In Practice
Central Vein Stenosis
Anil K. Agarwal, MD
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.
CASE PRESENTATION
A 44-year-old woman with a history of human immunodeficiency virus (HIV) infection and end-stage renal disease (ESRD)
initiated dialysis therapy through a right internal jugular tunneled
dialysis catheter in 2006. A month later, she developed catheterrelated infection, leading to its removal and placement of a left
internal jugular tunneled dialysis catheter. Recurrent infection of
this catheter within a month resulted in its removal and placement
of a new right internal jugular tunneled catheter. Due to cuff
exposure, this catheter was exchanged, and recurrent bacteremia
1 month later was treated with antibiotics and another catheter
exchange. Seven months after initiating dialysis therapy, her right
arm brachiocephalic arteriovenous (AV) fistula (AVF) was mature
and was cannulated successfully, and the catheter was removed.
Several months later, she was noted to have increased venous
pressure during dialysis. An angiogram showed 70%-80% stenosis
of the right brachiocephalic (innominate) vein, and angioplasty
was performed successfully. High pressures recurred 5 months
later, and this procedure was repeated for recurrent stenosis, only
to be repeated 5 months later for the same reason. In early 2008,
she underwent a third angioplasty of recurrent innominate stenosis
with placement of a 14⫻40-mm SMART stent (Cordis). Six
months later, in-stent stenosis was treated with angioplasty; however, 6 months after this, the stent required recanalization. This
was repeated twice in 2009 and twice in 2010. In late 2010, she
presented with swelling of the right arm, right side of the face, and
right breast that had progressed over several months. On examination, there was marked edema of the right upper extremity, neck,
and right side of the face with massive enlargement of the right
breast, and prominent tortuous veins were noted over the right
upper chest wall. A fistulogram was obtained that showed complete occlusion of the right innominate vein and stent (Fig 1).
INTRODUCTION
Venous outflow of the hemodialysis (HD) vascular
access completes the circuit that originates with cardiac output from the left side of the heart, providing
the arterial inflow for the AV vascular access. The
patency of all components of dialysis vascular access,
Am J Kidney Dis. 2013;61(6):1001-1015
including the arterial tree, AV anastomosis, peripheral
veins, and central veins, is critical for the provision of
consistent, adequate, comfortable, and uncomplicated
dialysis. The peripheral component of the venous
outflow of an AV access (which acts as the user
interface for cannulation) starts at the arterial anastomosis and ends at its confluence into the intracavitary
veins, demarcating the beginning of the “central”
veins. The major intrathoracic veins (subclavian vein,
brachiocephalic [also called innominate] vein, and
superior vena cava) are considered the central veins in
the upper extremity, and the veins cephalad to the
inguinal ligament in the lower extremity (iliac veins
and inferior vena cava) constitute the central veins
draining the lower extremity (Fig 2). The cephalic
arch in the upper extremity, although considered a
central vein by some, cannot be considered a central
vein by these criteria. The central veins are significantly larger and thicker, have higher blood flow, and
are more elastic than the peripheral veins. Overlapping bones make these central veins less accessible to
surgical intervention when central vein stenosis (CVS)
or occlusion impedes venous return from the whole
extremity (Fig 3). Pooling of blood behind the obstrucFrom Interventional Nephrology, The Ohio State University,
Columbus, OH.
Received April 3, 2012. Accepted in revised form October 22,
2012. Originally published online January 7, 2013.
Address correspondence to Anil K. Agarwal, MD, Interventional
Nephrology, The Ohio State University, 395 W 12th Ave, Ground
Fl, Columbus, OH 43210. E-mail: anil.agarwal@osumc.edu
© 2013 by the National Kidney Foundation, Inc.
0272-6386/$36.00
http://dx.doi.org/10.1053/j.ajkd.2012.10.024
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Anil K. Agarwal
Figure 1. Fistulogram shows central veins with complete
occlusion of the right subclavian-brachiocephalic (innominate)
junction with a thrombosis in the brachiocephalic vein. Note
collateralization in the neck and upper chest.
tion often results in symptoms due to venous hypertension, and complete occlusion renders the extremity
unsuitable for vascular access. Apart from compromising the ipsilateral side from the standpoint of vascular
access, CVS in patients with ESRD has other clinical
consequences, including increased morbidity, hospitalization, and mortality.
Previous or concomitant use of central venous
devices, including central venous catheters (CVCs)
and cardiac rhythm devices, is the most common
reason for the development of CVS. Device-unrelated
CVS is relatively uncommon and could be due to
external compression or may be idiopathic. This review focuses on CVS in patients on HD therapy in the
context of vascular access and intravascular device
use.
EPIDEMIOLOGY
A recent increase in the number of vascular access
procedures performed by nephrologists has resulted in
increased detection and awareness of CVS. Almost
80% of patients in the United States initiate dialysis
therapy with a catheter, and repeated attempts to
Figure 2. Anatomy of the venous system shows central veins
in the upper and lower extremities. The designations brachiocephalic and innominate are synonymous.
