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56.
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ENDOVASCULAR MANAGEMENT OF
ILIOCAVAL THROMBOSIS
Patricia E. orpe and Francisco J. Osse
INTRODUCTION
e term “endovenous” entered our vocabulary in the early
1990s to describe the percutaneous procedures performed
to treat successive patients presenting with acute lower
extremity deep vein thrombosis (DVT) superimposed on
varying stages of chronic venous occlusive disease. Rarely
did we see a case of “ rst episode” DVT. Gradually, the
procedures evolved to include staged endovascular reconstruction of extensive, purely chronic axial vein occlusion in very symptomatic patients. During this time, the
term “endovascular” had been touted, around the globe,
as the new frontier in vascular surgery. Techniques developed between 1950 and 1975 by Seldinger, Amplatz,
Dotter, Gruntzig, Judkins, and others, were “borrowed”
and incorporated into innovative, percutaneous methods of treating aortic aneurysm and carotid disease. But,
over the years, minimally invasive treatment of iliocaval
obstruction has not become part of the repertoire of most
vascular surgeons or interventional radiologists. is is
a re ection of many factors. First, consider that peripheral vascular arterial disease is so prevalent that there are
hardly enough physicians to care for the growing number
of patients. Although chronic venous disease is the most
common problem in vascular medicine, venous occlusive
disease is technically challenging, o en involving multiple
segments, damaged valves, and di cult terrain to navigate.
Few specialized tools have been developed, and those are
mainly for addressing acute thrombosis. Furthermore, residents and fellows training in fragmented programs have
trouble getting enough training in specialized areas of
endovascular surgery. With limited time and energy, most
focus on gaining experience with arterial disease. Catheter
skills are essential in performing endovenous procedures.
Venous cases can be more time-consuming than arterial
procedures, and reimbursement is o en less than for faster
arterial interventions. It is nonetheless as gratifying to successfully treat chronic venous obstruction and relieve the
heaviness and pain of venous hypertension as it is to open
an occluded iliac artery and relieve claudication. So here
we will begin with a chapter on the endovenous management of iliocaval thrombosis.
CLINICAL HISTORY AND
EVALUATION
It is not a surprise that the clinical manifestations of iliocaval
occlusion comprise a wide spectrum of signs and symptoms
of venous hypertension. e recruitment of collateral pathways may be adequate as well as occult; some thrombosed
individuals can remain symptom-free. Symptomatic individuals may present with variable lower extremity edema
and a variety of complaints related to venous hypertension. ere are three common clinical presentations among
patients with chronic venous obstruction; (1)asymptomatic, (2)acutely symptomatic with underlying pathology,
and (3)chronically symptomatic.
re ects the venous pathology. Asymptomatic patients may
have transient signs or symptoms that are not disabling.
For example, asymptomatic patients may have limb, vulvar, or abdominal varices indicating venous hypertension,
focal phlebitis within a varix or mild edema, intermittent
groin pain, and a tiny ulcer (Figure56.1). However, all of
these signs and symptoms can increase in intensity and frequency if the venous ow pattern is further compromised.
For example, super cial vein removal for varicosities, in
a patient with iliofemoral occlusion, can lead to severe
venous stasis and skin changes (Figure56.2).
Acute caval thrombosis commonly presents with unilateral or bilateral lower limb edema, unexplained recent
weight gain, and not infrequently, back pain. e lack of
collateral ow causes lower limb edema, discoloration,
and discomfort. e back pain re ects venous congestion
in the sacral plexus. Patients have no di culty recognizing
the seriousness of their condition, even though it may have
1
e clinical presentation
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Figure56.1 Le leg edema or nonthrombotic venous hypertension
related to le iliac compression. Lymphedema can be a component.
developed gradually. Early on, symptoms can mimic sciatica
and spinal, bowel, or bladder problems. However. when a
critical mass of thrombus nally interrupts deep venous ow,
venous hypertension progresses rapidly (Figures56.3,56.4).
Chronic iliocaval occlusion is o en more di cult to diagnose, since collaterals and recanalization alter the hemodynamics which dictate the severity of the venous hypertension.
