Vascular Access: global scenario - Annual Dialysis...

1

Creation and outcome of AV fistula

Surendra Shenoy M.D., Ph.D.

Section of Transplantation

Department of Surgery

Presentation outline

History of RRT

Role permanent access

Role of AVF as AV accessVein preservation

Pre surgical evaluation

Surgical techniques

Maturation evaluation

Maturation assist

Longterm followup

Management of complications

Outcome

Vascular access for Hemodialysiscreation and outcome of AVF

Disclosures

No specific disclosures pertaining to

the topic of presentation or the

materials discussed

Speaker will not be discussing

non FDA approved and investigational

products

Hemodialysis: External (access) shunts

Willem Johan Kolff

Belding H. Scribner

Internal (access) shunts

Brescia MJ, Cimino JE, Appel K , Hurwich BJ NEJM;1966:1089

Cimino Appel Brescia

Cimino Appel Brescia

Brescia Cimino AppelXXXXXXXXX

Brescia – Cimino fistula

Synonym

Distal Radiocephalic AVF

Vascular Access: global scenarioHealth care changes in US: Impact on VA

Social Security Amendments – 1972

All persons with ESRD eligible for medicare

Beneficiaries 10,000 (1970) to >150,000 (1990)

Assured reimbursementImproved access to healthcare

Physician’s Behavioral change

USRDS ADR Ch XII 1994

Patient profile: elderly, diabetics, ↑ co morbidities

Increased experience better care and longevity

2

AVG

Biologic

XenograftsAllograft

Cross linkedCross link

Synthetic

1978- Human Umbilical vein

(Biograft ®, Meadox Meds)- Saphenous vein

1972- Bovine carotid artery

(Artegraft ®, Artegraft Inc)

Non cross linked non antigenic

Cryopreserved(1985) antigenic

Non cross linked

1976

- ePTFE

Access problems and attempts to aid internal access (1972-1990)

Multitudes of sites with very little technical changes Snuff

box, high & low wrist fistula, brachiocephalic, Gracz’s,

basilic transposition UA, basilic transposition FA AVF

Same problems at different locations Not much invested to know why?

Anatomic suitability

Maturation period

Uncertainty of success

Background

Goodkin DA et.al. JASN 2003; 14: 3270

NKF-KDOQI (1995)

‘Fistula First’ (2003)

Access population differences

Access modality differences

Outcome differences

US ESRD population (200,000) ~ 80% AVG

Japan ESRD (175,00) ~ 85% AVF

European ESRD (30,000) ~ 80% AVF

Schena FP Kidney Int 2000; 57: S39-45

Strategies to improve ESRD mortality

Increased

dialysis dose

Decreased BP Phos control

Decreased LVH Better nutrition

Improved QOL

Williams AW. AJKD 2004;43:90 Kliger AS. CJASN 2009;4:S121

Quality of dialysis depends onfunctioning of vascular access

RAS inhibitors, statins, BP control, Phos control, fluid control etc.

(1990 - present)What is an Arteriovenous access?

AVA for dialysis

‘a conduit that gives access to patient’s

blood to provide adequate blood flow

to the dialyzer for cleansing’

Temporary PermanentPortsCatheters – Short term

– Long term(TDC)

AV Fistulae

AV grafts

AVG outcomeEarly Late

Failure to mature

DOQI <5% but probably 5-15%

• Around 25% within 6 mo

Thrombosis

Infection

Steal

Roy-Chaudhury, AJKD 2007:50:780 Chiang N. JVA 2014: online Huber TS. JVS 2003; 38:1005

1 Yr. Primary patency 23-47%

Cumulative patency 60-80%

Significant loss of patency with time

Graft body decay presenting as

Pseudoaneurysm,

Fibrous tissue ingrowth

AVG associated problemsNeed 3-5 weeks for safe cannulation

Average life of an AVG per site is ~2 yearsrequired ~ 2-3 procedures

AVF outcomeEarly Late

Thrombosis DAC 12-20%

Failure to mature 2-58%

Dember LM. JAMA 08: 2164-71

Chiang N. JVA 2014: online

AVF associated problemsNeed variable time to mature

AneurysmsNeedle access site problems

Steal

ThrombosisFailure to mature

Inadequate flowsInfection

Few thrombotic issues

Long term interventions 0.6 per functional year

Excellent long term outcome

3

UA cephalicLateral cephalic vein

Median cephalic vein

Median cubital

FA cephalic vein

Perforater veinAnterior branch basilic

UA basilicFA Basilic vein

Shenoy S. JVA 2009; 10 : 223

S.Shenoy©

Outflow

Superficial veins ‘primary options’

