Central Vein Stenosis: A Nephrologists
Perspective
Anil K. Agarwal, Bhairavi M. Patel, and Nabil J. Haddad
Division of Nephrology, Department of Internal Medicine, Ohio State University, Columbus, Ohio
ABSTRACT
Central vein stenosis is commonly associated with placement
of central venous catheters and devices. Central vein stenosis
can jeopardize the future of arteriovenous stula and arterio-
venous graft in the ipsilateral extremity. Occurrence of central
vein stenosis in association with indwelling intravascular
devices including short-term, small-diameter catheters such as
peripherally inserted central catheters, long-term hemodialysis
catheters, as well as pacemaker wires, has been recognized for
over two decades. Placement of multiple catheters, longer
duration, location in subclavian vein, and placement on the
left-hand side of neck seem to predispose to the development
of central vein stenosis. Endothelial injury with subsequent
changes in the vessel wall results in development of micro-
thrombi, smooth muscle proliferation, and central vein steno-
sis. Central vein stenosis is often asymptomatic in nondialysis
patients, but can result in edema of ipsilateral extremity and
breast when challenged by increased ow from an arterio-
venous stula or arteriovenous graft. Bilateral central vein
Dialysis vascular access-related expenditures cost the
Centers for Medicare and Medicaid Services (CMS)
over a billion dollars in 2001. Complications related to
vascular access account for 2030% of hospitalizations
of dialysis patients, primarily from sepsis and thrombo-
sis (1). Access thrombosis is usually a result of outow
obstruction because of stenosis at various points in the
anatomical course of access. While the most common
site of outow obstruction for arteriovenous grafts
(AVG) is at the venous anastomosis, occurrence of
central vein stenosis (CVS) compromises the ipsilateral
side for placement of any type of vascular access (Figs. 1
and 2).
Occurrence of CVS, commonly manifested by extrem-
ity and breast edema, pain, inadequate dialysis, and AV
access failure, has been well recognized since the early
1980s (28). The strikingly common theme of the reports
of CVS has been the association of central venous lesions
with previous placement of central venous catheters
(CVC). Well known to cause recurrent infections and
thrombosis, CVC can also result in less common but
Address correspondence to: Anil K. Agarwal, MD, FACP,
FASN, Division of Nephrology, Department of Internal Medi-
cine, Ohio State University, N 210 Means Hall, 1654 Upham
Drive, Columbus, OH 43210, or e-mail: aagarwal@
pol.net.
Seminars in DialysisVol 20, No 1 (JanuaryFebruary) 2007
pp. 5362
53
stenosis or superior vena cava stenosis can produce a clinical
picture of superior vena cava syndrome, associated with
engorgement of face and neck. Endovascular interventions
are the mainstay of management of central vein stenosis. Per-
cutaneous angioplasty and stent placement for elastic and
recurring lesions can restore the functionality of the vascular
access, at least temporarily. Frequent or multiple interven-
tions are usually required. In recalcitrant cases, surgical
bypass of the obstruction is an option. In resistant cases with
severe symptoms, occlusion of the functioning vascular access
will usually provide relief of symptoms. Further study of
mechanisms of development of central vein stenosis and
search for a targeted therapy is likely to lead to better ways
of managing central vein stenosis. Prevention of central vein
stenosis is the key to avoid access failure and other
complications from central vein stenosis and relies upon
avoidance of central vein stenosis placement and timely place-
ment of arteriovenous stula in prospective dialysis patient.
serious delayed complications, such as CVS. While it is
possible to have idiopathic CVS in the absence of history
of CVC or other device placement, the current review
will focus on the CVS associated with CVC due to its
higher prevalence and potential for prevention.
Prevalence
As CVS can be asymptomatic and routine or serial
venograms are not usual after CVC placement or
removal, the incidence of CVS is uncertain and is likely
to be underestimated. The high prevalence seen in dialy-
sis patients perhaps reects the fact that CVS only
becomes clinically manifest as the blood ow through
the maturing dialysis access increases, leading to venous
engorgement because of poor outow. Thus, the source
of most of the currently available data is limited to the
studies of symptomatic dialysis patients who required
imaging studies. Almost 25% of dialysis patients with
dysfunctional stulae were found to have subclavian
stenosis in one study, all with a history of previous
subclavian vein catheterization (7). Nineteen percent of
all patients (and 27% of those with history of previous
CVC) had CVS in one angiography series (9), similar to
the 16% incidence of CVS in another (10). A prospective
evaluation of functioning AVG by duplex scanning and
angiography showed CVS in 29% of patients (11). When
looked for, available studies in asymptomatic patients
54 Agarwal et al.
Fig. 1. Venogram of right upper extremity arteriovenous access
showing severe stenosis of right innominate vein. Note presence of
dilated collateral veins on the right-hand side of the neck with
reux of contrast into neck veins.