Chronic inferior vena cava (IVC) occlusion can result in either
bilateral or unilateral lower extremity edema. Prominent
collateral veins can be seen on the lower anterior abdominal wall and in the perineal or pubic region (Figures56.5,
56.6). Bilateral varicose veins may be present. Advanced skin
changes including hyperpigmentation, lipodermatosclerosis
and ulceration can develop. Venous stasis changes may lead to
below-the-knee amputation years before the venous obstruction is identi ed. Patients with iliocaval occlusion o en
report that leg elevation does little to alleviate edema. is
suggests a component of phlebolymphedema, perhaps sec-
2
ondary to venous obstruction.
Prolonged sitting can cause a
vague inguinal ache. Exertion may cause venous claudication.
Patients frequently report shortness of breath, even without
any history of pulmonary embolus or respiratory ailments.
Lower back discomfort or hematuria can be presenting signs.
As a rule, patients with long-standing venous insu ciency,
secondary to venous obstruction, are seen by primary care
physicians long before they are referred to vascular specialists.
Patients commonly report being told “there is not much we
can do for you other than compression.” Treatment of postthrombotic syndrome commonly means compression stockings. Patients may have a remote history of iliofemoral DVT
but no suspicion of central venous obstruction, since no one
ever evaluated this area. Alternatively, they may have a prior
diagnosis of iliocaval occlusion, or have been told that the
IVC is absent following phlebography or if cross-sectional
imaging. e chronically thrombosed cava becomes isodense
with surrounding so tissue, and large collaterals seen using
computed tomography (CT) and magnetic resonance imagery (MRI) may be interpreted as lymphadenopathy and
thereby prompt a search for malignancy.
Figure56.2 e right leg shows all the signs of advanced skin changes of chronic venous hypertension. e circumferential hyperpigmentation and
lipodermatosclerosis became worse, and ulcers developed, a er the patient underwent saphenous vein stripping for varicosities seven years before
this photo. Her remote history of iliofemoral DVT went undiscovered until she presented with acute DVT following the stripping surgery. She
responded to thrombolysis and iliac stenting, Her right leg improved, and the pain decreased signi cantly, which greatly enhanced her quality oflife.
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Figure56.3 Cyanosis secondary to massive venous obstruction in a
patient (Figure56.4) with chronic bilateral iliocaval occlusion and acute
le iliofemoral thrombosis.
Figure56.5 Abdominal varices indicating chronic occlusion of the
inferior vena cava in a 45-year-old man with bilateral stasis ulcers.
IMAGING ILIOCAVAL DISEASE
e evaluation of obstructive venous disease utilizes multiple imaging modalities. We begin with duplex ultrasound
(DU). e exam includes looking at the in ow and out ow
of the limb. is means the exam includes below-the-knee
veins as well as the iliac segments above the inguinal ligament. Wave-form analysis and velocity measurements
are important when suspecting proximal obstruction.
Speci cally look for high velocities in the le common iliac
segment, which can indicate a focal compression by the
right iliac artery. Large collaterals adjacent to the common
iliac might be present. However, they will show nonphasic
ow. Nonphasic ow is seen in collaterals and axial veins
distal to an obstructing lesion. A normal pattern returns
a er stenting (Figure 56.7). Patients must be monitored
for restenosis at 6-month intervals for the rst 1–2years
post-op or if they become symptomatic. Many patients have
a “normal” duplex exam even when they have restenosis. We
nd objective measurements are helpful. Labropoulos etal.
established criteria for de ning signi cant venous steno-
3
sis with DU.
Following baseline DU, patients underwent
phlebography and intravascular pull-back pressure measurements before treatment of an identi ed stenosis. e
data showed that a pressure gradient greater than or equal
to 3.0mmHg correlates with a greater than 50% stenosis.
Apeak velocity ratio of 2.5 correlated with a pressure gradient of 3.0mmHg. ese criteria pertain best to focal stenoses. In long-segment 12-mm stents, we nd that di use
intrastent hyperplasia will decrease the velocity. erefore,
Figure56.4 e initial thrombosis is this patient occurred a er an aortobifemoral bypass 20years prior to his presentation with hematuria and acute
lower extremity edema that was clearly greater on the le . e image on the le shows his legs at 1month follow-up a er iliocaval reconstruction.
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Figure56.6 Venograms of the IVC before and a er thrombolysis and stenting. is 17-year-old patient presented with acute le leg thrombosis. He
has a single kidney and a pattern of chronic caval obstruction that was unknown prior to the DVT. His initial treatment was in 1997, and he remains
patent with one subsequent intervention for focal caval and iliac in stent restenosis in2007.
we use serial velocity measurements to screen for restenosis
since visualization is unreliable.