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Figure 3. Near-complete occlusion of the right brachiocephalic (innominate) vein with retrograde flow to the internal
jugular vein and the presence of collaterals.
create and develop an AVF rather than place an AV
graft (AVG), even in those with suboptimal veins,
have the potential to prolong the duration of catheter use and cause CVS, although at present there
are no data to prove such an impact of current
fistula strategy.1
The true incidence and prevalence of CVS in the
ESRD population is unknown because most studies of
CVS are limited to symptomatic patients. CVS may
remain asymptomatic because clinical symptoms and
signs of CVS often develop only after an AVF or AVG
is placed in the ipsilateral extremity and the impediment to increased blood flow is unmasked.2 Additionally, if the stenosis is not critical or there is development of adequate collateral flow, the venous pooling
that occurs in the setting of a stenosis may remain
asymptomatic. Clinical signs may be subtle, and the
only indication of access dysfunction may be inadequate dialysis.
Angiographic studies of symptomatic patients demonstrate a high prevalence of CVS. Subclavian catheter placement is particularly high risk, with the
development of subclavian vein stenosis in approximately 25%-50% of patients in various studies.3,4 In
one cohort of 36 patients with a history of subclavian
catheter placement, angiographic evaluation prior to
AVF placement showed subclavian vein stenosis in
34%.5 Furthermore, in this study, of the 4 patients
already on HD therapy with fistula dysfunction, 3 had
stenosis of the subclavian vein and one had complete
occlusion. This contrasts with a control group of 30
patients with subclavian veins with no history of
cannulation in which no stenoses were noted. Retrospective investigations of symptomatic HD patients
Am J Kidney Dis. 2013;61(6):1001-1015
Central Vein Stenosis
Figure 4. (A) Right internal jugular
vein stenosis occurring only 1 week after
placement of a temporary hemodialysis
catheter. (B) During balloon angioplasty,
the waist on the balloon defines severe
stenosis of the vein. (Picture courtesy of
Tony Samaha, MD.)
with various accesses using duplex ultrasonography
or angiography have reported CVS prevalences of
19%-41%.6-8 The occurrence of CVS with internal
jugular catheters also has been demonstrated increasingly in more recent studies. Long-term femoral vein
catheters also are being used more frequently for
dialysis, and iliac vein and inferior vena cava stenoses
are not uncommon.
Although longer catheter duration has been implicated in CVS, temporary (nontunneled) dialysis catheters also have been associated with CVS (Fig 4A and
B). For example, a recent study of color Doppler
sonography of 100 consecutive patients receiving
temporary double-lumen dialysis catheters showed
CVS in 18%.9
Cause of and Risk Factors for CVS
CVS is associated with intravascular device or
central catheter placement in most cases, although it
occasionally can be idiopathic (Box 1). Preoperative
venography of patients prior to right internal jugular
vein tunneled catheter placement showed the presence
of CVS or angulation in 30% of patients without a
history of central catheter placement.10 The occur-
rence of CVS in HD patients has been reported on the
ipsilateral side of the AV access without a history of
previous CVC placement and is considered to be due
to increased flow and abnormal shear stress on the
side of access.11,12 Compression of the innominate
vein between arch vessels and the sternum also can
occur.13 The following sections review risk factors for
the occurrence of CVS in patients undergoing CVC or
device placement.
Number and Duration of CVCs
Irrespective of the location (subclavian or internal
jugular), a larger number and longer duration of CVC
use increases the risk of developing CVS.4,14 In one
study of subclavian vein stenosis, the mean number of
ipsilateral subclavian catheters was 1.6, and mean
duration of catheter use was 5.5 weeks.3 Further, a
prospective study of 42 consecutive subclavian vein
catheterizations demonstrated that stenosis more often was persistent (vs spontaneous recanalization) at 6
months in those with a larger number of inserted
catheters (2.0 vs 1.6), longer dwell time (49 vs 29
days), more dialysis sessions through the catheter (21
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
Central vein catheters
Tunneled dialysis catheters
Nontunneled dialysis catheters
Peripherally inserted central catheters
Other central venous catheters and ports
Cardiac rhythm devices
Pacemakers
Defibrillators
Unrelated to intravascular device
Idiopathic
Extrinsic compression of vein
Dialysis-associated venous thoracic outlet syndrome
Fibrosing mediastinitis
Retroperitoneal fibrosis
Post–radiation therapy
Am J Kidney Dis. 2013;61(6):1001-1015
Location of CVC
Anatomical configuration can expose a vein to a
unique degree of contact with catheters. Initial studies
demonstrated a much higher prevalence of CVS with
subclavian dialysis catheters (42%) than with internal
jugular dialysis catheters (10%).16 This may reflect in
part placement of 78% of internal jugular catheters on
the right side compared with 58% of subclavian
catheters. Similarly, a small study of short-term temporary dialysis catheters (32 subclavian and 20 internal jugular) showed a high incidence of CVS (50%) in
the subclavian group and none in the internal jugular
group,17 whereas another study of temporary HD
catheters in 57 HD patients showed no difference in
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Anil K. Agarwal
stenosis rates between subclavian and internal jugular
catheterization, with thrombus formation in 28%, subclavian stenosis in 14%, and superior vena cava
stenosis in 2% of the population.18 In this study, the
number of subclavian catheters was small and could
explain the lack of difference in the incidence of CVS
between anatomical locations.
Importantly, although the risk of CVS appears to be
lower than with subclavian catheters, internal jugular
catheters frequently are associated with venous thrombosis and CVS.19-21 In one study, a high incidence of
thrombosis (26%) and venous occlusion (62%) was
found by ultrasonography in 143 patients with a right
internal jugular dialysis catheter,22 whereas a second
study reporting results of routine evaluation of 133
patients found CVS in 41% of patients, despite only
18 (14%) patients having prior subclavian vein catheterization.6 Another routine venographic study of 69
patients undergoing placement of tunneled right internal jugular catheters showed CVS or angulation of the
central veins in 42% of patients; 65% of patients with
these findings had previous internal jugular catheters.12 These studies point to the frequency and
duration of CVC placement as being a more important
determinant of CVS than the specific location.