Deep veins ‘secondary option’

Radial artery

Ulnar artery

Brachial arteryInflow

S Shenoy©

AVA creation AV fistula - primary options

Anatomic snuff box

High and low radio-cephalic

Brachio-cephalic

Radio-median cephalic

Ulnar anterior basilic

Radio-basilic transposed

Proximal radial artery FA cephalic

Basilic transpostion

4

2

1

2

7× 2 =14

2 × 2 = 4

FA loop graft

Secondary options

UA loop graft

Clinical evaluationHistory of central vein abuse

Differential blood pressure

Arterial evaluation

Venous evaluation

Vein distention techniques1. Double tourniquets

2. Gravity

3. Tapping

4. Warmth

5. Exercise

Followed by duplex doppler ultra sound

Year Total Access

AV grafts

AV fistulae

% AVF

1993 65 51 14 22

1996 71 50 21 30 1998 158 82 76 48 1999 154 77 77 50 2000 125 50 75 60 2001 104 44 60 58 2003 83 36 48 57 2004 106 25 81 77 2005 179 26 153 86 2006 129 17 112 87

Washington University Single

surgeon experience

VascularLabUS

Surgeonviewed

US

Clinical exam

Pre KDOQI

Available options

& clinical

Evaluation

Primary

option

AVFFA/UA

1 stage

Primary

option

AVFFA/UA

2 stage

Primary

option

AVF Borderline

FA/UA

Secondary option

AVF AVG

Sup.

Vein

Deep

Vein

Fore

arm

Upper

arm

S. Shenoy©* Same option for a situation requires operator decision

** Algorithm does not take into account ‘early stick grafts’

Access planning – Tailoring access

Long

Expected

Survival

Short

Expected

Survival

Early

referral

Late

referral

On

dialysis

Early

referral

Late

referral

On

dialysis

1 2 3 4 6 5 7

1 2 3 3 4 3 5

1 2 5 2 4 2 3

1 2 3 4 6 5 7

1 2 3 3 4 3 5

1 2 3 2 4 2 5

1 2 3 3 5 4 6

1 2 5 3 4 2 4

1 2 5 2 4 2 3

Inflow

Central outflow

PeripheralOutflow

NAS(Needle access

Segment)

Stenosis is the cause for majority of access circuit failure

Capacity of the pump

diameter, stiffness & length

of the tubes

determines the flow

Physiology: AVA maturation & failure

AVG is NAS of the circuit

4

VNH Pathophysiology

Smooth muscle cell proliferation

Monocyte /Macrophage infiltration

Extracellular matrix deposition

Micro-vessel formation

Increase expression of cytokines TGF-

β1, PDGF, endothelin

Altered gene expression prior to the lesion

with up regulation of MCP-1, PAI-1, ET-1

Down regulation of TGF-β1Diskin CJ.N Clin Pra Neph 08;4:628

Roy-Chaudhry AJKD 07;50:782

Agarwal A. Am J Pathol 03; 1759

Proposed

mechanism Upstream events

Tissue quality

Surgical trauma

Genetic factors

Old vein injury

Blood flow changes

Down stream eventsIncreased production of free radicles

Upregulation of growth factors

Degradation of extra cellular matrix

Smooth muscle cell migrationVNH

Platelet activation

Approaches to mitigate biological responseSystemic therapy

Warfarin - Biggers JA et.al. Nepron 1977; 18: 109-13

Delays thrombosis but doesnot effect maturation

Aspirin - Harter HR et. al. NEJM 1979; 301: 577-79

- McCann RL et.al. Ann Surg 1980; 191: 328-339

- Endean ED et. al J Surg res 1986; 40: 297-304

- Andreucci VE et. al. DOPPS AJKD ‘04; 44:S61-7

- Yevzlin AS et.al. Sem Dial ‘06: 19: 535-39

Clopidogrel - Trimarchi H et.al Neph Cl Prct ‘06;102; c128-30

- Dember LM et. al. JAMA 2008; 299: 2164-71

Fish oil - Diskin CJ et. al. Nephron 1990; 155: 445-7

- Lok CE et. al. JAMA 2012; 307; 1809-16

Approaches to mitigate biological

response local therapy

Paclitaxil eluting mesh wrap(Angiotech)

Perivascular endothelial cell wrap

Conte M.S et.al. JVS ‘09; 50: 1359-68

Paulson WD et.al. NDT 2012; 27: 1219- 24

Peden EK et.al. JVA 2013; 14: 143-51

Coll - R: Sirolimus eluting wrapHuman pancreatic elastase

Why are we failing?