Fig. 2. Venogram of the left upper extremity arteriovenous access
showing complete occlusion of the left subclavian vein with dilated
collateral veins in the left shoulder area.
have found a relatively high incidence of CVS in those
with subclavian catheters (4250%) compared to those
with internal jugular (IJ) catheters (8,1214). Even occlu-
sion of the subclavian vein was frequently unaccompa-
nied by any clinical ndings (15).
Pathogenesis
The precise mechanisms of development of CVS and
exact sequence of events are still undened. Plausible
mechanisms are linked to the CVC-induced trauma to
the venous endothelium and the resultant inammatory
response within the vessel wall. Aside from the initial
trauma at the time of CVC placement, many factors,
including the presence of foreign body in the vein, sliding
movement of the catheter with respiration, postural and
head movements, increased ow and turbulence from
creation of AVF, alone or in combination, stimulate var-
ious processes within the vessel wall. Turbulence has
been shown to cause platelet deposition and venous wall
thickening (16). The physical damage to the vessel wall
can result in thrombin generation, platelet activation,
expression of P-selectin, and an inammatory response
(17). Formation of plateletleukocyte and plateletplate-
let aggregates and activation of leukocytes induces
release of myeloperoxidase. Intravascular thrombosis
results, perhaps with release of probrotic cytokines
(18). The high blood ow associated with dialysis, turbu-
lence, and vibration have the capability to stimulate
intimal hyperplasia (19,20).
Structural Changes in the Vein
The structural changes associated with CVC have not
been studied extensively. In vivo experimental models of
endothelial denudation using rabbit and rat veins involv-
ing air-drying, trypsin digestion, or monolament injury
showed development of platelet microthrombi within
24 hours and the presence of several layers of smooth
muscle cells after 78 days in the injured areas (21).
Some of the veins became completely occluded, a result
attributed to a thrombotic response to slower ow and
lesser shear force than in the arterial tree. The varying
responses to different levels of injury led to the postula-
tion that a critical area of endothelial denudation was
needed to stimulate a smooth muscle response. Having
less than the critical area of injury was associated with
complete healing in less than a week and no subsequent
intimal lesion.
Histologic examination of directional atherectomy
specimens from subclavian veins in patients with symp-
tomatic stenosis or occlusion has shown intimal hyper-
plasia of the vessel with presence of brous tissue (22). In
an autopsy study of six patients, the access vein, brachio-
cephalic vein, and superior vena cava (SVC) of three
patients with short-term (< 14 day) catheter use
showed focal areas of injury to the intima, denudation of
endothelium, and adherent clot reecting early injury
(23). The other three patients with long-term (> 90
days) catheter use had smooth muscle cell proliferation
causing thickening of the vein wall. These catheters were
attached to the vein wall in focal areas by the means of
organizing thrombus, endothelial cells, and collagen.
Two catheters were composed of polyurethane and four
of silicone in this small study. These observations and
similar evidence from animal models (see Catheter
Design section) reect a pattern of progressive injury
and vessel response. Thus, soon after the placement of
the venous catheter there is an early inammatory
response with development of intimal injury and cre-
ation of nonorganizing thrombus. With continued
inammation, as in the case of a long-term indwelling
 CENTRAL VEIN STENOSIS
catheter, there is organization of thrombus, smooth
muscle proliferation, thickening of vessel wall, and for-
mation of a bridge to the catheter. Whether this is a pre-
cursor to the development of CVS cannot be established
at this time.
Anatomical Considerations
There are many potential sites for creation of an
AVF; radiocephalic and brachiocephalic AVF are the
most common sites for reasons of convenience and
accessibility. The increased blood ow through extrem-
ity veins as a result of maturation of the AVF ultimately
needs to travel into the right atrium via the subclavian
vein, innominate vein (also known as brachiocephalic
vein), and SVC (Fig. 3). Obstruction of these central
veins caused by stenosis or venous thrombosis will inter-
rupt this ow, interfering with the development of a
functional AVF. Even though the AVF may develop
successfully, the impedance to the blood ow by the ana-
tomical stenosis will result in venous hypertension and
development of collaterals. Further development of the
collaterals may mitigate the symptoms, at least partially,
and allow continued development and, ultimately, use
of the access. If the AVF continues to function, symp-
toms related to venous hypertension, such as extremity
edema and pain usually dominate the clinical picture,
leading to clinical and angiographic discovery of CVS.