A higher prevalence of CVS with catheters placed
on the left rather than the right side may reflect the
longer and more tortuous course required of a leftsided catheter. The course of left-sided CVCs is remarkable for at least 3 sites of sharp angles: at the
transition from the left internal jugular vein to the left
brachiocephalic (innominate) vein, at the midpoint of
the left brachiocephalic (innominate) vein as it wraps
around the mediastinal vessels, and at the junction of
the left brachiocephalic (innominate) vein and the
superior vena cava (Fig 5).23 Higher wall contact with
a longer course, especially during physiologic movements associated with respiration, the cardiac cycle,
and external movements, may result in increased
endothelial injury that stimulates fibrotic pathways,
thereby resulting in future CVS. Additionally, an
ultrasound study demonstrated that the cross-sectional area of the left internal jugular vein was much
smaller than the right internal jugular vein in most
healthy adults, potentially making the left side more
vulnerable to CVS.24 An analysis of 403 right and 77
left internal jugular catheters in 294 HD patients
found a higher number of infectious and vascular
complications in the left internal jugular group25;
most notably, 4 patients with prior left internal jugular
catheters developed ipsilateral central venous occlusion resulting in permanent vascular access loss versus none in the right internal jugular group. Another
retrospective study of 127 patients with internal jugular catheters showed that 50% (7/14) of patients with
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Figure 5. (A) Thick slab maximum intensity projection image
shows a sharp angulation of the brachiocephalic vein as it
crosses the aorta and great vessels. (B) Coronal MIP image in
the same patient. The angulation of the brachiocephalic vein
cannot be appreciated in this projection. Reproduced from Salik
et al23 with permission of Elsevier.
left internal jugular catheters developed CVS compared to 0.9% (1/117) with right internal jugular
catheters (P⬍0.05). Of note, 7 of 13 patients with a
left-sided catheter and left AVF developed signs and
symptoms of CVS versus 1 of 24 patients with a
right-sided catheter and right AVF.14
External compression of the left brachiocephalic
(innominate) vein by the mediastinal structures also
may be responsible for CVS in some cases (Fig 6).26
An engorged subclavian vein can be compressed
between the clavicle and first rib, causing hemodialysis-associated thoracic outlet syndrome.27 CVS also
has been reported in association with femoral cathAm J Kidney Dis. 2013;61(6):1001-1015
Central Vein Stenosis
Figure 7. Stenosis of the left subclavian vein (arrow) due to
the presence of pacemaker wires. Note the presence of collateralization in the upper arm and retrograde filling of the cephalic
vein. Reproduced from Agarwal37 with permission of Elsevier.
eters, and the incidence of this complication might
increase as use of this access site increases.28
Peripherally Inserted Central Catheters
Smaller caliber CVCs (such as peripherally inserted central [PICC] and triple-lumen catheters) also
can be associated with thrombus formation and CVS
over a short term.29-32 In 150 patients undergoing
PICC placement who had no evidence of CVS or
occlusion on preplacement venography, 7% had CVS
or occlusion on subsequent venography; this was
particularly common in those with longer catheter
dwell time.33 It is difficult to ascertain the true clinical
incidence and prevalence of CVS in patients with
PICCs because few patients with a history of PICCs
are studied with angiography or challenged by high
blood flow from an AV access. Increasing use of
PICCs in patients with chronic kidney disease (CKD)
has the potential to result in difficulty obtaining vascular access in the future. A recent retrospective casecontrol study of dialysis patients found that 44.2% of
those using a nonfistula access (catheters and grafts)
had a history of PICC placement compared with only
19.7% of those using AVFs.34 Single-lumen tunneled
central infusion catheters may be less risky, although
no such evidence of their safety is available at present.
Figure 6. Left upper-extremity fistulogram shows different
degrees of left brachiocephalic (innominate) vein compression.
(A) Splaying of the left brachiocephalic vein (star) of a patient
with mild (grade 1) compression. (B) Indentation of the left
brachiocephalic vein (arrow) and collaterals (arrowhead) in a
patient with moderate (grade 2) compression. (C) Marked indentation of the left brachiocephalic vein (arrows) and prominent
collaterals (star) in a patient with severe (grade 3) compression
by what appear to be the brachiocephalic (innominate) and left
common carotid arteries. Reproduced from Maxim et al26 with
permission of Elsevier.
Am J Kidney Dis. 2013;61(6):1001-1015
Cardiac Rhythm Device–Associated CVS
Cardiovascular disease is a common comorbid condition in patients with advanced CKD, and use of
intravascular devices such as pacemakers or defibrillators is common.35,36 The left upper chest is the
preferred location for both vascular access placement
and cardiac rhythm device placement. Constant friction from pacemaker leads can cause persistent inflammation of the left central veins (Fig 7).37 In one study
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Anil K. Agarwal
of 30 patients with long-term transvenous defibrillators in place for 45 ⫾ 21 months, venography showed
a 50% prevalence of subclavian vein stenosis,38
whereas in another study, abnormalities of the central
veins were found in 64% of patients on routine
angiography after 6 months, suggesting that even a
relatively short duration of injury is not inconsequential.39 Other studies of such devices also have shown a
high prevalence of central vein abnormality,40-42 with
one recent retrospective review of HD patients showing 62% of individuals with cardiac rhythm devices
versus 32% of individuals without cardiac rhythm
devices having CVS.43 Critically, CVS can remain
asymptomatic and may manifest only when challenged by increased blood flow from a dialysis access.35,44,45
The presence of CVS should be suspected and
proactively investigated prior to placement of AV
access in patients with a cardiac rhythm device and
preemptively treated if an ipsilateral AV access is
necessary. Furthermore, a device should not be placed
ipsilateral to the AV access. Angioplasty and stent
placement of the CVS associated with device wires is
possible, but carries the risk of erosion of the leads
over months to years. Stent placement over the leads
should be avoided because stents may make wire
extraction very difficult in the event of an infection.
