thrombosis (after use for hemodialysis)	Very low	Moderate	High
Frequency of infection	Very low	Moderate (∼8/100 patient-years)	Very high (∼2 times/y/patient)
Longevity (after in use)	Longest (∼5 y)	Intermediate (∼2 y)	Shortest (<1 y)

History

I.First hemodialysis: 1924

II.First vascular access: 1943

III.Quinton-Scribner shunt: 1960 (Fig 1)

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Figure 1. Scribner shunt. The invention that made long-term hemodialysis possible in the early days was the removable U-shaped Teflon shunt connecting an artery to a vein in the arm of a patient. Reproduced with permission from Blagg et al.28

IV.Brescia-Cimino fistula: 1966

V.Synthetic polytetrafluoroethylene (PTFE) AV grafts: 1970s

VI.Permanent tunneled cuffed indwelling hemodialysis catheters: 1980s

VII.Synthetic polyurethane (Vectra; Thoratec Laboratories Corporation, Pleasanton, CA) AV grafts: 1990s

VIII.KDOQI Vascular Access guidelines first publicized in 1997, revised in 2001 and 2006. Highlights include:

A.Concerted measures to increase fistula placement and maturation

B.Concerted efforts to minimize use of dialysis catheters

C.Earlier guidelines strongly promoted surveillance for graft stenosis; latest version is more equivocal about its value

Epidemiology

I.More than 20% of dialysis patient hospitalizations are access related

II.Vascular access complications are associated with morbidity and mortality

III.Adjusted mortality is 40% to 70% greater in patients dialyzed through a catheter than those dialyzed through a fistula or graft. Mortality risk decreased in patients switched from catheter to AV access compared with patients who remain catheter dependent

IV.Fistula prevalence is lower in United States than Europe or Japan

V.Fistula prevalence varies by geographic region in United States:

A.Northeast and Northwest: 49% to 57%

B.Midwest: 36% to 42%

C.Southwest: 36% to 48%

D.Southeast: 30% to 35%

VI.75% of US patients initiate dialysis therapy with a catheter

VII.Fistula First initiative has increased both fistula and catheter use in United States

Preoperative Vascular Mapping

I.Routine preoperative vascular mapping with ultrasonography or venography increases fistula placement

II.High primary fistula failure persists despite preoperative mapping

III.Elements of preoperative mapping:

A.Minimum vein diameter, 2.5 mm for fistula

B.Minimum vein diameter, 4 mm for graft

C.Minimum artery diameter, 2 mm for fistula or graft

D.Exclude stenosis or thrombosis of proximal vein

IV.Order of preference of vascular access to be placed:

A.Distal (radiocephalic) fistula

B.Proximal (brachiocephalic) fistula

C.Proximal transposed brachiobasilic fistula

D.Upper-extremity graft

E.Thigh graft

F.Unusual grafts: necklace, unilateral chest wall

Vascular Access Monitoring and Surveillance

I.Identify access dysfunction as early as possible

II.Establish a monitoring/surveillance program

III.Clinical monitoring:

A.Physical examination: absent thrill, abnormal bruit, or distal edema; pulsatile swelling aneurysm (fistula) or pseudoaneurysm (graft)

B.Dialysis abnormalities: difficult cannulation, aspiration of clots, or prolonged bleeding from needle site

C.Unexplained decrease in Kt/V on constant dialysis prescription

IV.Access surveillance parameters (abnormal values in parentheses):

A.Static dialysis venous pressures (DVPs; ratio of DVP to systemic blood pressure >0.4)

B.Access blood flow (<600 mL/min or decrease by >25% from baseline)

C.Doppler ultrasound: peak systolic velocity (PSV) ratio greater than 2:1

D.Dynamic DVP and recirculation are not useful

V.Positive predictive value for greater than 50% stenosis is 70% to 100% for clinical monitoring, static venous pressures, flow monitoring, or duplex ultrasound

