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Central vein stenosis (CVS) is commonly seen in patients receiving hemodialysis through an arteriovenous
access, threatening the usability of arteriovenous access for dialysis. Subclavian and internal jugular catheters
are prime reasons for the development of CVS, especially in the setting of long-term use of multiple catheters.
CVS related to cardiac rhythm devices also is seen frequently. Idiopathic CVS can be encountered, although it
is less common. Clinical features ultimately become sufficiently prominent to prompt angiographic evaluation.
CVS should be evaluated carefully because management must be individualized. The primary method for
treatment of CVS is endovascular intervention, including angioplasty and stent placement, whereas surgical
options should be pursued in only refractory cases due to the invasiveness of the intervention. Early referral of
patients for chronic kidney disease care; timely discussion of kidney replacement modality choices, including
nonhemodialysis options such as peritoneal dialysis and kidney transplantation; placement of arteriovenous
access prior to the onset of dialysis; and avoidance of catheters and other central vein instrumentation will
prevent the development of CVS in most patients with kidney disease.
Am J Kidney Dis. 61(6):1001-1015. © 2013 by the National Kidney Foundation, Inc.
INDEX WORDS: Central vein stenosis; dialysis access; dialysis catheter complications; tunneled dialysis
catheter; vascular access.
with various accesses using duplex ultrasonography rence of CVS in HD patients has been reported on the
or angiography have reported CVS prevalences of ipsilateral side of the AV access without a history of
19%-41%.6-8 The occurrence of CVS with internal previous CVC placement and is considered to be due
jugular catheters also has been demonstrated increas- to increased flow and abnormal shear stress on the
ingly in more recent studies. Long-term femoral vein side of access.11,12 Compression of the innominate
catheters also are being used more frequently for vein between arch vessels and the sternum also can
dialysis, and iliac vein and inferior vena cava stenoses occur.13 The following sections review risk factors for
are not uncommon. the occurrence of CVS in patients undergoing CVC or
Although longer catheter duration has been impli- device placement.
cated in CVS, temporary (nontunneled) dialysis cath-
eters also have been associated with CVS (Fig 4A and Number and Duration of CVCs
B). For example, a recent study of color Doppler Irrespective of the location (subclavian or internal
sonography of 100 consecutive patients receiving jugular), a larger number and longer duration of CVC
temporary double-lumen dialysis catheters showed use increases the risk of developing CVS.4,14 In one
CVS in 18%.9 study of subclavian vein stenosis, the mean number of
ipsilateral subclavian catheters was 1.6, and mean
Cause of and Risk Factors for CVS
duration of catheter use was 5.5 weeks.3 Further, a
CVS is associated with intravascular device or prospective study of 42 consecutive subclavian vein
central catheter placement in most cases, although it catheterizations demonstrated that stenosis more of-
occasionally can be idiopathic (Box 1). Preoperative ten was persistent (vs spontaneous recanalization) at 6
venography of patients prior to right internal jugular months in those with a larger number of inserted
vein tunneled catheter placement showed the presence catheters (2.0 vs 1.6), longer dwell time (49 vs 29
of CVS or angulation in 30% of patients without a days), more dialysis sessions through the catheter (21
history of central catheter placement.10 The occur- vs 12), and more catheter-related infections (66.6% vs
33.3%).15
Box 1. Causes of Central Vein Stenosis in Dialysis Patients
Related to intravascular device
Location of CVC
Central vein catheters Anatomical configuration can expose a vein to a
Tunneled dialysis catheters unique degree of contact with catheters. Initial studies
Nontunneled dialysis catheters
Peripherally inserted central catheters
demonstrated a much higher prevalence of CVS with
Other central venous catheters and ports subclavian dialysis catheters (42%) than with internal
Cardiac rhythm devices jugular dialysis catheters (10%).16 This may reflect in
Pacemakers part placement of 78% of internal jugular catheters on
Defibrillators the right side compared with 58% of subclavian
Unrelated to intravascular device
Idiopathic
catheters. Similarly, a small study of short-term tem-
Extrinsic compression of vein porary dialysis catheters (32 subclavian and 20 inter-
Dialysis-associated venous thoracic outlet syndrome nal jugular) showed a high incidence of CVS (50%) in
Fibrosing mediastinitis the subclavian group and none in the internal jugular
Retroperitoneal fibrosis group,17 whereas another study of temporary HD
Post–radiation therapy
catheters in 57 HD patients showed no difference in
Figure 6. Left upper-extremity fistulogram shows different Cardiac Rhythm Device–Associated CVS
degrees of left brachiocephalic (innominate) vein compression.
(A) Splaying of the left brachiocephalic vein (star) of a patient Cardiovascular disease is a common comorbid con-
with mild (grade 1) compression. (B) Indentation of the left dition in patients with advanced CKD, and use of
brachiocephalic vein (arrow) and collaterals (arrowhead) in a intravascular devices such as pacemakers or defibril-
patient with moderate (grade 2) compression. (C) Marked inden-
tation of the left brachiocephalic vein (arrows) and prominent lators is common.35,36 The left upper chest is the
collaterals (star) in a patient with severe (grade 3) compression preferred location for both vascular access placement
by what appear to be the brachiocephalic (innominate) and left and cardiac rhythm device placement. Constant fric-
common carotid arteries. Reproduced from Maxim et al26 with
permission of Elsevier. tion from pacemaker leads can cause persistent inflam-
mation of the left central veins (Fig 7).37 In one study
of 30 patients with long-term transvenous defibrilla- at the tip of the catheter cause catheter dysfunction,
tors in place for 45 ⫾ 21 months, venography showed but an adherent thrombus also may be the first step in
a 50% prevalence of subclavian vein stenosis,38 the formation of a fibrin sleeve on the outer surface of
whereas in another study, abnormalities of the central the catheter. This process starts early, and a full-length
veins were found in 64% of patients on routine sleeve can form as early as within a week.51,52 Throm-
angiography after 6 months, suggesting that even a botic complications commonly occur in veins that
relatively short duration of injury is not inconsequen- have been catheterized and frequently are associated
tial.39 Other studies of such devices also have shown a with catheter sepsis.53 Stabilizing the tip of the cath-
high prevalence of central vein abnormality,40-42 with eter to the center of the vein lumen with a thin wire
one recent retrospective review of HD patients show- loop in a swine model caused less injury, thrombosis,
ing 62% of individuals with cardiac rhythm devices and thickening in the vessel wall.54 This supports the
versus 32% of individuals without cardiac rhythm mechanical theory of the development of CVS.