Finally, epicardial lead implantation, although more
invasive, may be preferable in the appropriate scenarios to avoid the risk of CVS.
PATHOPHYSIOLOGY
CVS due to venous catheters most likely is related
to heightened inflammation, increased oxidative stress,
activation of leukocytes, release of myeloperoxidase,
and activation of the coagulation cascade after catheter placement.46 The endothelial damage begins with
the initial trauma from vein cannulation that is perpetuated by an indwelling foreign body that is not biocompatible. Further, constant movement of the catheter
with respiration, movements of the head, and changes
in posture, as well as increased flow and turbulence
from the AV access, alter the shear stress, resulting in
platelet deposition and venous wall thickening.47
Trauma to the vessel wall results in thrombin generation, platelet activation, and expression of P-selectin
with inflammatory response,48 and subsequent activation of leukocytes results in release of myeloperoxidase and formation of platelet aggregates, culminating in intravascular thrombosis.49 Catheters frequently
are associated with formation of a thrombus, often in
conjunction with venous stenosis at the same site,
although it is unclear whether the thrombus and the
stenosis are causally related to each other.50 Not only
does the formation of platelet thrombi and a thrombus
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at the tip of the catheter cause catheter dysfunction,
but an adherent thrombus also may be the first step in
the formation of a fibrin sleeve on the outer surface of
the catheter. This process starts early, and a full-length
sleeve can form as early as within a week.51,52 Thrombotic complications commonly occur in veins that
have been catheterized and frequently are associated
with catheter sepsis.53 Stabilizing the tip of the catheter to the center of the vein lumen with a thin wire
loop in a swine model caused less injury, thrombosis,
and thickening in the vessel wall.54 This supports the
mechanical theory of the development of CVS.
Activation of coagulation factors may be an important element in the cause of CVS. Animal models
have shown that structural changes in the vein wall
occur within 24 hours after endothelial denudation,
marked by the development of platelet microthrombi.55
During the next 7-8 days, several layers of smooth
muscle cells develop in the injured areas, but apparently only if a “critical” area of injury is present,
without which the proliferative response does not
occur. Direct evidence for histopathologic changes is
scant in humans, but subclavian vein specimens from
directional atherectomy in patients with symptomatic
stenosis or occlusion show intimal hyperplasia and
the presence of fibrous tissue.56 Autopsy finding of an
adherent clot with intimal injury in patients with less
than 14 days of catheter use and the presence of
smooth muscle proliferation and thickened venous
wall in those with more than 90 days of catheter use
further support this hypothesis.57 Importantly, these
catheters also were found to be focally attached to the
vein wall by organizing thrombus, endothelial cells,
and collagen, perhaps suggesting imminent development of a fibrin sheath or CVS.
Bioincompatibility of the intravascular device likely
is one of the factors in the causation of venous injury
and inflammation. Catheter material may have different levels of antigenicity, potential for tissue growth,
and fibrogenesis, and this issue requires further study.
It has been suggested that Silastic internal jugular
catheters may produce less thrombosis,58 with one
study of the use of silicone catheters conducted in 22
patients with subclavian cannulation showing stenosis
in only 2 and thrombosis in only 3. In this study, there
was a lower incidence of subclavian vein stenosis
with these catheters than with polytetrafluoroethylene
(PTFE) and polyurethane catheters.59 In a rabbit model,
polyethylene and Teflon catheters caused more inflammation than silicone and polyurethane.60 Both silicone (eg, Tesio [Medcomp] and Schon [AngioDynamics]) and polyurethane (eg, Opti-Flow [Bard Access
Systems] and Ash Split [Medcomp]) commonly are
used to manufacture long-term dialysis catheters.
Am J Kidney Dis. 2013;61(6):1001-1015
Central Vein Stenosis
Figure 8. (A) Severe stenosis of the
superior vena cava (SVC) with edema of
face, lips, and thorax at presentation and
(B) dramatic resolution of edema after
successful angioplasty of SVC stenosis.
(Photographs courtesy of Arif Asif, MD.)
Infections associated with CVCs may aggravate
inflammation and predispose to the development of
CVS. In one study of 54 long-term HD patients,
venography performed 6 months after catheter removal showed a 75% prevalence of CVS in those with
previous catheter infections compared with 28% in
those with no infection.61 It also is plausible that CVS
was the predisposing factor for infection, pointing to a
possible vicious cycle.
It can be hypothesized that inflammation and activation of coagulation pathways act in combination and
are not sufficient by themselves to cause CVS. However, in a retrospective study of 77 patients with lupus
and ESRD, 17 patients (22%) had documented CVS,
similar to the nonlupus group.62 Number of CVCs,
but not degree of inflammation, was found to be
associated with CVS in this retrospective cohort study.