VI.Grafts with abnormal monitoring or surveillance should be referred for angioplasty

VII.Preemptive angioplasty should be performed if greater than 50% stenosis (technical success: <30% residual stenosis)

VIII.Approximately 50% of grafts with stenosis remain patent without preemptive angioplasty

IX.Approximately 25% of graft thrombosis not preceded by abnormal monitoring/surveillance results

X.Five of 6 randomized clinical trials did not observe decreased graft thrombosis or prolonged graft patency with surveillance and preemptive angioplasty

Pathogenesis of Access Stenosis

I.Stenosis due to venous neointimal hyperplasia (VNH)

II.VNH formed by smooth muscle cells, microfibroblasts, and microvessels

III.Cytokines (platelet-derived growth factor, endothelial growth factor, etc) modulate VNH progression

IV.Other potential factors for VNH:

A.Hemodynamic turbulence and shear forces

B.Dialysis needle injury

C.Surgical vascular damage

D.Uremia

E.Vascular damage from angioplasty

F.Expression of genes for cytokines

V.Novel therapies (local antiproliferative drug delivery systems) have decreased graft stenosis in animal models. Human studies are in progress (Fig 2)

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Figure 2. From pathogenesis to pathology to novel therapies. This figure identifies the different pathogenetic mechanisms that result in dialysis access stenosis and directs attention to potential novel therapies. Pathogenetic factors include hemodynamic and surgical stressors, inflammatory stimuli from dialysis needles and polytetrafluoroethylene (PTFE) graft material, and the unavoidable vascular injury that occurs at the time of angioplasty. Novel therapeutic modalities include perivascular drug delivery, drug-eluting stents, coated grafts, and novel balloons. Reproduced with permission from Roy-Chaudhury et al.24

AV Fistulas

I.Direct anastomosis between artery and vein

II.Three major types: radiocephalic (forearm), brachiocephalic (upper arm), transposed brachiobasilic (upper arm; Fig 3)

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Figure 3. Anatomy of arteriovenous (AV) fistulas (AVFs). The brachial artery bifurcates at the antecubital fossa into the radial and ulnar arteries, which perfuse the forearm. The cephalic vein runs superficially from the wrist to the shoulder on the radial (lateral) side. The basilic vein runs deep from the wrist to the shoulder on the ulnar (medial) side. The cephalic and basilic veins merge into the axillary vein near the shoulder. (A) A radiocephalic fistula is created by anastomosis of the end of the cephalic vein to the side of the radial artery near the wrist. (B) A brachiocephalic fistula is created by anastomosis of the end of the cephalic vein to the side of the brachial artery near the antecubital fossa. (C) A transposed brachiobasilic fistula is created by anastomosis of the end of the basilic vein to the side of the brachial artery near the antecubital fossa. Because the basilic vein runs deep and medial, the surgeon creates a longitudinal incision from the antecubital fossa to the shoulder. The basilic vein then is teased out of its native bed and tunneled superficially and laterally before its anastomosis to the artery to ensure ease of cannulation.

III.Time to cannulation: 6 to 12 weeks

IV.High primary failure rate (∼40%):

A.Early thrombosis

B.Failure to mature

C.Steal syndrome (1% to 4%)

V.Factors associated with primary failure: age older than 65 years, female sex, nonwhite race, cardiovascular disease, peripheral vascular disease, obesity

VI.Postoperative ultrasound to evaluate maturation (4 to 6 weeks after surgery)

VII.Ultrasound criteria for maturity:

A.Fistula diameter, 4 mm or greater

B.Access flow, 500 mL/min or greater

C.Distance from skin, 5 mm or less

VIII.Common anatomic lesions contributing to immaturity:

A.Juxta-anastomotic stenosis (repair by angioplasty or surgical revision)

B.Large accessory veins (can be ligated surgically or treated by coil embolization)

C.Excessively deep fistula (can be superficialized)

IX.Correction of anatomic lesions may convert immature to mature fistula

X.Late fistula failure is caused by stenosis:

1.60% at the venous outlet

2.25% at the arterial anastomosis

3.5% at central vessels

4.Rarely, a large aneurysm (unrelated to stenosis) may cause late fistula failure if surgical revision is not feasible

XI.Fistulas require 3- to 4-fold fewer interventions than grafts to maintain long-term patency for dialysis

XII.Thrombosed fistula requires thrombectomy within 48 hours (high technical success)

XIII.Primary patency after thrombectomy: 27% to 81% at 6 months; 18% to 70% at 1 year

AV Grafts

I.PTFE bridge interposed between artery and vein

II.Time to first cannulation: 2 to 3 weeks (24 to 48 hours for Vectra)

III.Primary failure: 15% to 20% (less than for fistulas)

IV.Causes of graft failure:

A.Thrombosis (∼80%)

B.Infection (∼20%), usually requires surgical excision

C.Occasionally graft failure may be due to a large pseudoaneurysm that is leaking or infected

V.Underlying stenosis in most thrombosed grafts:

A.Venous anastomosis (∼60%)

B.Venous outlet (15%)

C.Central veins (10%)

D.Intragraft (10%)

E.Arterial anastomosis (5%)

VI.Intervention-free patency after elective angioplasty: 70% to 85% at 3 months, 20% to 40% at 12 months

VII.Intervention-free patency after thrombectomy: 33% to 63% at 3 months, 10% to 39% at 6 months

VIII.Short-lived benefit of angioplasty: access flow back to preangioplasty level in 20% at 1 week and 40% at 1 month

IX.Stents may prolong patency in selected grafts (elastic lesion):

A.Metal stent (eg, nitinol) may require antiplatelet agent, such as clopidogrel

B.PTFE-covered stents potentially may improve patency compared with metal stents (limited data)

X.No clear advantage of bovine or cadaveric human vein grafts over PTFE grafts. Polyurethane (Vectra) grafts can be cannulated within 24 hours of use versus 2 weeks for PTFE grafts; they may be useful in patients with recurrent catheter dysfunction

Hemodialysis Catheters

I.May be nontunneled (temporary) or tunneled (more permanent)

II.Double-lumen and semirigid catheters made of polyurethane, polyethylene, or PTFE

III.Preferred sites of insertion:

A.Right internal jugular vein

B.Left internal jugular (IJ) vein

C.Subclavian vein

D.Femoral vein (if all thoracic veins occluded)

E.Translumbar or transhepatic (last resort)

IV.Catheter thrombosis prevented by using intraluminal anticoagulant (heparin or citrate)

V.Catheter thrombosis treated by instillation of thrombolytic agents (urokinase or tissue-type plasminogen activator); catheter exchange if unsuccessful

VI.Approximately 25% symptomatic ipsilateral deep vein thrombosis with femoral catheter

VII.May cause central vein stenosis (more common with subclavian than IJ)

VIII.Central vein stenosis presents with ipsilateral upper-extremity edema. Some patients have prominent chest wall collateral veins

IX.Treatment of central vein stenosis by using angioplasty (poor patency with or without stent placement)

X.Fibrin sheaths may occasionally encase the catheter tip, thereby impairing flow. Treatment requires balloon disruption or snare and removal of fibrin sheath by femoral approach

Catheter-Related Bacteremia (CRB)

I.Less likely with tunneled than nontunneled catheters

II.Frequency: 2.0 to 5.5 episodes/1,000 catheter-days

III.Suspected when patient has fever or chills; confirmed by positive catheter and peripheral blood culture results

IV.Serious complications in 5% to 10% of patients with CRB: endocarditis, osteomyelitis, septic arthritis, epidural abscess, death

V.60% to 70% caused by gram-positive organisms, 30% to 40% caused by gram-negative rods

VI.3 weeks of intravenous (IV) antibiotics for uncomplicated CRB

VII.Systemic antibiotics alone result in 75% recurrent infection

VIII.Catheter removal mandatory with persistent fever or bacteremia on antibiotic therapy or tunnel-track infection