devices having CVS.43 Critically, CVS can remain Activation of coagulation factors may be an impor-
asymptomatic and may manifest only when chal- tant element in the cause of CVS. Animal models
lenged by increased blood flow from a dialysis ac- have shown that structural changes in the vein wall
cess.35,44,45 occur within 24 hours after endothelial denudation,
The presence of CVS should be suspected and marked by the development of platelet microthrombi.55
proactively investigated prior to placement of AV
During the next 7-8 days, several layers of smooth
access in patients with a cardiac rhythm device and
muscle cells develop in the injured areas, but appar-
preemptively treated if an ipsilateral AV access is
ently only if a “critical” area of injury is present,
necessary. Furthermore, a device should not be placed
without which the proliferative response does not
ipsilateral to the AV access. Angioplasty and stent
placement of the CVS associated with device wires is occur. Direct evidence for histopathologic changes is
possible, but carries the risk of erosion of the leads scant in humans, but subclavian vein specimens from
over months to years. Stent placement over the leads directional atherectomy in patients with symptomatic
should be avoided because stents may make wire stenosis or occlusion show intimal hyperplasia and
extraction very difficult in the event of an infection. the presence of fibrous tissue.56 Autopsy finding of an
Finally, epicardial lead implantation, although more adherent clot with intimal injury in patients with less
invasive, may be preferable in the appropriate sce- than 14 days of catheter use and the presence of
narios to avoid the risk of CVS. smooth muscle proliferation and thickened venous
wall in those with more than 90 days of catheter use
PATHOPHYSIOLOGY further support this hypothesis.57 Importantly, these
catheters also were found to be focally attached to the
CVS due to venous catheters most likely is related
vein wall by organizing thrombus, endothelial cells,
to heightened inflammation, increased oxidative stress,
and collagen, perhaps suggesting imminent develop-
activation of leukocytes, release of myeloperoxidase,
ment of a fibrin sheath or CVS.
and activation of the coagulation cascade after cath-
Bioincompatibility of the intravascular device likely
eter placement.46 The endothelial damage begins with
is one of the factors in the causation of venous injury
the initial trauma from vein cannulation that is perpetu-
ated by an indwelling foreign body that is not biocom- and inflammation. Catheter material may have differ-
patible. Further, constant movement of the catheter ent levels of antigenicity, potential for tissue growth,
with respiration, movements of the head, and changes and fibrogenesis, and this issue requires further study.
in posture, as well as increased flow and turbulence It has been suggested that Silastic internal jugular
from the AV access, alter the shear stress, resulting in catheters may produce less thrombosis,58 with one
platelet deposition and venous wall thickening.47 study of the use of silicone catheters conducted in 22
Trauma to the vessel wall results in thrombin genera- patients with subclavian cannulation showing stenosis
tion, platelet activation, and expression of P-selectin in only 2 and thrombosis in only 3. In this study, there
with inflammatory response,48 and subsequent activa- was a lower incidence of subclavian vein stenosis
tion of leukocytes results in release of myeloperoxi- with these catheters than with polytetrafluoroethylene
dase and formation of platelet aggregates, culminat- (PTFE) and polyurethane catheters.59 In a rabbit model,
ing in intravascular thrombosis.49 Catheters frequently polyethylene and Teflon catheters caused more inflam-
are associated with formation of a thrombus, often in mation than silicone and polyurethane.60 Both sili-
conjunction with venous stenosis at the same site, cone (eg, Tesio [Medcomp] and Schon [AngioDynam-
although it is unclear whether the thrombus and the ics]) and polyurethane (eg, Opti-Flow [Bard Access
stenosis are causally related to each other.50 Not only Systems] and Ash Split [Medcomp]) commonly are
does the formation of platelet thrombi and a thrombus used to manufacture long-term dialysis catheters.
Infections associated with CVCs may aggravate The clinical features of CVS vary according to the site
inflammation and predispose to the development of of obstruction and mechanism of development.
CVS. In one study of 54 long-term HD patients,
venography performed 6 months after catheter re- Related to Venous Hypertension Peripheral
moval showed a 75% prevalence of CVS in those with to the Obstruction
previous catheter infections compared with 28% in
Venous engorgement from CVS may result in
those with no infection.61 It also is plausible that CVS
edema, swelling, pain, tenderness, and erythema of
was the predisposing factor for infection, pointing to a
the ipsilateral extremity, along with ipsilateral breast
possible vicious cycle.
swelling. Pleural effusions may develop in severe
It can be hypothesized that inflammation and activa-
cases. In cases of stenosis of the bilateral brachioce-
tion of coagulation pathways act in combination and
phalic veins or if superior vena cava syndrome develops,
are not sufficient by themselves to cause CVS. How-
this typically responds to angioplasty (Fig 8A and B). In
ever, in a retrospective study of 77 patients with lupus
chronic superior vena cava obstruction, alternative
and ESRD, 17 patients (22%) had documented CVS,
venous drainage into the azygous system can develop,
similar to the nonlupus group.62 Number of CVCs,
although clinical features of CVS are always present
but not degree of inflammation, was found to be
(Fig 9).37 Intercostal veins often can be dilated as well
associated with CVS in this retrospective cohort study.
(Fig 10).