Thus, it is possible that a systemic inflammatory
disease such as lupus may not result in a particularly
higher incidence or prevalence of CVS due to competing inflammation present in patients with ESRD,
although the small size of this retrospective study
cannot be considered conclusive.
Anatomical factors also may contribute to the pathophysiology 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 brachiocephalic (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
CVS becomes symptomatic in HD patients with an
increase in extremity blood flow from an AV access.
Am J Kidney Dis. 2013;61(6):1001-1015
The clinical features of CVS vary according to the site
of obstruction and mechanism of development.
Related to Venous Hypertension Peripheral
to the Obstruction
Venous engorgement from CVS may result in
edema, swelling, pain, tenderness, and erythema of
the ipsilateral extremity, along with ipsilateral breast
swelling. Pleural effusions may develop in severe
cases. In cases of stenosis of the bilateral brachiocephalic veins or if superior vena cava syndrome develops,
this typically responds to angioplasty (Fig 8A and B). In
chronic superior vena cava obstruction, alternative
venous drainage into the azygous system can develop,
although clinical features of CVS are always present
(Fig 9).37 Intercostal veins often can be dilated as well
(Fig 10).
Rarely, abnormal flow in the left jugular bulb and
inferior petrosal sinuses can be caused by retrograde
flow from brachiocephalic vein stenosis, leading to
false suspicion of the presence of a carotid cavernous
fistula.64
Figure 9. Severe stenosis of the superior vena cava with a
significantly dilated azygous vein (arrowhead). Reproduced from
Agarwal37 with permission of Elsevier.
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Anil K. Agarwal
Figure 10. Occlusion of the subclavian vein with development of alternative venous drainage through the intercostal and
internal thoracic veins. (Photo courtesy of Rizwan Qazi, MD.)
Related to Vascular Access Dysfunction
During Dialysis
Venous engorgement due to CVS can cause tortuosity and aneurysmal dilatation of veins, collateral formation, prolonged bleeding after dialysis, elevated
venous pressures during dialysis, and thrombosis of
the vascular access. Poor adequacy of dialysis and its
consequences, including recurrent hyperkalemia, can
develop if CVS is untreated.
It is possible to have CVS without specific symptoms. For example, only about half the patients with
subclavian vein obstruction develop edema of the
arm.3 Clinically asymptomatic CVS is detected incidentally by angiography done in preparation of AV
access placement or during investigation of unrelated
access dysfunction.
DIAGNOSIS
A high index of suspicion, especially in those with
a history of multiple catheter placements or longstanding catheter use, can lead to clinical diagnosis of
CVS. Careful physical examination may reveal limb
or breast swelling and the development of collaterals,
particularly around the neck and upper part of the
chest, and retrograde flow in collateral veins detected
on physical examination may indicate the presence of
more central outflow obstruction. However, the definitive diagnosis of CVS is made by angiography.
Angiography is superior to duplex ultrasonography
and is recommended prior to placement of an AV
access in dialysis patients with a history of previous
CVC placement, especially subclavian catheters.65,66
A minimal amount of an iso-osmolar radiocontrast
can be used safely for a venogram in patients not yet
on dialysis therapy. Duplex ultrasonography is suboptimal for the evaluation of central veins due to interfer1008
ence by the bony thorax and overlapping soft tissue in
obese individuals. However, color flow duplex ultrasonography avoids the use of radiocontrast and can
suggest CVS when there is an absence of respiratory
variation in vessel diameter, lack of polyphasic atrial
waves, and presence of collateral channels.67 In a
study comparing duplex ultrasonography to venography in symptomatic patients with a liver transplant,
dialysis, or cancer, there was significant yield with
duplex and 90% agreement with venography.68 In this
study, the optimal threshold for detection of a ⬎50%
stenosis by duplex ultrasonography was a poststenotic
to prestenotic peak vein velocity ratio of 2.5. These
results suggest that duplex ultrasonography can be
used not only to select which patients should receive
an intervention, but also for monitoring how successful the treatment is during follow-up.
Magnetic resonance angiography to evaluate central veins has been used previously, but should be
avoided due to the possibility of nephrogenic systemic fibrosis after gadolinium use in patients with
advanced kidney disease.69 Newer techniques, such
as time-of-flight magnetic resonance angiography, may
be able to visualize veins without using contrast.
APPROACH TO THE TREATMENT OF CVS
Prior to considering intervention, it is important to
evaluate the patient carefully and individually, keeping in mind the often temporary improvement associated with current methods of treatment, clinical care,
and needs and all available options for kidney replacement therapy for that individual patient.
Conservative Approach
Close observation of patients with chronic obstruction and adequately developed collaterals may be
sufficient. Intervention is indicated when either HD is
inadequate or if symptoms appear. Occasionally, symptoms may improve as collaterals develop. Simple
measures such as elevation of the extremity can help
in very mild cases of CVS. For an associated thrombus in the central vein, anticoagulation therapy is
indicated, as suggested by available guidelines.70,71
The catheter, if still functional, asymptomatic, and
needed, should not be removed. These measures may
only be able to bridge a dysfunctional access while
more definitive therapy is planned for correction of
obstruction or creation of a new access to allow
catheter avoidance.