The clinical manifestations of CVS result in a variety of
Fig. 3. Venous anatomy. Note the tortuous route of a central
venous catheter from left internal jugular vein with rightward
curve at junction with subclavian vein, and then leftward curve at
conuence of innominate veins to form the superior vena cava.
The route from the right internal jugular vein into the right atrium
is almost vertically down requiring less intimate contact with the
vein wall.
55
symptoms, which may differ depending on the level and
degree of obstruction, as described later.
Asymmetry of the Venous Drainage
There are signicant anatomical differences in the
path of right and left central veins. The right IJ vein trav-
erses the neck almost straight into the innominate and
SVC. The vein on the left, merging with the subclavian
vein, has to take a longer, tortuous course with two
opposite incurvations to reach the cavo-atrial junction.
In addition, in about a third of the patients, the left IJ
vein has a smaller cross-sectional area than the vein on
the right-hand side (24). These anatomic factors can lead
to greater contact of an indwelling foreign body with the
vessel wall when it is placed from the left-hand side. Not
only can this cause CVS on the left-hand side, it is also
capable of causing CVS on the right-hand side. This is
due to the close contact of the indwelling CVC with
the conuence of the veins causing turbulence in blood
ow; it is more likely with shorter than with longer
catheters.
Movement and Position of the Catheter Tip
The length of the mediastinum increases upon assum-
ing the upright position causing the tip of the catheter to
move up from its position in supine posture. The shift is
more evident in females with a large amount of breast tis-
sue, with larger-diameter catheters, and with subclavian
vein placement (25,26). Left-sided IJ catheters also move
more than right-sided catheters with rotation of the
head and neck, causing more endothelial trauma (27).
Risk Factors for CVS
Although in one study CVS was twice as common in
females as in males with subclavian dialysis catheters,
such a gender-related difference has not been well sub-
stantiated (14). There is no reported difference between
diabetics and nondiabetics as well. The prevalence of
idiopathic CVS or CVS resulting from causes other than
CVC has not been studied in dialysis patients, although
the SVC syndrome associated with bronchogenic carci-
noma and lymphoma is well described (28). Compres-
sion of the vein by an external mass can produce similar
symptoms and should be excluded.
Risk Factors for CVS Associated with CVC
Number and Duration of Previous CVC
Placement
It is relatively rare for CVS to occur in the absence of
previous venous catheterization. Multiple CVC place-
ments (14,29) and longer catheter dwell times (8,14,29)
have been associated with a higher risk of CVS. In case
of subclavian vein stenosis, the mean number of ipsilate-
ral catheters was 1.6 with mean duration of 5.5 weeks (7).
56 Agarwal et al.
Longer dwell time of CVC increases the duration of wall
injury. A prospective study of 42 consecutive hemodialy-
sis patients who underwent subclavian vein catheteriza-
tion with serial venograms at 0, 1, 3, and 6 months after
catheter removal, subclavian vein stenosis (>30% nar-
rowing) was found in 52.4% of patients (30). Sponta-
neous recanalization occurred in 45.4% of these patients
at 3 months. Patients with persistent stenosis at
6 months had a greater number of inserted catheters
(1.58 vs. 1.2), longer time in place (49 days vs. 29 days),
more dialysis sessions (21 vs. 12), and more catheter-
related infections (66.6% vs. 33.3%) than those who re-
canalized spontaneously.
Short-term hemodialysis catheters are commonplace
in those initiating hemodialysis, those with maturing
access, and those with a malfunctioning access awaiting
intervention. Though CVS is not as common with short-
term catheters, these catheters are not completely benign
(31,32). Pericatheter sleeves, thrombus formation, and
brachiocephalic vein stenoses have all been reported
with catheters that had been in place on average of
21 days (31).
Location of CVC
It is an important factor in causation of CVS. Sub-
clavian catheters have an especially high risk (8,1214)
with a 42% incidence of CVS compared to a 10% rate
with IJ vein catheters (13). However, a recent study
showed higher frequency of CVS with IJ catheters (33).
CVS was detected by venography in 27% of the patients
with history of IJ vein catheterization, 16% on the side
ipsilateral to the catheter and 11% on the contralateral
side (9). Another recent study of 133 dialysis patients
undergoing venography revealed a 41% prevalence
of CVS; 83% of those with a history of subclavian cathe-
ters had CVS and 36% of those with IJ catheters had
CVS (29).
from infection adding to that from the indwelling
catheter, this may not necessarily be so. It is possible
that CVS develops rst, and the impediment to the
blood ow due to it predisposes to infection. Why
infection has not been noted with CVS associated
with IJ vein catheterization is not clear, but may be
related to the limited studies that have been per-
formed in this area.