Thus, it is possible that a systemic inflammatory
Rarely, abnormal flow in the left jugular bulb and
disease such as lupus may not result in a particularly
inferior petrosal sinuses can be caused by retrograde
higher incidence or prevalence of CVS due to compet-
flow from brachiocephalic vein stenosis, leading to
ing inflammation present in patients with ESRD,
false suspicion of the presence of a carotid cavernous
although the small size of this retrospective study
fistula.64
cannot be considered conclusive.
Anatomical factors also may contribute to the patho-
physiology and pathogenesis of CVS. The anatomy of
the left-sided central veins, as previously mentioned, is
more conducive to the development of CVS,23,24,26,63
with 3-dimensional models of the left-sided veins
suggesting an additional angulation of the brachioce-
phalic (innominate) vein over the brachiocephalic
artery and the aortic arch that is not present on the
right.23
Other risk factors for CVS, such as sex-specific
differences, need to be studied further. In the absence
of intravascular device placement, the occurrence of
CVS is unexplained. It is plausible that the altered
shear stress and turbulence with changes in blood flow
pattern and speed due to an AV access in conjunction
with oxidative stress lead to venous wall hyperplasia
and eventual stenosis.
CLINICAL FEATURES
Figure 9. Severe stenosis of the superior vena cava with a
CVS becomes symptomatic in HD patients with an significantly dilated azygous vein (arrowhead). Reproduced from
increase in extremity blood flow from an AV access. Agarwal37 with permission of Elsevier.
sia and proliferative lesions were found in restenotic angioplasty without use of a stent. Critically, a lack of
areas after angioplasty than were found in the original large randomized controlled studies of PTA in patients
stenosis.72 In another study of ⬎50% CVS in 35 with CVS does not allow fair comparison of outcomes
asymptomatic HD patients with 38 AVGs, 86 veno- of PTA vis à vis other treatment modalities.
grams were reviewed.73 No intervention was done in Intravascular ultrasound study after angioplasty of
28% of cases, and none of these patients progressed to the central veins has shown that central veins are
symptoms, stent placement, or additional CVS. In much more likely to recoil than the peripheral veins.85
contrast, in the 72% of cases in which percutaneous Thus, the success of PTA often depends on the elastic
transluminal angioplasty (PTA) was performed, esca- or nonelastic nature of the lesion, which may have
lation of CVS after PTA was seen in 8% of these different structural characteristics of the stenosis as
cases, resulting in further interventions. Although shown by intravascular ultrasound.78.
there is possible indication bias, these findings sup-
port the theory that endothelial damage from angio-
plasty can aggravate the venous response and acceler- STENTS
ate the stenotic process. It also is possible that a rather Lack of sustained results with PTA led to the use of
high residual stenosis (40%) in the intervention group stents for CVS.86 Guidelines for CVS recommend
was an indication of its already refractory nature and placement of a stent for elastic recoil of the vein that
that a more aggressive approach with stent placement leads to significant residual stenosis after PTA or for
might have been beneficial.74 Thus, endovascular in- lesions recurring within 3 months after angioplasty.76,87
tervention for CVS requires careful planning while Placement of self-expandable stents in the treatment
using restraint when feasible. Endovascular interven- of CVS typically achieves a high degree of technical
tion also can be used as a palliative approach. Coil success. For example, use of self-expanding metallic
embolization of the long thoracic vein has been shown
stents for elastic lesions was associated with better
to reduce breast edema in HD patients who have
outcomes than angioplasty alone. However, the pri-
elevated venous hydrostatic pressure due to central
mary and secondary patency of stents is modest at
venous occlusion.75
best (Table 1).88 It also is difficult to compare results
of different studies done over a period of time because
Percutaneous Transluminal Angioplasty
stainless steel stents were used in earlier studies. In
PTA, either on its own or with stent placement, is one study of 52 HD patients with 56 lesions, 51
the preferred approach to CVS, depending on the self-expandable metallic stents were placed.89 Pri-
rapidity of recurrence (guideline 20 of the National mary and secondary patency rates were 46% and 76%
Kidney Foundation–Kidney Disease Outcomes Qual- at 6 months and 20% and 33% at 12 months, respec-
ity Initiative [NKF-KDOQI]).76 PTA for central ve- tively. However, another study of 57 self-expandable
nous disease has been in vogue for almost 3 decades metallic stents in 50 patients with CVS had far better
and has very high technical success rates, ranging results, with primary patency rates of 92%, 84%,
from 70%-90%.47,77-82 The variable patency rates in
56%, and 28% at 3, 6, 12, and 24 months, respec-
these studies may be due to the variety of criteria used
tively.90 Secondary patency also was significantly
by authors in reporting their results, as well as the
better: 97% after 6 and 12 months, 89% after 24
wide variety of techniques and equipment used. Ac-
months, and 81% after both 36 and 48 months. In a
cording to these studies, at 6 months, unassisted
patency after PTA varies from 23%-63%, with a retrospective study, 23 patients with symptomatic
cumulative patency rate range of 29%-100%, whereas refractory CVS were treated with various types of
at 12 months, unassisted patency after PTA ranges stent placement.91 In this study, median primary pa-
from 12%-50%, with a cumulative patency rate of tency was 138 days, with 1-year patency of only 19%,
13%-100%. Although poor patency rates after PTA whereas median secondary patency was 1,036 days
alone were seen in 2 earlier studies of patients with with 64% patency at 1 year. A recent retrospective
CVS (28.9% at 180 days and 25% at 1 year),75,83 a analysis of the Nitinol shape memory alloy stents in
more recent study using high-pressure balloons noted 64 patients (with 15 central and 54 peripheral vein
better results with PTA alone, with unassisted patency stents) showed primary patency of 14.9 months in
after PTA of 60% at 6 months and 30% at 12 months.84 central veins and 8.9 months in peripheral veins.92
Results in this study and similar results from a second Significantly better results in this retrospective study
more recent study81 suggest either a difference in may reflect the more advanced nature of the stent
patient population or technical advances, including material, although this conclusion remains conjecture.
the use of high-pressure balloons. Significant second- Repeated interventions are needed to maintain pa-
ary patency often can be achieved with repeated tency achieved by the stents over longer periods.