Endovascular Intervention
Endovascular intervention should be considered
with caution because the approaches to correction of
CVS remain suboptimal and possibly even detrimental. In one study, more aggressive neointimal hyperplaAm J Kidney Dis. 2013;61(6):1001-1015
Central Vein Stenosis
sia and proliferative lesions were found in restenotic
areas after angioplasty than were found in the original
stenosis.72 In another study of ⬎50% CVS in 35
asymptomatic HD patients with 38 AVGs, 86 venograms were reviewed.73 No intervention was done in
28% of cases, and none of these patients progressed to
symptoms, stent placement, or additional CVS. In
contrast, in the 72% of cases in which percutaneous
transluminal angioplasty (PTA) was performed, escalation of CVS after PTA was seen in 8% of these
cases, resulting in further interventions. Although
there is possible indication bias, these findings support the theory that endothelial damage from angioplasty can aggravate the venous response and accelerate the stenotic process. It also is possible that a rather
high residual stenosis (40%) in the intervention group
was an indication of its already refractory nature and
that a more aggressive approach with stent placement
might have been beneficial.74 Thus, endovascular intervention for CVS requires careful planning while
using restraint when feasible. Endovascular intervention also can be used as a palliative approach. Coil
embolization of the long thoracic vein has been shown
to reduce breast edema in HD patients who have
elevated venous hydrostatic pressure due to central
venous occlusion.75
Percutaneous Transluminal Angioplasty
PTA, either on its own or with stent placement, is
the preferred approach to CVS, depending on the
rapidity of recurrence (guideline 20 of the National
Kidney Foundation–Kidney Disease Outcomes Quality Initiative [NKF-KDOQI]).76 PTA for central venous disease has been in vogue for almost 3 decades
and has very high technical success rates, ranging
from 70%-90%.47,77-82 The variable patency rates in
these studies may be due to the variety of criteria used
by authors in reporting their results, as well as the
wide variety of techniques and equipment used. According to these studies, at 6 months, unassisted
patency after PTA varies from 23%-63%, with a
cumulative patency rate range of 29%-100%, whereas
at 12 months, unassisted patency after PTA ranges
from 12%-50%, with a cumulative patency rate of
13%-100%. Although poor patency rates after PTA
alone were seen in 2 earlier studies of patients with
CVS (28.9% at 180 days and 25% at 1 year),75,83 a
more recent study using high-pressure balloons noted
better results with PTA alone, with unassisted patency
after PTA of 60% at 6 months and 30% at 12 months.84
Results in this study and similar results from a second
more recent study81 suggest either a difference in
patient population or technical advances, including
the use of high-pressure balloons. Significant secondary patency often can be achieved with repeated
Am J Kidney Dis. 2013;61(6):1001-1015
angioplasty without use of a stent. Critically, a lack of
large randomized controlled studies of PTA in patients
with CVS does not allow fair comparison of outcomes
of PTA vis à vis other treatment modalities.
Intravascular ultrasound study after angioplasty of
the central veins has shown that central veins are
much more likely to recoil than the peripheral veins.85
Thus, the success of PTA often depends on the elastic
or nonelastic nature of the lesion, which may have
different structural characteristics of the stenosis as
shown by intravascular ultrasound.78.
STENTS
Lack of sustained results with PTA led to the use of
stents for CVS.86 Guidelines for CVS recommend
placement of a stent for elastic recoil of the vein that
leads to significant residual stenosis after PTA or for
lesions recurring within 3 months after angioplasty.76,87
Placement of self-expandable stents in the treatment
of CVS typically achieves a high degree of technical
success. For example, use of self-expanding metallic
stents for elastic lesions was associated with better
outcomes than angioplasty alone. However, the primary and secondary patency of stents is modest at
best (Table 1).88 It also is difficult to compare results
of different studies done over a period of time because
stainless steel stents were used in earlier studies. In
one study of 52 HD patients with 56 lesions, 51
self-expandable metallic stents were placed.89 Primary and secondary patency rates were 46% and 76%
at 6 months and 20% and 33% at 12 months, respectively. However, another study of 57 self-expandable
metallic stents in 50 patients with CVS had far better
results, with primary patency rates of 92%, 84%,
56%, and 28% at 3, 6, 12, and 24 months, respectively.90 Secondary patency also was significantly
better: 97% after 6 and 12 months, 89% after 24
months, and 81% after both 36 and 48 months. In a
retrospective study, 23 patients with symptomatic
refractory CVS were treated with various types of
stent placement.91 In this study, median primary patency was 138 days, with 1-year patency of only 19%,
whereas median secondary patency was 1,036 days
with 64% patency at 1 year. A recent retrospective
analysis of the Nitinol shape memory alloy stents in
64 patients (with 15 central and 54 peripheral vein
stents) showed primary patency of 14.9 months in
central veins and 8.9 months in peripheral veins.92
Significantly better results in this retrospective study
may reflect the more advanced nature of the stent
material, although this conclusion remains conjecture.
Repeated interventions are needed to maintain patency achieved by the stents over longer periods.