Contrast phlebography provides the clearest understand-
ing of obstructive disease. real-time digital phlebography
shows rate of contrast clearance and contrast density patterns that can be helpful. Awide le common iliac segment
indicates compression.
Demonstration of collaterals pathopneumonic for
obstruction is clearly seen in patients with iliocaval obstruction. Magnetic resonance venography (MRV) and computed tomographic venography (CTV) reconstructions
can demonstrate le vein iliac compression with multiple
views (Figures56.8, 56.9). However, both gadolinium and
CO2 have been shown to be less e ective contrast agents
3
than iodinated contrast in the venous system.
in-slice
CT, widely used for diagnosis of pulmonary embolus, is
4
not always sensitive for distal DVT.
e 64-slice CTV
can produce impressive images of the lower extremities
when contrast is injected distally via pedal intravenous
access. We recommend that cross-sectional imaging and
duplex be combined with phlebography if intervention
is planned. Imaging of iliac compression is best done
with intravascular ultrasound (IVUS). A decrease in
cross-sectional area can be calculated, and the tightness of
the anterior-posterior diameter relative to the transverse
diameter indicates a hemodynamically signi cant lesion.
We recommend documentation of the lesion with IVUS
p r e a n d p o s t s t e n t i n g .
Figure56.7 Duplex waveforms show the loss of phasicity when there is a
proximal iliac obstruction. Following stent placement, the waveform is
phasic, and the peak systolic velocity is similar to the other limb, which
serves as a control.
TREATMENT OPTIONS
S Y M P T O M A T I C I V C O C C L U S I O N
Symptomatic IVC occlusion, whether acute or chronic,
responds poorly to conservative therapy. Medical treatment
with anticoagulation alone will do little to alleviate the multisegmental occlusion of large axial veins. Despite heparin,
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Figure56.8 CTA showing where the right common iliac artery crosses
the le common iliacvein.
warfarin, and autolysis, the risk of pulmonary embolus is
high, and the threat of phlegmasia exists. Over time, the
IVC syndrome may develop, leading to discomfort and disability. Historically, surgical intervention was reserved for
severe cases and clinical results were mixed due to the morbidity of such high-risk surgery. In 2001, Jost etal. reported
overall 3-year primary and secondary patency rates of
54% and 62% in patients undergoing surgical reconstruc-
5
tion for nonmalignant obstruction from 1985 to 1999.
In
view of these limitations, endovascular repair of acute and
Figure56.9 An image from MRV allows measurement of vessel diameters
and shows the le common iliac vein compression and ascending
lumbar collateral.
chronic IVC and combination iliocaval obstruction has
evolved over the past 25years. Early stainless steel stents
were e ective in strutting caval lesions, and they were asso-
6,7
ciated with signi cant restenosis.
As early as April 1993,
we began placing self-expanding metallic stents in chronically occluded iliac veins and the IVC. We have followed
hundreds of patients over the years to track the long-term
clinical outcomes and perform reinterventions to maintain
8
patency.
Published reports since 2000 have shown endo-
venous reconstruction to be a safe, e ective, and durable
9–22
treatment option.
Following two decades of clinical
experience, absent any large randomized trials, the minimally invasive, percutaneous approach has been declared
an acceptable, if not preferred, treatment for symptomatic
20
iliocaval obstruction or stenosis.
e 2008 guidelines
published by the American College of Chest Physicians
(ACCP) recommend phamacomechanical thrombolysis in
preference to catheter-directed thrombolysis alone in the
23
treatment of selected cases of acuteDVT.
N O N T H R O M B O T I C
LEFT COMMON ILIAC
OBSTRUCTION:MAYTHURNER
e prevalence of le iliac vein compression may be
higher than concluded from autopsy studies in the 1940s.
Originally described by Cockett and omas, the anatomical lesion was thought to be hemodynamically signi cant
24,25
in approximately 30% of the population.