No. of Central
Study Lesions Primary Patency Secondary Patency
Rajan DK (2007) 6 83.3% (95% CI, 50%-120%) at 3 mo, and Secondary patency: 100% at 12 mo with 3
66.7% at 6 and 12 mo (95% CIs, 20%- patients censored over that time
110% and 10%-120%)
Rajan DK (2007) 89 Fistula group rates: 88.5% ⫾ 4.8%, 59.4% ⫾ NA
7.6%, and 46% ⫾ 7.9% at 3, 6, and 9 mo;
graft group rates: 78.1% ⫾ 7.3%, 40.7% ⫾
9%, and 16% ⫾ 7.3% at 3, 6, and 9 mo
Maya ID (2007) 23 19% at 1 ya 64% at 1 ya
Sprouse LR (2004) 32 NA Symptoms related to central stenosis were
controlled for 6.5 mo on average
Aytekin C (2004) 14 1-, 3-, 6-, and 12-mo primary stent patency 3-, 6-, 12-mo and 2-y secondary patency
rates: 92.8%, 85.7%, 50%, and 14.3% rates: 100%, 88.8%, 55.5%, and 33.3%
Chen CY (2003) 18 3, 6, 12 and 18 mo: 100% and 89%, 73% 100% after 3 mo, 93% and 100% after 6
and 68%, 49% and 42%, and 16% and mo, 85% and 91% after 12 mo and, 68%
0%c and 72% after 24 mo
Hatzimpaloglou A (2002) 15 70% at 12 and 24 mo NA
Smayra T (2001) 9 56% at 1 y 75% 1 y
Haage P (1999) 50 3, 6, 12, and 24 mo: 92%, 84%, 56%, and 97% after 6 and 12 mo, 89% after 24 mo,
2% and 81% after 36 and 48 mo
Vesely TM (1997) 20 1, 3, 6 mo, and 1 y: 90%, 67%, 42%, and 3, 6 mo, 1 and 2 y: 89%, 64%, 56%, and
25% 22%
Mickley V (1997) 15 1 y: 100%; 2 y: 85% 1 y: 70%; 2 y: 50%
Lumsden AB (1997) 25 84% at 1 mo, 42% at 6 mo, and 17% at 1 y —
Vesely TM (1997) 20 1, 3, 6 mo and 1 y: 90%, 67%, 42%, and 3, 6 mo, 1 and 2 y: 89%, 64%, 56%, and
25% 22%
Mickley V (1997) 15 100% at 1 y, 85% at 2 y 70% at 1 y, 50% at 2 y
Gray RJ (1995) 32 46% at 6 mo, 20% at 12 mob 76% at 6 mo, 33% at 12 mob
Beathard GA (1992) 24 NA 70.4% at 1 mo, 62.1% at 2 mo, 48.6% at 3
mo, and 28.9% at 4 mo
Matthews R (1992) 2 NA NA
Note: All studies are observational studies except for Matthews 1992, which is a case report.
Abbreviations: CI, confidence interval; NA, not available.
Modified and reproduced from Yevzlin88 with permission of John Wiley and Sons.
a
All stents had restenosis on follow-up venogram.
b
Peripheral and central outcomes were mixed in the data reporting. Two central stents migrated after catheter placement.
c
Primary patency rates given for stent and hemodialysis access at each time point.
Because some of these accesses are terminal, stent dografts” have the advantage of providing a rela-
placement and multiple periodic interventions may be tively inert and stable intravascular matrix for
appropriate. Bare-metal stents are associated with endothelialization, thereby reducing restenosis.97
shortening, migration, fracture, and neointimal hyper- Studies of the efficacy of covered stents are now
plasia and require repeated treatments with PTA.93-96 emerging.3,98 One study evaluating PTFE-covered
The type of stent used also may be a factor in the stent placement showed 360-day primary patency
variable success rates of these stents. First-generation of 32% and secondary patency of 39%,96 whereas a
stents, such as self-expandable metallic stents, are low similar study evaluating Dacron (polyethylene te-
profile, flexible, and radiopaque, but have disadvan- rephthalate)-covered stents showed primary and
tages of foreshortening at the time of placement, secondary patency rates of 29% and 64%, respec-
delayed shortening, and migration.97 Second-genera- tively, at 1 year.99 Immediate and long-term results
tion stents made of nickel-titanium alloy transform of stent grafts are encouraging in more recent
according to temperature, are superelastic, and can studies.100-102
return to their original shape after the deforming force Outcomes of PTA alone and stent placement have
is removed. not been compared in randomized controlled trials. A
Use of covered stents also is becoming increas- study of central vein angioplasty (n ⫽ 101) and stent
ingly common, and these “stent grafts” or “en- placement (n ⫽ 46) showed that angioplasty alone
maintenance dialysis. Saudi J Kidney Dis Transplant. 1997;8: 25. Salgado OJ, Urdaneta B, Colmenares B, Garcia R, Flores C.
119-122. Right versus left internal jugular vein catheterization for hemodi-
6. MacRae JM, Ahmed A, Johnson N, Levin A, Kiaii M. alysis: complications and impact on ipsilateral access creation.
Central vein stenosis: a common problem in patients on hemodialy- Artif Organs. 2004;28:728-733.
sis. ASAIO J. 2005;51:77-81. 26. Maxim I, Kraus MJ, Trerotola SO. Extrinsic compression of
7. Agarwal AK, Patel BM, Farhan NJ. Central venous stenosis the left innominate vein in hemodialysis patients. J Vasc Interv
in hemodialysis patients is a common complication of ipsilateral Radiol. 2004;15:51-56.
central vein catheterization [abstract]. J Am Soc Nephrol. 2004;15: 27. Illig KA. Management of central vein stenoses and occlu-
368A-369A. sions: the critical importance of the costoclavicular junction.