Vascular injury response

‘Neointimal response results with any form of

vascular injury including infection,

inflammation, immune injury, toxic exposure,

physical trauma (HTN, balloon catheter),

alteration in blood flow’

‘Intimal thickening is a stereotypic response of

vessel wall for any injury’

‘With restoration or normalization of the

endothelial cell layer intimal smooth muscle cells

can get back to their non proliferative state ….. ’

Robbins – Basic Pathology

Factors for AVF failure ’upstream events’

Technical

Handling of tissue

Clamp injury Suture material

Vein distention technique

Physiological

Suture technique

Tissue bands and kinks

Rheologic factors

Blood pressure

Tissue alignment

Shenoy S. et.al. JVS ‘03; 28:229 Tordoir JH Neph Dail Trans ‘03;18:378

Vassaloti JA. Sem Dial’ 04;17:243 Dember LM. JAMA 2008;299:2164

Cardiac outputBlood flow

Stripping adventitia destruction

of vassa vassorum

Demographics

Vessel quality/size

5

Alteration in configuration and blood flow are only 2

permanent factors related to creation of AVF

Physiology of AV access

Normal blood flow10 – 250 ml/min

With AVFblood flow increase600 -1200 ml/min

Intra operative increase250 -500ml/min

Increase in outflow vein 50- 100 fold

10-250 ml/min

250-500 ml/min

50-100 foldimmediate increasein the outflow vein

HypothesisAcute increase in the blood flow caused

by AV communication creates flow

related ‘stress zones’ in the access

circuit. Stress trauma that exceeds

physiological threshold results in injury

response (VNH). Flow modulation can

alter this stress in ‘stress zones’.……. S. Shenoy

Laminar blood flowSpiral Effect of flow on blood vesselsWall shear stress

(WSS)

Circumferential stress(Oscillatory or Hoop stress)

Stress/strain effects intact endothelial cell

morphologic and biochemical response

Prostacyclin and nitric oxide are vasodilatory

compounds, Endothelin -1 vasoconstrictor

Qui Y. J Vasc Res 2000; 37:147-57

Steady WSS is vasodilator, Oscillatory shear

vasoconstrictor, effect of combination enhances

vasodilator and inhibits vasoconstrictor based on the

stress phase angle

What does this mean?

Is there a clinical correlation?

Swing point stenosis(e.g. JAS)

6

Torsion and swing point stenosis

Shenoy S. JVS 2007; 152-154

Results of RCW AVF

‘Piggy back’ SLOT

N = 123

Exclusion = 9

End to side

N = 54

Side to side

N = 12

Piggy Back

N = 48

Mature vs. fail

(%)

36 : 18

(67 : 33)

9 : 3

(75 : 25)

40 : 8

(83 : 17)

Fail due to

Early JAS

8

44%

2

67%

2

20%

Late JAS8

22%

2

22%

1

2.5%

Total JAS16

30%

4

33 %

3

6%

Bharat A. JVS 2012; 55:274

Hull J. JVS 2013; 58:187-93

Computational fluid dynamic evaluation

Pressure drop is closely related to angleSLOT has the least shear stress

Post operative follow-up10-14 days

Wound healing problems

Infection, dehiscence, hematoma, lymphocoele

Vascular problems

Insufficiency, steal, venous hypertension,

thrombosis

Neurologic problems

Sensory, motor loss

If problems detected consider CDDUS

Venous side Arterial side

350-500 ml/min 350-500 ml/min

venous needle arterial needle

Needs of a well functioning access

AV Fistula

dialysis machine

Flow <600ml/minA good AVF 800-1200ml/min

>10cm straight NSS

<5mm deep from skin

Needle access segment (NAS)

K-DOQI

Rule of 6’s

US maturation evaluation

AVF flow 1.2 liter/min

Out flow vein 6-8cm diameter

>12cm long, 2-4 mm deep from skin

Objective evaluation

7

AVF 3-4 weeks

US evaluation

Meets maturation

criteria

Readyto use

Borderline 400-600ml/min

Exam - okay

Wait 4 more weeks

Mature

Good flows Poor vein

Poor<400ml/min

Exam - okay

Fistulograminflow study

No problem

UnlikelymatureEnhancement

Superficialization

Patch venoplasty


Clinical exam + Duplex

Initial post op visit

10-14 days

Non mature

Fistulogram

ProblemAngioplasty


WASHU experience

Inkollu S et.al. JVS 2016; 63: 1018-25

Superficial vein based AVF 89%

Basilic transposition (deep vein) 11%

Fistula needing 2º procedures for outflow veins 38.6%

N= 226

(2007 – 2013, N=585)