1009
Anil K. Agarwal
Table 1. Studies of Stent Placement in Central Vein Stenosis
Study
No. of Central
Lesions
Primary Patency
Secondary Patency
83.3% (95% CI, 50%-120%) at 3 mo, and
66.7% at 6 and 12 mo (95% CIs, 20%110% and 10%-120%)
Fistula group rates: 88.5% ⫾ 4.8%, 59.4% ⫾
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
19% at 1 ya
NA
Secondary patency: 100% at 12 mo with 3
patients censored over that time
Rajan DK (2007)
6
Rajan DK (2007)
89
Maya ID (2007)
Sprouse LR (2004)
23
32
Aytekin C (2004)
14
Chen CY (2003)
18
Hatzimpaloglou A (2002)
Smayra T (2001)
Haage P (1999)
15
9
50
Vesely TM (1997)
20
Mickley V (1997)
Lumsden AB (1997)
Vesely TM (1997)
15
25
20
Mickley V (1997)
Gray RJ (1995)
Beathard GA (1992)
15
32
24
1-, 3-, 6-, and 12-mo primary stent patency
rates: 92.8%, 85.7%, 50%, and 14.3%
3, 6, 12 and 18 mo: 100% and 89%, 73%
and 68%, 49% and 42%, and 16% and
0%c
70% at 12 and 24 mo
56% at 1 y
3, 6, 12, and 24 mo: 92%, 84%, 56%, and
2%
1, 3, 6 mo, and 1 y: 90%, 67%, 42%, and
25%
1 y: 100%; 2 y: 85%
84% at 1 mo, 42% at 6 mo, and 17% at 1 y
1, 3, 6 mo and 1 y: 90%, 67%, 42%, and
25%
100% at 1 y, 85% at 2 y
46% at 6 mo, 20% at 12 mob
NA
Matthews R (1992)
2
NA
NA
64% at 1 ya
Symptoms related to central stenosis were
controlled for 6.5 mo on average
3-, 6-, 12-mo and 2-y secondary patency
rates: 100%, 88.8%, 55.5%, and 33.3%
100% after 3 mo, 93% and 100% after 6
mo, 85% and 91% after 12 mo and, 68%
and 72% after 24 mo
NA
75% 1 y
97% after 6 and 12 mo, 89% after 24 mo,
and 81% after 36 and 48 mo
3, 6 mo, 1 and 2 y: 89%, 64%, 56%, and
22%
1 y: 70%; 2 y: 50%
—
3, 6 mo, 1 and 2 y: 89%, 64%, 56%, and
22%
70% at 1 y, 50% at 2 y
76% at 6 mo, 33% at 12 mob
70.4% at 1 mo, 62.1% at 2 mo, 48.6% at 3
mo, and 28.9% at 4 mo
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
placement and multiple periodic interventions may be
appropriate. Bare-metal stents are associated with
shortening, migration, fracture, and neointimal hyperplasia and require repeated treatments with PTA.93-96
The type of stent used also may be a factor in the
variable success rates of these stents. First-generation
stents, such as self-expandable metallic stents, are low
profile, flexible, and radiopaque, but have disadvantages of foreshortening at the time of placement,
delayed shortening, and migration.97 Second-generation stents made of nickel-titanium alloy transform
according to temperature, are superelastic, and can
return to their original shape after the deforming force
is removed.
Use of covered stents also is becoming increasingly common, and these “stent grafts” or “en1010
dografts” have the advantage of providing a relatively inert and stable intravascular matrix for
endothelialization, thereby reducing restenosis.97
Studies of the efficacy of covered stents are now
emerging.3,98 One study evaluating PTFE-covered
stent placement showed 360-day primary patency
of 32% and secondary patency of 39%,96 whereas a
similar study evaluating Dacron (polyethylene terephthalate)-covered stents showed primary and
secondary patency rates of 29% and 64%, respectively, at 1 year.99 Immediate and long-term results
of stent grafts are encouraging in more recent
studies.100-102
Outcomes of PTA alone and stent placement have
not been compared in randomized controlled trials. A
study of central vein angioplasty (n ⫽ 101) and stent
placement (n ⫽ 46) showed that angioplasty alone
Am J Kidney Dis. 2013;61(6):1001-1015
Central Vein Stenosis
was superior to stent placement in terms of primary
patency, but assisted (secondary) patency of both
angioplasty and stent placement was similar, pointing
to a benefit with stent placement in angioplastyresistant lesions.103 Of note, these authors used cutting balloons prior to placing stents. Similar patency
with angioplasty and stent placement was seen in
other recent studies.104,105 Thus, use of stents can
improve initial technical success in patients resistant
to PTA alone.
In summary, venous stents have many limitations,
such as migration, fracture, intrastent neointimal hyperplasia, and appearance of unrelated stenoses. Stents
placed in the low-pressure venous system are inherently less likely to remain patent than in the highpressure arterial system. Despite these shortcomings,
stent placement offers an immediate access-saving
intervention for those with difficult access with refractory lesions who require a bridge to more definitive
treatment later.
Hybrid Graft-Catheter Device
A novel approach to CVS recently has become
available in the form of a hybrid graft-catheter. When
CVS is refractory to the traditional approach but
placement of a CVC is possible, this approach allows
use of an internal AV access with reduced risk of
infection.106 The graft portion of the device is placed
in the arm and is connected to the catheter component
that traverses the CVS. The indication for such a
device currently is limited to the population with
near-exhaustion of access sites, and long-term results
will define its place in maintaining vascular access in
the future.
Cardiac Rhythm Device–Related CVS
The management of CVS related to cardiac rhythm
devices may require angioplasty, stent placement, or
as a last resort, ligation of access to reduce symptoms.