8. MacDonald MJ, Martin LG, Hughes JD, Kikeri D, Scout DC, Semin Vasc Surg. 2011;24:113-118.
Harker LA. Distribution and severity of stenoses in functioning 28. Hegarty J, Picton M, Chalmers N, Kalra PA. Iliac vein
arteriovenous grafts: a duplex and angiographic study. J Vasc stenosis secondary to femoral catheter placement. Nephrol Dial
Technol. 1996;20:131-136. Transplant. 2001;16:1520-1521.
9. Naroienejad M, Saedi D, Rezvani A. Prevalence of central 29. Wu X, Studer W, Skarvan K, Seeberger MD. High inci-
vein stenosis following catheterization in patients with end-stage dence of intravenous thrombi after short-term central venous
renal disease. Saudi J Kidney Dis Transplant. 2010;21:975-978. catheterization of the internal jugular vein. J Clin Anesth. 1999;11:
10. Taal MW. Chesterton IJ, McIntyre CW. Venography at 482-485.
insertion of tunneled internal jugular vein dialysis catheters reveals 30. Grove JR, Pevec WC. Venous thrombosis related to periph-
significant occult stenosis. Nephrol Dial Transplant. 2004;19:1542- erally inserted venous catheters. J Vasc Interv Radiol. 2000;11:837-
1545. 840.
11. Morosetti M, Meloni C, Gandini R, et al. Late symptomatic 31. Ryder MA. Peripherally inserted central venous catheters.
venous stenosis in three hemodialysis patients without previous Nurs Clin North Am. 1993;28:937-971.
central venous catheters. Artif Organs. 2000;24:929-931. 32. Allen AW, Megargell JL, Brown DB, et al. Venous thrombo-
12. Oguzkurt L, Tercan F, Yildirim S, Torun D. Central venous sis associated with placement of peripherally inserted central
stenosis in hemodialysis patients without a previous history of catheters. J Vasc Interv Radiol. 2000;11:1309-1314.
catheter placement. Eur J Radiol. 2005;55:237-242. 33. Gonsalves CF, Eschelman DJ, Sullivan KL, DuBois N,
13. Komodo A, Akimoto T, Kato M, et al. Central venous Bonn J. Incidence of central vein stenosis and occlusion following
stenosis among hemodialysis patients is often not associated with upper extremity PICC and port placement. Cardiovasc Intervent
previous central venous catheters. ASAIO J. 2011;57:439-443. Radiol. 2003;26:123-127.
34. El Ters M, Schears GJ, Taler SJ, et al. Association between
14. Kohl KH, Tan C. Central vein stenosis in end stage renal
prior peripherally inserted central catheters and lack of functioning
failure patients. J R Coll Physicians Edinb. 2005;35:116-122.
arteriovenous fistulas: a case-control study in hemodialysis pa-
15. Hernandez D, Diaz F, Refine M, et al. Subclavian vascular
tients. Am J Kidney Dis. 2012;60:601-608.
access stenosis in dialysis patients: natural history and risk factors.
35. Korzets A, Chagnac A, Ori Y, Katz M, Zevin D. Subclavian
J Am Soc Nephrol. 1998;9:1507-1510.
vein stenosis, permanent cardiac pacemakers and the haemodia-
16. Schilling F, Schilling D, Montagne R, Millicent T. Post
lysed patient. Nephron. 1991;58:103-105.
catheterization vein stenosis in hemodialysis: comparative angio-
36. Chuang C, Tarng D, Yang W, Huang T. An occult cause of
graphic study of 50 subclavian and 50 internal jugular accesses.
arteriovenous access failure: central vein stenosis from permanent
Nephrol Dial Transplant. 1991;6:722-724.
pacemaker wire. Am J Nephrol. 2001;21:406-409.
17. Cimochowski GE, Worley E, Rutherford WE, Sartain J,
37. Agarwal AK. Central vein stenosis: current concepts. Adv
Blondin J, Harter H. Superiority of the internal jugular over the Chronic Kidney Dis. 2009;16:360-370.
subclavian access for temporary dialysis. Nephron. 1990;54:154- 38. Sticherling C, Chough SP, Baker RL, et al. Prevalence of
161. central venous occlusion in patients with chronic defibrillator
18. Oguzkurt L, Tercan F, Torun D, Yildirim T, Zum̈rü tidal A, leads. Am Heart J. 2001;141:813-816.
Kizilkilic O. Impact of short-term hemodialysis catheters on the 39. Da Costa SS, Scalabrini Neto A, Costa R, et al. Incidence
central veins: a catheter venographic study. Eur J Radiol. 2004;52: and risk factors of upper extremity deep vein lesions after perma-
293-299. nent transvenous pacemaker implant: a 6-month follow-up prospec-
19. Jean G, Vanel T, Chazot C, Charra B, Terrat JC, Hurot JM. tive study. Pacing Clin Electrophysiol. 2002;25:1301-1306.
Prevalence of stenosis and thrombosis of central veins in hemodi- 40. Lickfett L, Bizen A, Arepally A, et al. Incidence of venous
alysis after a tunneled jugular catheter. Nephrologie. 2001;22:501- obstruction following insertion of an implantable cardioverter
504. defibrillator. A study of systematic contrast venography on patients
20. Jassal SV, Pierratos A, Roscoe JM. Venous stenosis and presenting for their first elective ICD generator replacement.
thrombosis associated with the use of internal jugular vein cath- Europace. 2004; 6:25-31.
eters for hemodialysis. ASAIO J. 1999;45:356-359. 41. Rozmus G, Daubert JP, Huang DT, Rosero S, Hall B,
21. Forauer AR, Glockner JF. Importance of US findings in Francis C. Venous thrombosis and stenosis after implantation of
access planning during jugular vein hemodialysis catheter place- pacemakers and defibrillators. J Interv Cardiac Electrophys. 2005;
ments. J Vasc Interv Radiol. 2000;11:233-238. 13:9-19.