Superficialization (n=176)(78%)

Complex repair (n=50)(22%)

Forearm (n=32)(28%)

UA cephalic (n=14)(24%)

Forearm (n=73)(63%)

UA cephalic (n=42)(71%)

~ 40% of AVF show outflow vein problems

~ 80% of the outflow problems deeply situated veins

Flap elevation technique

Superficialization using flap elevation

Weyde W et.al. Kid Int. 2002; 61: 1170

Cull DL et.al. Ann Vasc Surg 2002; 16:84

Weyde W et.al. K I 2002

Forearm AVF 23 pts.

AVF patency 1yr 95.6%

Cull D. et.al. 45 pts.

Brachiocephalic 20

Radiocephalic 7

Brachiobasilic 8

Exclusion 10

AVF patency 1yr 53%

Conventional single incision technique

8

10 cms

Wound complications

Single incision techniques Minimal incision superficialization

Bharat A et.al. in Wilson SE (ed) Vasc Access 2012: p196-205


MIST results


Getting vein closer to skinLipectomy & Liposucction

Primary patency 1yr 71%

Primary patency 3 yr 63%

Secondary patency 3yrs 88%Bourquelot P et.al. J Vasc Surg 2009; 50:369


Secondary patency 2 yr 91%Maliska III CM et.al. J am Col Surg 2015;221: 1067

Suction assisted lipectomy 3 cases Krochmal DJ et.al. Can J Pl Surg 2010; 18: 25


Secondary patency 1yr 83%Ladenheim ED et.al. J Vasc Surg 2014; 15: 358

Vein enhancement techniques

Side branch venoplasty

Enhancement venopexy

Tortuous veins

Bifid veins

Complex reconstruction

Reconstruction with superficialization

….. S. Shenoy

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Tortuous veins Bifid veins

ESRD: RRT planningMultidisciplinary care : training the staffIMPACT study improved AVF/AV & mortality at 1Yr.

Care co-ordination: Role of access coordinatorHigher percentage started dialysis with AVF

Patient educationLower mortality & all cause hospitalization

Wilson SM, et. al. AJKD 2012; 60:435-43

Polkinghorne KR, et.al. AJKD 2009;53:99-106

Wu IW, et.al. Neph Dial Trans 2009;24:3426-33

Vein PreservationPatient referral for access evaluation: ?CKD stage 4 or earlier

Timing of creation ??AVF

AVG

Adverse effects of high flow

Central effects Peripheral Local

Uncommon

CHF Distal ischemia Aneurysms

occasional Common

AV stenosis diameters and flowswith varying mean blood pressures

Stenosis

diameter1mm 2 mm 3.5 mm

Stenosis

length (mm)

5 mm 60 mm 5 mm 60 mm 5 mm 60 mm

PressureMean (mmHg)

Blood flow (ml/min)

50

80

100

120

160

Hoganson D. J Vasc Acc 2014;15:409

AV stenosis diameters and flowswith varying mean blood pressures

Stenosis

diameter1mm 2 mm 3.5 mm

Stenosis

length (mm)5 mm 60 mm 5 mm 60 mm 5 mm 60 mm

PressureMean (mmHg)

Blood flow (ml/min)

50 117 40 626 329 2099 1338

80 896 475 3271 1888

100 1060 564 3761 2191

120 1207 642 4483 2469

160 269 117 1471 795 5103 3006

Hoganson D. J Vasc Acc 2014;15:409

Small diameters do not permit high flows

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Pathophysiology

Venous aneurysms are a result of

dilation of needle access

segment over a period of time

Every needle access heals with a scar

when the pressure in the system is

high the scar tends to thin out

resulting in aneurysmal dilation

……. S. Shenoy

Venous aneurysmsArea cannulation

AVF Cannulation related aneurysms

Clinical presentation and

Indications for aneurysm repair

UrgentEmergent Elective

•H/O Bleed

•Pulsatile clot

• No H/O Bleed

• Chronic Needle

access site ulcer

•Expanding

aneurysm

•Thinned out skin

Cannulation infiltration CV infectionsMost infections start with

small infiltration

Infiltrations more common

with higher pressure

Management options

Non-surgical

Surgical

CV infections and aneurysms

Aneurysms: Conservative management

Cannulation evaluation

Problem identification & prevention

Timely referral for evaluation

Treatment plan in place

Infections : conservative management

AVF autologous tissue : early infections

can be managed with antibiotics like any

other soft tissue infection

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When fistula outflow is superficial