Angioplasty has been shown to be safe and provides
poor primary but acceptable secondary patency rates
at 1 year.107 If necessary, the stent can be placed over
the lead wire, but this is not recommended because it
will “jail the leads,” making removal of the wire
difficult in case of infection in dialysis patients.108,109
If stent placement is needed, ideally the device first
should be removed and replaced after the stent has
been placed, although this is a much more complex
procedure.110 Placement of epicardial leads should be
considered in such cases, as well as in high-risk cases
with advanced CKD proactively (prior to access placement) to preserve central veins and avoid lead infection.111
Am J Kidney Dis. 2013;61(6):1001-1015
Surgery
In severely symptomatic cases, access occlusion
can be achieved either manually, by surgical ligation,
or by inflating a balloon inside the access for a
prolonged period. When another access site is available, new access should be created, preferably preemptively (to avoid catheter use), and symptomatic CVS
can be treated with ligation of access. A precision
banding procedure to reduce access flow using realtime intravascular flow monitoring has been shown to
reduce symptoms related to venous hypertension.112
Surgery for correction of CVS is difficult, often
requiring claviculectomy or even median sternotomy.
Accordingly, surgery usually is considered a last resort when percutaneous treatment has failed. Surgical
intervention consists of direct repair using saphenous
vein grafts or ringed PTFE grafts, jugular vein turndown to bypass a stenosed subclavian vein, or use of
surgical techniques to create anastomosis of vein to
vein or even vein to right atrium. Approaches include
axillary to jugular vein, subclavian vein to superior
vena cava, cephalic vein to external jugular vein, and
axillary vein (or artery) to superior vena cava or
auricular appendage anastomosis.113 In the lower extremity, common femoral vein to iliac vein or inferior
vena cava and external iliac vein to inferior vena cava
bypass can be done.114
Alternative Approaches for Kidney Replacement
Therapy in CVS
When vascular access is failing due to CVS, a
different location for access should be considered. It
also is reasonable to consider another modality of
kidney replacement therapy, including changing to
peritoneal dialysis and expediting kidney transplantation. These options should be discussed with the
patient each time an access fails, irrespective of the
cause or regardless of whether all vascular access
options have been exhausted.
PREVENTION
CVS is likely to remain a major concern in the
future because ⬎80% of patients initiating HD therapy
in the United States do so with a CVC.1,115 Inadequate
education and planning for vascular access during late
CKD care, due to either late patient referral to a
nephrologist or late referral to an access surgeon,
needs to be addressed. Because the number and duration of CVCs remain the most important cause of
CVS, avoidance of catheters is critical. In appropriate
situations, all possible approaches should be considered at the onset of kidney failure, including fistula,
graft, peritoneal dialysis, and preemptive kidney transplantation, with a focus on the “catheter last” approach. Early referral to a nephrologist and early
1011
Anil K. Agarwal
placement of an AVF are essential. In patients with
earlier stages of CKD, strategies to preserve vessels
(both arteries and veins) should be followed. Risks of
using catheters, especially subclavian catheters but
also including infusion catheters and PICCs, should
be emphasized. In patients with CKD, use of a singlelumen central venous infusion catheter may be preferable, although data about their safety are not available
at this time. Additionally, the initiation of dialysis
therapy can be delayed to allow time for access
creation. In this regard, it is important to note that
during the past decade, dialysis is being initiated at
higher levels of estimated kidney function with little
evidence for the benefits of such a practice.116 Once
created, effective early salvage of immature AVFs and
methods to improve the use of relatively difficult
AVFs, such as creation of buttonholes, are important
methods to increase initial and ongoing fistula usability.117 Finally, a femoral access is preferable to using a
subclavian catheter for HD access.
FUTURE DIRECTIONS IN MANAGEMENT OF CVS
With controversial benefits and risks of angioplasty
and stent placement, optimal treatment of CVS is
elusive at this time. Because CVCs remain a “necessary evil,” approaches to improve catheters (less antigenic material and better hemodynamics) should be
investigated. Animal and in vitro studies of the newer
heparin-coated catheters have shown lower thrombosis and fibrin-sheath formation, although data for
humans are limited. The impact of these newer catheters on the development of CVS should become a
routine end point in such studies. Improvement in
balloon and stent technology, including better cutting
balloons and drug-eluting stents, may improve results,
but these have not undergone systematic evaluation
for treatment of central vein lesions. Initial results of
using brachytherapy were encouraging, but it has not
been shown to prolong the patency of the vein because of recurrent stenosis in new locations.118 Radiofrequency wire techniques are being evaluated for the
treatment of central vein occlusion. Pharmacologic
agents reducing inflammation and fibrosis also should
be investigated.
CASE REVIEW
The patient had recurrent occlusion of a brachiocephalic vein stent with significant symptoms of venous
hypertension. Although the left upper extremity was a
potential site to create a secondary AVF, we wanted to
preserve her current access if possible. Moreover,
given the high number of catheters she had previously, it was likely that she also could have left
brachiocephalic vein stenosis. We considered placement of a femoral AV access, but were reluctant on
1012
Figure 11. Recanalization of the brachiocephalic (innominate) vein stent with re-establishment of central flow in our
patient.
account of her morbid obesity, although that remains a
viable future option. The patient did not have an ideal
situation to perform peritoneal dialysis and was not an
acceptable candidate for transplantation due to morbid obesity. Accordingly, she underwent recanalization of her right brachiocephalic vein stent using a
traditional technique without using radiofrequency
wire (Fig 11). Interestingly, she reported after the
procedure that hearing in her right ear slowly started
improving. The AVF was used without difficulty until
she required another recanalization 10 months later,
along with covered stent placement. She presently is
using the same access for HD.
ACKNOWLEDGEMENTS
Support: None.
Financial Disclosures: The author declares that he has no
relevant financial interests.
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