22. Wilkin TD, Krause MA, Lane KA, Trerotola SA. Internal 42. Oginosawa Y, Abe H, Nakashima Y. The incidence and risk
jugular vein thrombosis associated with hemodialysis catheters. factors for venous obstruction after implantation of transvenous
Radiology. 2003;228:697-700. pacing leads. PACE. 2002;25:1605-1611.
23. Salik E, Daftary A, Tal MG. Three-dimensional anatomy of 43. Drew DA, Meyer KB, Weiner DE. Transvenous cardiac
the left central veins: implications for dialysis catheter placement. device wires and vascular access in hemodialysis patients. Am J
J Vasc Interv Radiol. 2007;18:361-364. Kidney Dis. 2011;58(3):494-496.
24. Lobato EB, Sulek CA, Moody RL, Morey TE. Cross 44. Deighan CJ, McLaughlin KJ, Simipson K, Boulton JM.
sectional area of the right and left internal jugular veins. J Cardio- Unsuspected subclavian stenosis resulting from a permanent pac-
thorac Vasc Anesth. 1999;13:136-138. ing wire. Nephrol Dial Transplant. 1996;11:2333-2334.
45. Teruya TH, Abou-Zamzam AM, Limm W, Wong L, Wong 66. National Kidney Foundation. Dialysis Outcomes Quality
L. Symptomatic subclavian vein stenosis and occlusion in hemodi- Initiative: Clinical Practice Guidelines for Vascular Access. New
alysis patients with transvenous pacemakers. Ann Vasc Surg. York, NY: National Kidney Foundation; 1997:20-21.
2003;17:526-529. 67. Rose SC, Kinney TB, Bundens WP, Valji K, Roberts AC.
46. Weiss MF, Scivittaro V, Anderson JM. Oxidative stress and Importance of Doppler analysis of transmitted atrial waveforms
increased expression of growth factors in lesions of failed hemodi- prior to placement of central venous access catheters. J Vasc Interv
alysis access. Am J Kidney Dis. 2001;37:970-980. Radiol. 1998;9:927-934.
47. Glanz S, Gordon DH, Lipkowitz GS, Butt KM, Hong J, 68. Labropoulos N, Borge M, Pierce K, et al. Criteria for
Sclafani SJ. Axillary and subclavian vein stenosis: percutaneous defining significant central vein stenosis with duplex ultrasound. J
angioplasty. Radiology. 1988;168:371-373. Vasc Surg. 2007;46:101-107.
48. Palabrica T, Lobb R, Furie BC, et al. Leukocyte accumula- 69. Kearon C, Kahn SR, Agnelli G, Goldhaber S, Raskob GE,
tion promoting fibrin deposition is mediated by P-selectin on Comerota AJ; American College of Chest Physicians. Antithrom-
adherent platelets. Nature. 1992;359:848-851. botic therapy for venous thromboembolic disease: American Col-
49. Weiss MF, Scivittaro V, Anderson JM. Oxidative stress and lege of Chest Physicians Evidence-Based Clinical Practice Guide-
increased expression of growth factors in lesions of failed hemodi- lines (8th edition). Chest. 2008;133:454S-545S.
alysis access. Am J Kidney Dis. 2001;37:970-980. 70. Debourdeau P, Kassab Chahmi D, Le Gal G, et al; on behalf
50. Vanherweghem JL, Yassine T, Goldman M, et al. Subcla- of the Working Group of the SOR. 2008 SOR guidelines for the
vian vein thrombosis: a frequent complication of subclavian vein prevention and treatment of thrombosis associated with central
cannulation for hemodialysis. Clin Nephrol. 1986;26:235-238. venous catheters in patients with cancer: report from the working
51. Hoshal VL Jr, Ause RG, Hoskins PA. Fibrin sleeve forma- group. Ann Oncol. 2009;20:1459-1471.
tion on indwelling subclavian central venous catheters. Arch Surg. 71. Paksoy Y, Gormus N, Tercan MA. Three-dimensional con-
1971;102:253-258. trast enhanced magnetic resonance angiography (3-D CE-MRA) in
52. Forauer AR, Theoharis CGA, Dasika NL. Jugular vein cath- the evaluation of hemodialysis access complications, and the
eter placement: histologic features and development of catheter- condition of central veins in patients who are candidates for
related (fibrin) sheaths in a swine model. Radiology. 2006;240:427- hemodialysis access. J Nephrol. 2004;7:57-65.
434. 72. Chang CJ, Ko PJ, Hsu LA, et al. Highly increased cell
53. Raad I I, Luna M, Khalil SM, Costerton JW, Lam C, Bodey proliferation activity in the restenotic hemodialysis vascular access
GP. The relationship between the thrombotic and infectious compli- after percutaneous transluminal angioplasty: implication in preven-
cations of central venous catheters. JAMA. 1994;271:1014-1016. tion of restenosis. Am J Kidney Dis. 2004;43:74-84.
54. Kohler TR, Kirkman TR. Central venous catheter failure is 73. Levit RD, Cohen RM, Kwak A, et al. Asymptomatic central
induced by injury and can be prevented by stabilizing the catheter venous stenosis in hemodialysis patients. Radiology. 2006;238:
tip. J Vasc Surg. 1998;28:59-66. 1051-1056.
55. Manderson J, Campbell GR. Venous response to endothelial 74. Aruny JE, Lewis CA, Cardella JF, et al; Society of Interven-
denudation. Pathology. 1986;18:77-87. tional Radiology Standards of Practice Committee. Quality im-
56. Gray RJ, Dolmatch BL, Buick MK. Directional atherec- provement guidelines for percutaneous management of the throm-
tomy treatment for hemodialysis access: early results. J Vasc Interv bosed or dysfunctional dialysis access. J Vasc Interv Radiol.
