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Cephalic arch and

Central venous stenoses:

best practices

AQ Urbanes, MD

ASDIN Annual Scientific Meeting

25. February 2012

Disclosures

Vice-President, Lifeline Vascular Access

Consultant, Bard PV

Cephalic arch

Deltopectoral groove

Clavipectoral faschia

Multifactorial causes of arch pathology

• shear stress

– high flow

– angulation of vein

• relatively immobile

– tethered to fascia and muscle

– impaired remodeling

• hypertrophied valves

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Extent of the problem

• 15-40% of dysfunctional fistulae

• brachiocephalic >> radiocephalic

• non-DM > DM

• high-flow AVF

• Ca x iP product

• ESRD 2o renovascular disease

Hammes NDT 2009; 24 (7): 2190.

Heerwagen J Vasc Access 2010; 11 (1): 41.

Jaberi J Vasc Access 2007; 8 (4): 287.

Rajan JVIR 2003; 14 (5): 567.

What is the problem?

• resistant to high-pressure balloons

• non-durable results

• prone to rupture

• endovascular stents may limit future surgical options

– translocation

– use of basilic/axillary venous outflow

Non-surgical options

6 mo. 1o patency 12 mo. 1o patency

#

procedures/patie

nt year

Rajan (PTA only) 83 ± 8 75 ± 10 1.6

Shemesh (BMS vs.

stent-graft)

BMS

stent-graft

39.1

81.8

0

31.8

1.9

0.9

Heerwagen (CBA) 81 ± 10 38 ± 14 0.9

Miller (inflow

reduction)76 57 0.9

Heerwagen J Vasc Access 2010; 11 (1): 41.

Miller J Vasc Access 2010; 11 (4): 281.

Rajan JVIR 2003; 14 (5): 567.

Shemesh J Vasc Surg 2008; 48 (6): 1524.

Surgical options

Chen Ann Vasc Surg 2005: 19 (5); 629.

Surgical outcomes

Chen 2005 Kian 2008

n 7 13

immediate surgical success 86% 100%

primary patency15.7 ± 14.3 months

(range = 0 to 39)

6 mo. primary patency

before revision

after revision

8%

69%

12 mo. primary patency

before revision

after revision

0%

39%

# interventions per patient year

before surgery

after surgery 0.54

3.5

1.0

Chen Ann Vasc Surg 2005: 19 (5); 629.

Kian Semin Dialysis 2008: 21 (1); 93.

Review

6 mo. 1o patency 12 mo. 1o patency

#

procedures/patie

nt year

Rajan (PTA only) 83 ± 8 75 ± 10 1.6

Shemesh (BMS vs.

stent-graft)

BMS

stent-graft

39.1

81.8

0

31.8

1.9

0.9

Heerwagen (CBA) 81 ± 10 38 ± 14 0.9

Miller (inflow

reduction)76 57 0.9

Kian (surgery) 69 39 1.0

Heerwagen J Vasc Access 2010; 11 (1): 41.

Miller J Vasc Access 2010; 11 (4): 281.

Rajan JVIR 2003; 14 (5): 567.

Shemesh J Vasc Surg 2008; 48 (6): 1524.

Kian Semin Dialysis 2008: 21 (1); 93.

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Best practices

• Anticipate the problem– high-flow mature brachiocephalic AVF

• Treat the patient, not the lesion– clinical presentation

– multi-segment stenoses

– judicious angioplasty

• Treatment choices– PTA

– then ?• endovascular stenting vs. flow re-equilibration vs. both

– vessel translocation

Central venous stenosis

Etiology

• central venous catheters

• PICC

• cardiac rhythm devices (PPM/AICD)

• not associated with hardware

Central venous catheter & stenosis

• risk is related to

– side (left 2x risk vs. right)

– vein (subclavian 42% > IJ 10%)

–multiple catheters

– duration of catheter use

• no data relating risk to catheter caliber

Catheter-related injury

• underlying venous pathology in CKD

• injury during or after insertion

• mechanical irritation

• inflammation from catheter-related infection

• irritation to endothelium during cardiac and

respiratory motion

normal vs. CKD vein

Feinfeld 1999. AJKD. 34: 702.

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Cephalic wall ∆s in CKD

Change number %

intimal hyperplasia 20 100%

wall collagenosis 20 100%

disruption/loss of internal elastic lamina 9 45%

disruption/loss of endothelial cell layer 6 30%

muscle loss or atrophy 6 30%

mucoid or myxoid degeneration 6 30%

inflammatory reaction – erythrocyte/histiocyte infiltration 5 25%

mural calcification 3 15%

telangiectasia 2 10%

Wali 2006. Ann Thorac Cardiovasc Surg. 12: 341.

Review

• Vascular hardware use is the single most important modifiable factor in the genesis of CV disease.

• Changes consistent with neo-myointimalhyperplasia are present in the CKD patient even before access creation.

• Changes are mediated by neuro-humoralmechanisms which are more prominent in the uremic environment.

Clinical presentation

from G Beathard, MD

Central venous stenosis

Subclavian vein log-jamming

Brachiocephalic vein stenosis

with collaterals

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Prevalence of Central Venous disease

• in general population

– not known

Prevalence

GroupIncidence of

Central Venous disease

CKD (-)

hardware (+)

hardware (-)

4.4% asymptomatic

25-50% asymptomatic

CKD (+)

hardware (-) vascular access (-)

hardware (-) vascular access (+)

hardware (+) vascular access (-)

hardware (+) vascular access (+)

30-65% asymptomatic

41% asymptomatic

65% asymptomatic

71% symptomatic

Sticherling 2001. Am Heart J. 141: 183.

Gonsalvez 2003. Cardiovasc Interven Radiol. 26: 123.