Peripherally Inserted Central Catheters (PICC
lines) and Venous Ports
Peripherally inserted central catheters (PICC lines)
and venous ports are emerging as signicant contribu-
tors to CVS. A study of 154 patients with previous
indwelling catheters and normal initial venograms
showed a 7% incidence of CVS or occlusion (39). There
was no association of CVS with catheter caliber, but the
mean dwell time of those who developed CVS (138 days)
was signicantly longer than those who did not develop
CVS (68 days). Quite remarkably, none of the patients
with CVS had symptoms. Venous thrombosis can also
develop with tunneled small-bore infusion catheters,
which may be a precursor of CVS if the irritation is pro-
longed due to long-term use of the catheter (40).
Pacemaker and Defibrillator Wires
It is common to see dialysis patients with multiple
comorbidities who require placement of pacemakers
and debrillators (Fig. 4). Maturation and function of
an ipsilateral AVF is often hampered by the presence of
such a device. Device-related CV wires are not a contra-
indication to ipsilateral placement of permanent AV
access (3,4144). However, attempts to place an AV

Right- or Left-Sided Catheterization

There is a predilection for CVS to occur with left-
sided catheter placement, possibly related to the more
tortuous route catheters take on that side (13,3436).
Catheter ow problems, infection, and central vein
obstruction were signicantly more common with left-
sided catheters in a study of 294 patients with 403
right and 77 left IJ catheterizations (36). AV access
ligation was necessary in four instances, all with left-
sided CVS. All patients with left-sided CVS were dia-
betics and had more severe symptoms.

Catheter Infections
Catheter infections can be associated with the
development of CVS, especially with subclavian vein
catheterization (30,36,37). In a study of 42 dialysis
patients with subclavian catheters, those with persis-
tent venous stenosis 6 months after removal of the Fig. 4. Occlusion of the left subclavian vein due to the presence
catheter had more catheter insertions and catheter- of pacemaker wires. Dilated collateral veins are present. Straight
related infections (38). Although it is possible that arrow demonstrates the site of stenosis while curved arrow shows
this latter association is due to the inammation the pacemaker (courtesy: Arif Asif, MD).
 CENTRAL VEIN STENOSIS
access on the same side may result in symptoms such as
extremity edema caused by CVS from the wires.
Caliber of CVC
There is a high incidence of CVS with hemodialysis
catheters, suggesting an association with their larger
diameter (12-14 French) compared with relatively smal-
ler size (4-8 French) of CVC used for other purposes.
Whereas one study showed a linear relationship between
catheter size and venous thrombosis rates in smaller
diameter catheters 1% with 4-F, 6.6% with 5-F, and
9.8% with 6-F catheters in upper arm veins (45) there
is no comparative study of larger-diameter catheters
such as those used for dialysis in central veins. Small cal-
iber catheters should, nevertheless, not be considered
benign. Triple lumen CVC placed in the IJ vein for
short-term (34 days) use were associated with intraven-
ous thrombi in 56% (with brin sleeve development in
56% of these patients) despite the use of prophylactic
heparin and aspirin (32). Whether this indicates an ear-
lier stage in the development of CVS is not certain.
Recent recognition of CVS associated with PICC lines
and pacemaker wires is also concerning. As the number
and use of such catheters is increasing tremendously for
various reasons, this may become an important cause of
CVS in patients needing vascular access for hemodialysis
in the future. It is quite possible that small-caliber cathe-
ters incite a similar degree of CVS, but that it is the CVS
associated with large (dialysis) catheters that is more
likely to be detected because of symptoms resulting from
increased blood ow from a functioning access.
Catheter Tip Position
Many complications of CVC may be related to the
position of the catheter tip, which has traditionally been
placed in the central part of SVC or at the cavoatrial
junction (46). It has now become common to place the
tip of the dialysis catheter in the lower part of the right
atrium for better performance, although it may occa-
sionally be complicated by intraatrial thrombus. More
CVC movement with the cardiac cycle when the tip is
within the heart may predispose to CVS. However, a
short catheter, especially if placed from the left-hand side
with close approximation of its tip to the wall of SVC, is
especially likely to result in endothelial damage and
inammatory response which, over the long term, may
lead to CVS.
Catheter Composition
The vessel wall may respond variably to different
catheter materials a concept related to stiffness and
presumed biocompatibility of the polymer. In a rabbit
model, polyethylene and Teon catheters were associ-
ated with more inammation than was seen with cathe-
ters composed of silicon and polyurethane; the stiff
nature of polyethylene and Teon was considered etio-
logic (47). In addition, silicone dialysis catheters were
associated with a lower incidence of CVS than were
polyurethane catheters (48). Search for more bio-
57
compatible material for construction of CVC may
prove fruitful.