Radiol. 1992;3:497-503. 2003;14(9 Pt 2):S247-S253.
57. Forauer AR, Theoharis C. Histologic changes in the human 75. Miller GA, Friedman A, Khariton A, Jotwani MC, Savran-
vein wall adjacent to central venous catheters. J Vasc Interv sky Y. Long thoracic vein embolization for the treatment of breast
Radiol. 2003;14:1163-1168. edema associated with central venous occlusion and venous hyper-
58. Agraharkar M, Isaacson S, Mendelssohn D, et al. Percutane- tension. J Vasc Access. 2010;11:115-121.
ously inserted Silastic jugular hemodialysis catheters seldom cause 76. National Kidney Foundation. Guideline 20. K/DOQI Clini-
jugular vein thrombosis. ASAIO J. 1995;41:169-172. cal Practice Guidelines for Vascular Access, 2000. Am J Kidney
59. Beenen L, van Leusen R, Deenik B, Bosch FH. The inci- Dis. 2001;37(suppl 1):S137-S181.
dence of subclavian vein stenosis using silicone catheters for 77. Beathard GA. Percutaneous transvenous angioplasty in the
hemodialysis. Artif Organs. 1994;18:289-292. treatment of vascular access stenosis. Kidney Int. 1992;42:1390-1397.
60. Di Costanzo J, Sastre B, Choux R, Kasparian M. Mechanism 78. Kovalik EC, Newman GE, Suhocki P, Knelson M, Schwab
of thrombogenesis during total parenteral nutrition: role of catheter SJ. Correction of central venous stenoses: use of angioplasty and
composition. JPEN J Parenter Enteral Nutr. 1988;12:190-194. vascular Wallstents. Kidney Int. 1994;45:1177-1181.
61. Hernandez D, Dıaz F, Suria S, et al. Subclavian catheter- 79. Quinn SF, Schuman ES, Demlow TA, et al. Percutaneous
related infection is a major risk factor for the late development of transluminal angioplasty versus endovascular stent placement in
subclavian vein stenosis. Nephrol Dial Transplant. 1993;8:227-230. the treatment of venous stenosis in patients undergoing hemodialy-
62. Waheed U, Brown C, Haddad N, Van Cleef S, Agarwal A, sis: intermediate results. J Vasc Interv Radiol. 1995;5:851-855.
Bhatt U. Central venous stenosis in systemic lupus erythematosus 80. Dammers R, de Haan MW, Planken NR, van der Sande FM,
associated ESRD. Semin Dial. 2008;21:106-107. Tordoir JHM. Central vein obstruction in hemodialysis patients:
63. Nazarian G, Bjarnason H, Dietz CA, Bernadas CA, Hunter results of radiological and surgical intervention. Eur J Vasc Endo-
DW. Changes in catheter tip position when a patient is upright. J vasc Surg. 2003;26:317-321.
Vasc Interv Radiol. 1997;8:437-441. 81. Surowiec SM, Fegley AJ, Tanski WJ, et al. Endovascular
64. Paksoy Y, Genc BO, Genc E. Retrograde flow in the left management of central venous stenoses in the hemodialysis pa-
inferior petrosal sinus and blood steal of the cavernous sinus tient: results of percutaneous therapy. Vasc Endovasc Surg. 2004;
associated with central vein stenosis: MR angiographic findings. 38:349-354.
AJNR Am J Neuroradiol. 2003;24:1364-1368. 82. Bakken AM, Protack CD, Saad WE, Lee DE, Waldman DL,
65. Lumsden AB, MacDonald MJ, Isiklar H, et al. Central Davies MG. Long-term outcomes of primary angioplasty and
venous stenosis in the hemodialysis patient: incidence and efficacy primary stenting of central venous stenosis in hemodialysis pa-
of endovascular treatment. Cardiovasc Surg. 1997;5:504-509. tients. J Vasc Surg. 2007;45:776-783.
83. Beathard GA. The treatment of vascular access graft dysfunc- 102. Anaya-Ayala JE, Smolock CJ, Colvard BD, et al. Efficacy
tion: a nephrologist’s view and experience. Adv Ren Replace Ther. of covered stent placement for central venous occlusive disease in
1994;1:131-147. hemodialysis patients. J Vasc Surg. 2011;54:754-759.
84. Buriankova E, Kocher M, Bachleda P, et al. Endovascular 103. Ozyer U, Harman A, Yildirim E, Aytekin C, Karakayali F,
treatment of central venous stenoses in patients with dialysis Boyvat F. Long-term results of angioplasty and stent placement for
shunts. Biomed Papers. 2003;147:203-206. treatment of central venous obstruction in 126 hemodialysis pa-
85. Davidson CJ, Newman GE, Sheikh KH, et al. Mechanisms tients: a 10-year single-center experience. AJR Am J Roentgenol.
of angioplasty in hemodialysis fistula stenoses evaluated by intra- 2009;193:1672-1679.
vascular ultrasound. Kidney Int. 1991;40(1):91-95. 104. Kim YC, Won JY, Choi SY, et al. Percutaneous treatment
86. Gunther RW, Vorwerk D, Bohndorf K, et al. Venous steno- of central venous stenosis in hemodialysis patients: long-term
ses in dialysis shunts: treatment with self-expanding metallic outcomes. Cardiovasc Intervent Radiol. 2009;32:271-278.
stents. Radiology. 1989;170:401-405. 105. Bakken AM, Protack CD, Saad WE, Lee DE, Waldman
87. Aruny JE, Lewis CA, Cardella JF, et al. Quality improve- DL, Davies MG. Long-term outcomes of primary angioplasty and
ment guidelines for percutaneous management of the thrombosed primary stenting of central venous stenosis in hemodialysis pa-
or dysfunctional dialysis access. Standards of Practice Committee tients. J Vasc Surg. 2007;45:776-783.
of the Society of Cardiovascular & Interventional Radiology. J 106. Katzman HE, McLafferty RB, Ross JR, Glickman MH,
Vasc Interv Radiol. 2003;14(9 Pt 2):S247-S253. Peden EK, Lawson JH. Initial experience and outcome of a new
88. Yevzlin AS. Hemodialysis catheter-associated central ve- hemodialysis access device for catheter-dependent patients. J Vasc
nous stenosis. Semin Dial. 2008;21:522-527. Surg. 2009;50:600-607.