Keep needle as parallel to skin as possible

Stick on side

of vessel

Not on top

Lateral approach

for cannulation may

prevent aneurysms

Short

tract

Surgical management Rest area of repair

Decide perioperative site for dialysis

Antibiotic coverage if needed

Excision of redundant skin and outflow

Reconstruction of outflow

Provision of healthy skin coverage

Management of outflow stenosis

And/or Inflow flow reduction

End to End

Tubular reconstruct

Techniques to plan for skin coverageRhomboid flap (Limberg flap)

Z-W plasty

Bi-convex advancement

Bi – convex advancement flap Hemodynamic changes - AVA

Normal flow to the limb 30-120 ml/min

Flow by 5 - 10 folds immediately in OR

Flow range for mature AVA 500-1200 ml/min

response to maintain distal circulation

UA AVF direct feed gets single vessel feed

Forearm vessels usually get dual inflow

Suding PN et.al. Sem Vasc Surg. 2007;20:184-8

Mickley V. Neph Dial Tx 2008;23:19-24

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Hemodynamics of

asymptomatic patients

High flows AVF

often cause decrease

in distal perfusion in less

compliant distal vessels

Normal compliant vessels

Hemodynamics of

symptomatic patients

distal vascular disease

Valentine RJ et.al. J Vasc. Surg. 2002;36:351-6

Tynan-Cuisinier GS et.al. Eu J Vas Eno V Surg. 2003;37:179-84

Any flow diversion can

become

symptomatic

in the presence of

distal vascular disease

IncidenceWith forearm arm access 1-2%

With upper arm 5-15%

With femoral access 16-36%

DiabeticsCoronary artery diseasePeripheral vascular diseaseTobacco use Female gender ~ equivocalHypertension - no good evidenceIncreased age – no good evidence

Population at risk

Stage I Asymptomatic retrograde flow

Stage II Pain on exertion, stress or dialysis

Stage III Rest pain

Stage IV Ischemic changes motor, sensory or cutaneous

Grade 0 No steal

Grade 1 Mild – cool extremity, no symptoms, flow augmentation

Grade 2 Moderate – intermittent ischemia with stress

Grade 3 Severe – ischemic pain at rest/tissue loss

Clinical classification of steal

Sidawy AN, et.al. JVS 2003;35:603-10

Mickley V. Neph. Dial Tx. 2008; 23:19-24

Clinical considerationAny symptom that is persistent e.g. pain, coolness, altered movements

associated with clinical signs of pallor, difference in temperature, should be further evaluated

Rest pain, loss of sensation, loss of movement require urgent clinical evaluation as they may be reversible

Irreversible problems result in functional/limb loss

Clinical management of stealAVG ~600 ml/min; AVF ~500ml/min

Symptomatic steal is due to distal limb ischemia

Ischemia can be reduced by increasing perfusion

Limb perfusion is function of blood flow and pressure

achieved with

Decreasing the fistula

flow

in high flow fistula

Increasing distal

perfusion

in low flow fistula

High flow Low flow

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Management of steal

LigationAccess loss but may be necessary

to prevent complications

High flow - Flow reductionPrecision Banding

Using tapered grafts

RUDI - Revascularization using distal inflow

DRAL – Distal radial artery ligation

Low flow – distal revascularizationDRIL (distal revascularization with interval ligation)

PAI (proximalization of arterial inflow)

Individual data with a protocol based approach AVF 79%

AVG 21%

Functional AVF maturation 81.7%

Committed to catheter 3.5%

AVF maturation (ITT) 72%

1 yr. Primary patency 42.5%

1 yr. Secondary patency 81.8 %

Median (range 1.2 - 97.7 mon) followup 36.1 mon

AVF procedures per functional year 0.68

Patient outcome >85% AVF

Hemodialysis fistula maturation (HFM) study by

NIH completed 602 patients from 7 institutions

SummaryHD is the back bone of life with ESRD

Longevity in HD is directly linked to dialysis dose

Modality of AV access should be tailored

Functional AVA is key to provide adequate dialysis

Goal is to provide the longest

lasting

access needing least number

of interventions

Summary

Hemodynamics play a key role in the development of access pathology

Technical alterations modulating hemodynamics have shown promising results

Duplex Doppler US has evolved as an essential tool in planning and management of AVA

Effective utilization of US along with anincreasing understanding of VA

hemodynamics has a potential to increasethe incidence of functional AVA

Vascular Access: global scenario - Annual Dialysis...

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