IX.Guidewire exchange of catheter possible if fever resolves on antibiotic therapy

X.Catheter biofilm is the major source of CRB

XI.Antibiotic lock (concentrated antibiotic-heparin solution instilled into catheter lumen after dialysis) can kill bacteria in the biofilm

XII.IV antibiotics plus antibiotic lock cures CRB with catheter salvage in approximately two thirds of cases (Fig 4)

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Figure 4. Clinical approach to management of dialysis catheter–related bacteremia (CRB). In catheter-dependent patients with suspected CRB (fever or rigors), after blood cultures (BCs) are obtained, empiric antibiotic therapy (Abx) is started with vancomycin (for coverage of methicillin-resistant Staphylococcus species) and ceftazidime or gentamicin (for broad-spectrum gram-negative coverage). In conjunction, an antibiotic lock (Fig 4) is instilled into each catheter lumen at the end of the dialysis session. Abx is discontinued in patients with negative culture results. If culture results are positive for coagulase-negative Staphylococcus species or gram-negative bacilli, the 2 treatment options are to: (1) continue appropriate systemic Abx with an antibiotic lock or (2) exchange the infected catheter over a new one over a guidewire. If fever and bacteremia persist despite antibiotic therapy, the catheter is removed and workup (WU) is initiated for metastatic infection. In infections caused by Staphylococcus aureus or Candida species, catheter replacement is mandatory. Abbreviations: HD, hemodialysis; CVC, central venous catheter; ECHO, echocardiography; Ampho B, amphotericin B. Adapted with permission from Allon.2

XIII.Success of antibiotic lock depends on organism: 87% to 100% for gram-negative, 75% to 84% for Staphylococcus epidermidis, and 40% to 55% for Staphylococcus aureus

XIV.Prophylaxis of CRB was reported with a variety of antibiotic locks, 30% citrate, or taurolidine. None is currently approved by the US Food and Drug Administration for this indication

Acknowledgements

Support: None.

Financial Disclosure: None.

Additional Readings

1. 1National Kidney Foundation: KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Vascular Access 2006. Am J Kidney Dis. 2006;48(suppl 1):S176–S322.

2. 2Allon M. Dialysis catheter-related bacteremia: Treatment and prophylaxis. Am J Kidney Dis. 2004;44:779–791.

3. 3Allon M. Current management of vascular access. Clin J Am Soc Nephrol. 2007;2:786–800.

4. 4Feldman HI, Kobrin S, Wasserstein A. Hemodialysis vascular access morbidity. J Am Soc Nephrol. 1996;7:523–535.

5. 5Pisoni RL, Young EW, Dykstra DM, et al. Vascular access use in Europe and in the United States: Results from the DOPPS. Kidney Int. 2002;61:305–316.

6. 6Stehman-Breen CO, Sherrard DJ, Gillen D, Caps M. Determinants of type and timing of initial permanent hemodialysis vascular access. Kidney Int. 2000;57:639–645.

7. 7Allon M, Daugirdas JT, Depner TA, Greene T, Ornt D, Schwab SJ. Effect of change in vascular access on patient mortality in hemodialysis patients. Am J Kidney Dis. 2006;47:469–477.

8. 8Xue JL, Dahl D, Ebben JP, Collins AJ. The association of initial hemodialysis access type with mortality outcomes in elderly Medicare ESRD patients. Am J Kidney Dis. 2003;42:1013–1019.

9. 9Agarwal AK, Patel BM, Haddad NJ. Central vein stenosis: A nephrologist’s perspective. Semin Dial. 2007;20:53–62.

10. 10Allon M, Lockhart ME, Lilly RZ, et al. Effect of preoperative sonographic mapping on vascular access outcomes in hemodialysis patients. Kidney Int. 2001;60:2013–2020.