89. Gray RJ, Horton KM, Dolmatch BL, et al. Use of Wallstents 107. Asif A, Salman L, Carrillo RG, et al. Patency rates for
for hemodialysis access-related venous stenoses and occlusions untreat- angioplasty in the treatment of pacemaker-induced central venous
able with balloon angioplasty. Radiology. 1995;195:479-484. stenosis in hemodialysis patients: results of a multicenter study.
90. Haage P, Vorwerk D, Piroth W, Schuermann K, Guenther Semin Dial. 2009;22:671-676.
RW. Treatment of hemodialysis-related central venous stenosis or 108. Saad TF, Myers GR, Cicone J. Central vein stenosis or
occlusion: results of primary Wallstent placement and follow-up in occlusion associated with cardiac rhythm management device
50 patients. Radiology. 1999;212:175-180. leads in hemodialysis patients with ipsilateral arteriovenous ac-
91. Maya ID, Saddekhi S, Allon M. Treatment of refractory cess: a retrospective study of treatment using stents or stent-grafts.
J Vasc Access. 2010;11:293-302.
central vein stenosis in hemodialysis patients with stents. Semin
109. Baddour LM, Epstein AE, Erickson CC, et al. Update on
Dial. 2006;20:78-82.
cardiovascular implantable electronic device infections and their
92. Vogel PM, Parise C. SMART stent for salvage of hemodialy-
management: a scientific statement from the American Heart
sis access grafts. J Vasc Interv Radiol. 2004;15:1051-1060.
Association. Circulation. 2010;121:458-477.
93. Trerotola SO, Fair JH, Davidson D, et al. Comparison of
110. Wilkoff BL, Love CJ, Byrd CL, et al. Transvenous lead
Gianturco Z stents and Wallstents in a hemodialysis access graft
extraction: Heart Rhythm Society expert consensus on facilities,
animal model. J Vasc Interv Radiol. 1995;6:387-396.
training, indications, and patient management: this document was
94. Verstandig AG, Bloom AI, Sasson T, Haviv YS, Rubinger
endorsed by American Heart Association. Heart Rhythm. 2009;6:
D. Shortening and migration of Wallstents after stenting of central
1085-1104.
venous stenoses in hemodialysis patients. Cardiovasc Intervent
111. Asif A, Carrillo R, Juan-Domingo G, et al. Epicardial
Radiol. 2003;26:58-64. cardiac rhythm devices for dialysis patients: minimizing the risk of
95. Chen CY, Liang HL, Pan HB, et al. Metallic stenting for infection and preserving central veins. Semin Dial. 2012;25(1):88-
treatment of central venous obstruction in hemodialysis patients. 94.
J Chin Med Assoc. 2003;66:166-172. 112. Jennings WC, Miller GA, Coburn MZ, Howard CA, Law-
96. Oderich GS, Treiman GS, Schneider P, Bhirangi K. Stent less MA. Vascular access flow reduction for arteriovenous fistula
placement for treatment of central and peripheral venous obstruc- salvage in symptomatic patients with central venous occlusion. J
tion: a long-term multi-institutional experience. J Vasc Surg. Vasc Access. 2012;13(2):157-162.
2000;32:760-769. 113. Currier CB Jr, Widder S, Ali A, et al. Surgical manage-
97. Kundu S. Review of central venous disease in hemodialysis ment of subclavian and axillary vein thrombosis in patients with a
patients. J Vasc Interv Radiol. 2010;21:963-968. functioning arteriovenous fistula. Surgery. 1986;100:25-28.
98. Sapoval MR, Turmel-Rodrigues LA, Raynaud AC, Bourque- 114. Anaya-Ayala JE, Bellows PH, Ismail N, et al. Surgical
lot P, Rodrigue H, Gaux JC. Cragg covered stents in hemodialysis management of hemodialysis-related central venous occlusive
access: initial and midterm results. J Vasc Interv Radiol. 1996;7: disease: a treatment algorithm. Ann Vasc Surg. 2011;25:108-119.
335-342. 115. Pisoni RL, Young EW, Dykstra DM, et al. Vascular access
99. Farber A, Barbey MM, Grunert JH, Gmelin E. Access- use in Europe and the United States: results from the DOPPS.
related venous stenoses and occlusions: treatment with percutane- Kidney Int. 2002;16:305-316.
ous transluminal angioplasty and Dacron-covered stents. Cardio- 116. Cooper BA, Branley P, Bulfone L, et al. A randomized,
vasc Intervent Radiol. 1999;22:214-218. controlled trial of early versus late initiation of dialysis. N Engl
100. Jones RG, Willis AP, Jones C, McCafferty IJ, Riley PL. J Med. 2010;363:609-619.
Long-term results of stent-graft placement to treat central venous 117. Falk A. Use of the brachiocephalic vein for placement of
stenosis and occlusion in hemodialysis patients with arteriovenous tunneled hemodialysis catheters. AJR Am J Roentgenol. 2006;187:
fistulas. J Vasc Interv Radiol. 2011;22:1240-1245. 773-777.
101. Kundu S, Modabber M, You JM, Tam P, Nagai G, Ting R. 118. Kwok PC, Wong KM, Ngan RK, et al. Prevention of
Use of PTFE stent grafts for hemodialysis-related central venous recurrent central venous stenosis using endovascular irradiation
occlusions: intermediate-term results. Cardiovasc Intervent Ra- following stent placement in hemodialysis patients. Cardiovasc
diol. 2011;34:949-957. Intervent Radiol. 2001;4:400-406.