Catheter Design
Many different designs of CVC have been used for
dialysis, though there is no conclusive evidence that one
is better than the other. If a catheter was to cause less tur-
bulence or movement within the vein, it could poten-
tially be less inammatory. In a swine model, controlling
the movement of the catheter tip with a thin wire loop
indeed resulted in less injury to the vein wall, less devel-
opment of thrombus, and less wall thickening (49).
Thus, modication of the design of the catheter (such as
direction and location of holes, curvature, split or non-
split design) affecting tip movement could have a role in
prevention of CVS and is a subject deserving further
study.
Relationship with Thrombosis
Thrombosis is frequently encountered in association
with CVC and CVS and could be a cause or effect of the
CVS. Evidence from animal models and autopsy studies
suggests that endothelial damage results in thrombus
organization, preceding the development of CVS.
Venous thrombosis has been reported in 38% of those
receiving multiple PICC lines (50). Alternatively, the
CVS can lead to stagnation of blood ow, causing
venous or access thrombosis, especially if the CVC is still
indwelling. Endothelial damage, stasis due to the cath-
eter, and a hypercoagulable state resulting from expres-
sion of thrombogenic factors (Virchows triad) provide
an ideal setting for intravascular clotting and could be
the common denominator of occurrence of CVS as well.
Clinical Features
Central vein stenosis may be completely asympto-
matic and be detected only by a venogram taken in pre-
paration for access placement (7,15). After an ipsilateral
access is created, CVS is likely to become symptomatic
in short order. The symptoms depend upon the specic
site of stenosis. While obstruction of the subclavian vein
is associated with edema and venous hypertension of the
corresponding extremity and breast, brachiocephalic
vein stenosis impedes blood ow from the same side of
the face as well as the upper extremity. Bilateral brachio-
cephalic vein obstruction or SVC obstruction results in
SVC syndrome, the symptoms of which are described
below.
Extremity Edema
It is estimated that only 50% of patients with signi-
cant subclavian vein stenosis develop ipsilateral arm
edema (7). Edema can occur without a functioning
access in that extremity, but is much more likely once
such a high ow system is created (51). Use of this access
for dialysis often exacerbates the edema further, and can
cause pain in the extremity. Swelling, tenderness, and
58 Agarwal et al.
associated erythema can resemble cellulitis. Edema of
the breast on the ipsilateral side may occur, and pleural
effusion can develop as well (52,53).
Aneurysmal Dilatation of the Extremity Veins
and AVF
Development of tortuous, aneurysmal dilatation of
an AVF may complicate stenosis-related partial obstruc-
tion to AVF blood ow. Prompt stulogram and correc-
tion of stenosis may halt progressive deterioration. Thin
and shiny skin over the dilatation may herald impending
rupture of the aneurysm, which can be life threatening.
Prompt surgical repair of the aneurysm is important in
such cases.
Development of Collaterals
As the CVS develops gradually, it permits develop-
ment of collateral veins, diverting the blood ow cen-
trally via other patent veins. This often results in visible,
palpable, tortuous veins over the extremity, chest, and
neck. Occasionally, the collaterals are large enough to
divert sufcient blood ow to abate or stabilize the signs
and symptoms of CVS; however, intervention is required
in most cases.
SVC Syndrome
Recognized for over a decade, SVC syndrome is a
dreaded complication of SVC obstruction (28,54). Bilat-
eral innominate vein stenosis can produce a similar pic-
ture. The syndrome is characterized by edema of both
upper extremities, the face and neck together with
numerous dilated collaterals over the chest and neck.
Unrelieved, it can be life threatening and can cause soft
tissue edema of the neck and airway compression. Occa-
sionally, the blood ow can be maintained via a dilated
azygous vein. Recanalization, angioplasty, and stenting
of the SVC are usually required.
Thrombosis of Access
Often a late symptom of CVS, it is usually preceded
by elevated venous pressures during hemodialysis, epi-
sodes of prolonged bleeding from needle sites after dialy-
sis, and a signicant decline in access blood ow.
Thrombectomy of such accesses without attempts to
diagnose and treat CVS can be complicated by recurrent
thrombosis and worsening of symptoms.
Venous Thrombosis
The combination of a CVC, venous hypertension,
and turbulent blood ow associated with CVS can pre-
dispose to venous thrombosis. Most central venous
thromboses are asymptomatic and are detected inciden-
tally. Venous thrombosis is common with PICC lines
23% after initial placement and 38% after multiple
placements (50). Subclavian vein thrombosis was diag-
nosed in 10 patients receiving parenteral nutrition and
was treated with removal of catheter and anticoagula-
tion with good results (55). In an intensive care unit non-
dialysis CVC caused jugular vein thrombosis in 63.5%
of patients as detected by duplex ultrasound after
removal of the catheter (56).
