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2/29/2012
1
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
2/29/2012
2
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.
2/29/2012
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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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4
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
2/29/2012
7
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
2/29/2012
8
titanium connector
ePTFE catheter
titanium connector
stenosis ≠ stenosis
Itkin. JVIR 2004: 15 (1); 51-56.
2/29/2012
9
BEFORE AFTER
Effect of respiration
2/29/2012
10
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
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