Teruya 2003. Ann Vasc Surg. 17: 526.

Taal 2004. NDT. 19: 1542.

Lickfett 2004. Europace. 6: 25.

MacRae 2005. ASAIO. 51: 77.

Oginosawa 2005. Pacing Clin Electrophysiol. 28: 425.

Review

• Incidence of CV disease in generalpopulation is not known.

• Vascular hardware increases incidence of CV disease in both CKD and non-CKD population.

• The contribution of a peripheral AV access to the development of CV disease is not well established. ? More likely symptomatic

When to treat

Treated Not treated

n 62 24

BC/SC 32/30 15/8

% stenosis 74 72

progression 88% 17%

stenosis

progression0.50 %/day 0.25 %/day

Treated

(+sx)

Not treated

(-sx)

n 50 53

prior cath

use

48% 26%

1o 6 mo.

patency

lesion

access

68 ± 6

68 ± 6

77 ± 6

72 ± 7

1o 12 mo.

patency

lesion

access

55 ± 4

50 ± 4

77 ± 6

66 ± 5

2o 12 mo.

patency89 ± 5 100

Levit Radiology 2006; 238 (3): 1051.

Renaud NDT; epub 26 Aug 2011.

PTA only

Author #6 mo 1o

patency

12 mo

1opatency

12 mo

2opatency

Ozyer 2009 94 83 77

Bakken 2007 47 62 29 73

Maya 2007 32 38 20

Surowiec 2004 35 43 80

Quinn 1995 10 23 12 100

Kovalik 1994 30 50

Wisselink 1993 15 36 86

Beathard 1992 27 29

12 mo. 2o patency 73-100% for PTA only

Stent after failed PTA or recurrence

Author Stent n6 mo.

1opatency

12 mo.

1opatency

12 mo.

2opatency

Kundu 2011 PTFE 14 100 100

Jones 2011 PTFE 30 81 45

Anaya-Ayala 2011 PTFE 25 56 100

Ozyer 2009 mix 43 68 33

Rajan 2007 nitinol 6 67 67 100

Maya 2007 mix 23 33 19 64

Sprouse 2004 mix 29 50 100

Vogel 2004 nitinol 16 74 67 55

Aytekin 2004 mix 14 50 14 55

Quinn 2003 PTFE 6 40 32 39

Oderich 2000 mix 37 41 18 59

Vesely 1998 Wallstent 20 42 25 56

Gray 1995 Wallstent 32 46 20 33

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Author Stent n6 mo.

1opatency

12 mo.

1opatency

12 mo.

2opatency

Kundu 2011 PTFE 14 100 100

Jones 2011 PTFE 30 81 45

Anaya-Ayala 2011 PTFE 25 56 100

Quinn 2003 PTFE 6 40 32 39

Ozyer 2009 mix 43 68 33

Maya 2007 mix 23 33 19 64

Sprouse 2004 mix 29 50 100

Aytekin 2004 mix 14 50 14 55

Oderich 2000 mix 37 41 18 59

Rajan 2007 nitinol 6 67 67 100

Vogel 2004 nitinol 16 74 67 55

Vesely 1998 Wallstent 20 42 25 56

Gray 1995 Wallstent 32 46 20 33

12 mo. 2o patency 39-100% for stent-grafts

12 mo. 2o patency 55-100% for BMS

Flow re-equilibration

• Premise:

– Central venous disease is not uncommon in CKD.

– Central venous disease is not symptomatic until an

access is created.

– Presence of vascular access causes dysequilibrium

of a previously compensated system.

– Inflow reduction returns patient to equilibrium.

Flow re-equilibration

• Inflow reduction

– 22 patients with symptomatic central venous

hypertension

– inflow reduction performed

• Qa 1640 mL/min to 840 mL/min

– 20/22 successful

• 2/22: thrombosis; aneurysm formation

–mean follow-up 8 months

– patency data pending

Jennings 2011. J Vasc Access. epub 10.11.2011

Review

12 month secondary patency

Treatment Patency

PTA only 73-100%

BMS

stent-graft

55-100%

39-100%

Surgery

Author #6 mo. 1o

patency

12 mo. 1o

patency

12 mo. 2o

patency

Illig 2011 12 75

Dammers 2003 10 75 75

Mickley 2001 6 83 100

El-Sabrout 1999 9 88 100

Haug 1999 6 100 100

Bhatia 1995 13 92 83 100

Surgical options

• access ligation or reduction of flow

– flow re-equilibration

– allow just enough flow that the collateral circulation can handle

• extra-anatomic bypass

– jugular vein turn-down

– subclavian vein to EJ or IJ bypass

– axillary to femoral vein bypass

– high morbidity; uncommonly done

• largest series in publication with n=13

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Surgical option

• HeRO® graft

HeRO®

(hemodialysis reliable outflow)

HeRO intended use

• HeRO® vascular access device is intended for

use

– in maintaining long-term vascular access

– for chronic hemodialysis patients

– exhausted peripheral venous access sites suitable

for fistulae or grafts

• FDA classifies the HeRO® device as a graft

HeRO patient candidates

• catheter-dependent or approaching catheter-

dependency

• non-candidates for fistulae or grafts

• compromised central venous circulation

HeRO® components

outflow (catheter) component

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titanium connector

ePTFE catheter

titanium connector

stenosis ≠ stenosis

Itkin. JVIR 2004: 15 (1); 51-56.

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BEFORE AFTER

Effect of respiration

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Best practices

• Prevention

• Treat the patient, not the lesion– anatomy, imaging, position, respiration

– clinical presentation

– judicious angioplasty

• Treatment choices– PTA

– endovascular stenting• stent-graft vs. BMS

– flow re-equilibration

– HeRO® graft

– surgical repair