Venous thrombosis, by itself, is not always inconse-
quential. A review of axillary and subclavian vein throm-
bosis revealed post-treatment symptoms in 34%,
pulmonary embolism in 9.4%, and death in 1.2%,
regardless of the etiology of thromboses (57). Develop-
ment of intraatrial thrombus is not unusual with tunnel-
ed dialysis catheters and can also lead to pulmonary
embolization (58). Catheter-related thrombus can pro-
pagate to the dural venous sinuses and result in pseudo-
tumor cerebri. Diagnosis of venous thrombosis can be
made accurately with venograms or duplex ultrasound.
Removal of the catheter and systemic anticoagulation
are the cornerstone of treatment of venous thrombosis
associated with CVS. Early catheter removal and antico-
agulation may produce a prompt response to treatment
(59). Acute thrombosis can be treated effectively
with thrombolysis (60,61). Thrombolytic therapy and
surgical removal of thrombus may have a role in specic
cases (62).
Inadequate Dialysis
Central vein stenosis may reduce access blood ow.
When it falls below dialyzer blood ow, access recircula-
tion usually follows resulting in inadequate dialysis. An
AVF tends to stay patent even at low blood ow and is
more likely to be associated with occurrence of recircula-
tion. In contrast, an AVG is more likely to thrombose
before blood ow is low enough to produce recirculation.
Recurrent Infections
Although infection may be a causative factor for
CVS, CVS may also predispose to infection. Certainly
the consequences of CVS, such as excessive bleeding
from access, need for thrombectomy, and repeated inter-
ventions, can increase the risk of infection.
Diagnosis
The diagnosis of the CVS can most often be made or
suspected based upon a careful history and clinical
examination. History of previous CVC placement, espe-
cially if multiple, should alert one to the possibility of
CVS. Presence of pacemakers or automatic cardioverter
debrillators should prompt careful investigation to
look for the presence of CVS and its resolution prior to
placing a vascular access on the ipsilateral side. Exam-
ination revealing numerous dilated collaterals in the
neck or chest and arm edema on the ipsilateral side indi-
cates obstruction to outow. In case of bilateral CVS, a
clinical picture of SVC syndrome can be seen, with facial
edema. The direction of blood ow in collateral veins
can be ascertained by careful examination.
Central vein stenosis can often be conrmed by color-
ow duplex venous ultrasound. A normal respiratory
variation in the diameter of central veins and polyphasic
 CENTRAL VEIN STENOSIS
atrial waves are present in most patients with patent cen-
tral veins (63). The presence of numerous collaterals in
the neck is usually indicative of CVS. However, Doppler
may mistake a dilated collateral vein as a patent central
vein, unless attention is paid to the absence of respira-
tory variation (64). It may be difcult to visualize central
veins with ultrasound in those with signicant muscle
mass or obesity.
Central venography is the gold standard for the diag-
nosis of CVS. In a series of 141 patients, 54 stenoses were
diagnosed in 41 patients by color-ow duplex and 64 ste-
noses were diagnosed by angiography (11). There were
13 CVS (20.3%), with 9 of the 13 CVS diagnosed by an-
giography only. Digital subtraction angiography is more
sensitive than color duplex sonography in the evaluation
of dialysis access. The DOQI guidelines recommend
venography prior to placement of a permanent access in
patients with previous subclavian catheterization (65).
Magnetic resonance venogram permits avoidance of
radiocontrast in a patient with advanced chronic kidney
disease (CKD), where preservation of residual renal
function is important (66). This may also be useful in
those with radiocontrast allergy.
Management of CVS
Nonsurgical Approach
Elevation of the limb and anticoagulation can some-
times relieve edema associated with CVS, especially
when complicated by acute thrombus. These measures
are not useful in chronic occlusion. The access remains
at higher risk of thrombosis if the stenosis is not relieved.
The adequacy of dialysis from such an access is unlikely
to be optimal. As development of collaterals may be
associated with resolution of symptoms, treatment may
be deferred in asymptomatic patients who can achieve
adequate dialysis.