11. 11Robbin ML, Gallichio ML, Deierhoi MH, Young CJ, Weber TM, Allon M. US vascular mapping before hemodialysis access placement. Radiology. 2000;217:83–88.

12. 12Silva MB, Hobson RW, Pappas PJ, et al. A strategy for increasing use of autogenous hemodialysis access procedures: Impact of preoperative noninvasive evaluation. J Vasc Surg. 1998;27:302–308.

13. 13Asif A, Cherla G, Merrill D, Cipleu CD, Briones P, Pennell P. Conversion of tunneled hemodialysis catheter-consigned patients to arteriovenous fistula. Kidney Int. 2005;67:2399–2406.

14. 14Beathard GA, Arnold P, Jackson J, Litchfield T. Aggressive treatment of early fistula failure. Kidney Int. 2003;64:1487–1494.

15. 15Moist LM, Hemmelgarn BR, Lok CE. Relationship between blood flow in central venous catheters and hemodialysis adequacy. Clin J Am Soc Nephrol. 2006;1:965–971.

16. 16Ram SJ, Work J, Caldito GC, Eason JM, Pervez A, Paulson WD. A randomized controlled trial of blood flow and stenosis surveillance of hemodialysis grafts. Kidney Int. 2003;64:272–280.

17. 17Robbin ML, Oser RF, Lee JY, Heudebert GR, Mennemeyer ST, Allon M. Randomized comparison of ultrasound surveillance and clinical monitoring on arteriovenous graft outcomes. Kidney Int. 2006;69:730–735.

18. 18Malik J, Slavikova M, Svobodova J, Tuka V. Regular ultrasound screening significantly prolongs patency of PTFE grafts. Kidney Int. 2005;67:1554–1558.

19. 19Poole CV, Carlton D, Bimbo L, Allon M. Treatment of catheter-related bacteremia with an antibiotic lock protocol: Effect of bacterial pathogen. Nephrol Dial Transplant. 2004;19:1237–1244.

20. 20Beathard GA. Catheter management protocol for catheter-related bacteremia prophylaxis. Semin Dial. 2003;16:403–405.

21. 21Beathard GA, Welch BR, Maidment HJ. Mechanical thrombolysis for the treatment of thrombosed hemodialysis access grafts. Radiology. 1996;200:711–716.

22. 22Oliver MJ, McCann RL, Indridason OS, Butterly DW, Schwab SJ. Comparison of transposed brachiobasilic fistulas to upper arm grafts and brachiocephalic fistulas. Kidney Int. 2001;60:1532–1539.

23. 23Dixon BS. Why don’t fistulas mature?. Kidney Int. 2006;70:1413–1422.

24. 24Roy-Chaudhury P, Sukhatme VP, Cheung AK. Hemodialysis vascular access dysfunction: A cellular and molecular viewpoint. J Am Soc Nephrol. 2006;17:1112–1127.

25. 25Robbin ML, Chamberlain NE, Lockhart ME, et al. Hemodialysis arteriovenous fistula maturity: US evaluation. Radiology. 2002;225:59–64.

26. 26Lok CE, Allon M, Moist LM, Oliver MJ, Shah H, Zimmerman D. REDUCE FTM I (Risk equation determining unsuccessful cannulation events and failure to maturation in arteriovenous fistulas). J Am Soc Nephrol. 2006;17:3204–3212.

27. 27Allon M, Robbin ML. Increasing arteriovenous fistulas in hemodialysis patients: Problems and solutions. Kidney Int. 2002;62:1109–1124.

28. 28Blagg CR. The early history of dialysis for chronic renal failure in the United States: A view from Seattle. Am J Kidney Disease. 2007;49:482–496.

Division of Nephrology, University of Alabama at Birmingham, Birmingham, AL.

Address correspondence to Michael Allon, MD, Division of Nephrology, PB, Rm 226, 728 Richard Arrington Blvd, Birmingham, AL 35294.

PII: S0272-6386(08)00045-0

doi:10.1053/j.ajkd.2007.10.046

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