Endovascular Intervention
Angioplasty. Guideline 20 of K/DOQI recom-
mends percutaneous transluminal balloon angioplasty
(PTA), with or without stent placement and is consid-
ered the preferred approach to CVS (67). PTA usually
provides excellent initial results, but the long-term pri-
mary patency is not optimal. Among 50 CVS in a series
of 862 venous stenoses, an initial success rate of 89%
was followed by primary 6-month patency of only 25%
(41). In contrast, peripheral venous angioplasty had an
initial success rate of 94%, and 6-month primary paten-
cy of 77% indicating a different response of central veins
to angioplasty. This is probably due to their greater elas-
ticity and recoil than peripheral veins. In another study,
treatment of 25 CVS with PTA was reviewed retrospec-
tively; and 88% technical success rate was followed by a
42% primary patency at 6 months and 17% primary
patency at 1 year (11). Mean primary patency was
5.7 months. Similar results were reported in another
angioplasty series of 26 patients with central vein angio-
plasty (68). Technical success rate was 96% (100% in
59
stenoses and 50% in occlusions), with primary patency
rate of 70% at 3 months, 60% at 6 months, and 30% at
12 months. A 43% one-year patency and 100% secon-
dary patency rates were described in another study (69).
Postoperative surveillance, either by clinical examina-
tion or by angiography, is necessary to detect recurrence
of the lesion. Multiple procedures are usually needed. It
is important to note that in patients with a pacemaker,
angioplasty can be successfully performed with pacema-
ker wires in place (4244).
The histologic basis for recurrent stenosis after PTA
has been studied in stenotic AVF but not in CVS. Im-
munohistochemical measurement of proliferating cell
nuclear antigen showed a very high proliferative index
in 20 restenotic AVF, when compared with 10 primary
stenotic AVF (70). The process was even more signi-
cant in diabetic individuals. However, the process of
neointimal hyperplasia seen in AVF stenosis may not
be applicable to the process of smooth muscle hyper-
plasia in CVS.
Directional Atherectomy. Directional atherecto-
my combined with PTA is a potential treatment of CVS.
This procedure fell out of favor due to the possibility of
central vein rupture with this technique (22).
Stent Placement. For lesions that do not respond
to PTA or recur quickly, stent placement is indicated
(60). Using a Wallstent, the 3-, 6-, 12-, and 24-month pri-
mary patency rates were 92%, 84%, 56%, and 28%,
respectively; cumulative overall stent patency was 97%
after 6 and 12 months, 89% after 24 months, and 81%
after 36 and 48 months (71). However, the characteris-
tics of the lesions inuence the response to stenting. Elas-
tic lesions have a poor outcome with angioplasty alone
(time to occlusion 2.9 months), but a longer time to
recurrence when treated with Wallstent (8.6 months);
nonelastic lesions treated with these stents had shorter
patency (4.2 months) (72). Various types of stents can
effectively counter the immediate elastic recoil of the
vein, and can provide better patency rates for such
lesions (7375). DOQI recommends stent placement for
elastic lesions recurring within 3 months (67).
The benets of stenting may be overstated. A recent
retrospective study of CVS treatment did not nd a dif-
ference between primary patency between the stent and
the angioplasty groups at day 30 (89% vs. 94%), day 90
(63% vs. 67%), or day 180 (38% vs. 40%) (76). The sec-
ondary patency at day 90 (95% vs. 94%), day 180 (76%
vs. 84%), and day 360 (69% vs. 59%) was also similar.
The median survival of the access was 618 days versus
586 days.
These results reect rather a modest benet of using
stents over angioplasty alone. The long-term primary
patency of the stent is compromised by neointimal
hyperplasia in and around the stent. Only about a quar-
ter to a third of the stents remain patent without another
intervention at 1 year because of recurrent stenosis.
However, in selected cases, this may allow lifesaving
transition to another modality of renal replacement or
even provide an opportunity to create another AVF on
the contralateral side.
60 Agarwal et al.
Surgery
When endovascular treatment fails, surgical exposure
of the vein and repair of the lesion can be performed,
often requiring claviculectomy (77). Veno-venous
bypass of the CVS can also be performed in such cases
(78). Many techniques have been described, including
axillary vein to IJ vein bypass (7980), IJ vein to axillary
vein transposition (81,82), axillary to saphenous vein
bypass (83), and patch angioplasty of the axillosubclavi-
an stenosis. Right atrial bypass grafting for central
venous obstruction (84) and many other bypass tech-
niques have been used. With improvement in endovas-
cular techniques, these procedures are reserved for
recalcitrant cases.
Occlusion of the Vascular Access
This is the treatment of last resort to relieve the edema
and pain, and results in abandonment of that extremity
for future access. This can be done by manual compres-
sion, balloon occlusion, surgical ligation (3), or percuta-
neous embolization (85).
Future Directions
The current management of CVS is far from being
effective for the long term, although achievement of
short-term relief is possible. Most of the therapies for
CVS have evolved from those designed for arterial
lesions; there is paucity of vein-specic studies. In AVF
stenoses, neointimal hyperplasia is the primary lesion,
similar to that in coronary arteries. Examination of
results of PTA in AVF has shown occurrence of more
endovascular injury, leading to accelerated neointimal
hyperplasia (70). Newer treatments, including drug elut-
ing stents with rapamycin or paclitaxel, stents coated
with endothelial progenitor cell antibodies (anti-CD 34)
to improve endothelial healing inside the stent, treat-
ment with statin drugs, and brachytherapy with beta
radiation have demonstrated benet in coronary arter-
ies, ndings that cannot be directly extrapolated to cen-
tral veins.
Brachytherapy has been used experimentally for pre-
vention of recurrent stenosis of AVG after angioplasty
(86,87). However, the prominent histologic element in
CVS is that of smooth muscle hyperplasia, different
from neointimal hyperplasia of AVG or coronary arter-
ies. It is quite likely that accelerated tissue growth occurs
after endovascular intervention in CVS as well. Brachy-
therapy for prevention of restenosis after angioplasty
and stenting of CVS was not helpful in a small study
(88). Use of brachytherapy in central veins, much larger
than peripheral veins or coronary arteries, would require
a higher dose of radiation. The role of intravascular beta
radiation in CVS is undened at this time. Considering
the paradigm of management of restenosis in coronary
arteries, it may prove useful to investigate the use of ther-
apies targeted at reducing proliferative changes after
endovascular therapy. Further elucidation of hemody-
namic and molecular mechanisms of CVS, and develop-
ment of strategies to counteract those mechanisms may
result in more effective preventive therapies for CVS
with better outcomes in dialysis vascular access.
Alternative Approaches to Renal Replacement
Therapy in CVS
Contralateral Access. Once the attempts at resol-
ving CVS on the ipsilateral side have been exhausted, it
is often necessary to place another access on the contra-
lateral side. If the CVS is identied before access throm-
bosis, the new access can be developed and a CVC
avoided. Femoral AVG and permanent CVC are often
used in these patients, with high morbidity.
Peritoneal Dialysis. Peritoneal dialysis is an under-
utilized form of dialysis in the United States. Patients
with difcult hemodialysis access problems, such as
CVS, can often be switched to peritoneal dialysis.
Renal Transplantation. The patients with immi-
nent failure of their last access should be given emergent
consideration for an expedited renal transplant, which
remains difcult due to the shortage of cadaveric kid-
neys. A living donor is an excellent option, as in anyone
else with end-stage renal disease (ESRD).
Measures to Prevent CVS: Improving
Outcomes in ESRD
Central venous catheter placement is the most import-
ant cause of CVS. In those with existing CKD or those
at substantial risk of CKD, avoiding CVC of any kind is
desirable, especially in the subclavian vein and on the
left-hand side. Indiscriminate use of PICC lines should
be discouraged. In those with a history of CVC, it is pru-
dent to take a venogram before placing an AV access on
the ipsilateral side (89).
It is very important to briey consider the common
reasons for placement and use of CVC. Late referral of
dialysis patients to the nephrologist, delayed referral to
the surgeon for creation of vascular access, concerns
with AVF comorbidity, personnel preference, lack of
initiative, placement due to poor use of advanced
techniques for stula placement (such as transposition,
secondary AVF) result in placement of AVG and CVC,
both less desirable but more readily available forms of
accesses. USRDS data from Dialysis Morbidity and
Mortality Wave 1 study showed a signicantly higher
overall relative risk of mortality for diabetic patients
with AVG and CVC (1.41 and 1.54, respectively) com-
pared to those with AVF (9091). The data from multi-
national Dialysis Outcomes Practice Patterns Study
(DOPPS) also revealed unfavorable outcomes for AVG
even in those dialysis facilities that favored AVG (92).
The AVG have worse survival and higher need for
intervention for maintenance than the AVF.
In the United States, dialysis is initiated using CVC in
60% of new patients, and AVF has only been used in a
minority of incident and prevalent patients (93). The
efforts to increase AVF rates are often compromised by
 CENTRAL VEIN STENOSIS
a relatively high rate of primary failure (50% overall,
> 80% in diabetics, elderly, and females) after initial
placement, to the frustration of patient, surgeon, and
the nephrologist (94). Timely placement of AVF and
prompt intervention for malfunctioning or thrombosed
accesses, as recommended by DOQI can avoid much
morbidity from CVC. Early referral of patients with
CKD to the care of a nephrologist, and early referral of
CKD stage 4 patients (GFR 1530 ml/min/1.73 m2) to
the surgeon for creation of AVF hold the key to the pre-
vention of CVS and other complications and better out-
comes in ESRD.
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