Two German
pathologists, May and urner rst described their iliac
compression ndings in 1957. eir names are associated
with the clinical syndrome that re ects the mechanical risk
factor for le leg thrombosis. Nonthrombotic manifestation of unilateral venous hypertension, due to common iliac
vein narrowing, is now considered by some as an indica-
17
tion for stent placement,
e presence and persistence of
such a lesion helps explain the high rethrombosis rate a er
balloon thrombectomy or early catheter-directed thrombolysis. Removal of acute iliofemoral thrombus without
correction of the underlying lesion will almost invariably
result in rethrombosis. Investigation with IVUS provides
valuable information about the appearance and function
of the common iliac vein near the bifurcation. Although in
most patients duplex can identify the presence of collaterals
or a focal shi in velocity (at the area of right iliac artery
compression of the vein), direct visualization and measurement with IVUS are ideal. In the absence of thrombosis,
a high-grade lesion is characterized by anteroposterior
(AP) diameter of less than 3.0mm, pressure gradient of
≥ 3.0mmHg, distal stasis, and visible collateral veins. Such
lesions merit consideration of stenting to prevent thrombosis in the future.
Neglen reported that a single anatomical lesion was
identi ed in the proximal le common iliac vein in 36% of
17
the 255 patients included in their study.
Asmaller group,
472 • CHRONIC VENOUS INSUFFICIENCY
8%, had a compressive lesion near the internal iliac bifurca-
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tion. In 46% of the patients, a combination of proximal and
distal lesion was observed. Whereas the proximal lesion is
more common on the le , there is an equal incidence of the
distal narrowing. e cause of the distal lesions is extrinsic
compression from the iliac artery, but relatively little brosis
occurs at this level compared to the proximal lesions. e
arterial compression and proximity of the spine can result
in intrinsic vein wall thickening in the proximal le iliac.
Bilateral common iliac compression is found in approximately 2% of the population. Whereas IVUS measurements
and images are de nitive, the phlebographic image is o en
misinterpreted as normal. e wider transverse diameter,
and lighter contrast density, in the common iliac segment
are consistent with AP narrowing of the vein. But, if collaterals are not seen, and the characteristic impression of
the right iliac artery is not identi ed, the diagnosis can be
missed with phlebography. Collaterals that are visualized
with valsalva may not be apparent with normal respiration
in a supine position.
A C U T E T H R O M B O T I C
OBSTRUCTION
Catheter-directed thrombolysis, mechanical thrombectomy, and combination therapy have evolved over the past
two decades. For the most part, patients presenting with
phlegmasia cerulean dolens are referred for catheter-directed
thrombolysis in centers where interventionalists are available. Patients not responding to standard heparin and warfarin therapy may also be referred for catheter-directed
lysis. However, the majority of DVT patients treated in the
emergency room are discharged with low molecular weight
heparin and are no longer routinely hospitalized for bed
rest. A multidisciplinary, multicenter clinical trial, under
the auspices of the NIH, was initiated in 2007 to investigate
the bene ts of early endovascular thrombus removal (with
thrombolysis and mechanical thrombectomy and adjunctive use of stents) compared with standard anticoagulation
27
therapy.
Prevention of postthrombotic syndrome is a primary goal of early endovascular intervention. e objective
of the study is the acquisition of Level Idata, comparing anticoagulation alone with thrombus removal plus anticoagulation. e strategy of early thrombus removal reduces the
likelihood of pulmonary embolus as well as postthrombotic
syndrome.
Early observations of the natural history of DVT and
subsequent evaluations following lysis revealed several ndings. Distal valvular incompetence can develop in patients
with persistent proximal obstruction, even if distal veins are
28,29
not a ected by the DVT.
is associated with a higher incidence of recurrent DVT.
Persistent residual thrombus
30
Finally, the combination of obstruction and re ux leads to
more severe postthrombotic syndrome than either condi-
29
tion alone.
CHRONIC THROMBOTIC
OBSTRUCTION:MAYTHURNER +
THROMBOSIS
Prior to 2000, reports detailing the use of thrombolytic
therapy and stents for use in venous thrombosis focused on
patients with acute thrombosis, in whom about 50% have
an underlying iliac lesion or May- urner compression.
Ver y o en, the acute clinical presentation is deceptive, since
the “critical mass” of thrombus that causes the clinical symptoms is composed of newer thrombus superimposed on a
substrate of subacute or even chronic thrombus.
Endovascular stenting of chronic iliac occlusions, a er
removal of acute thrombus, has become familiar to interventionalists treating venous obstruction. Balloon angioplasty proved to be inadequate in treating iliac lesions.
We frequently use catheter-directed thrombolysis, with
tissue plasminogen activator, to so en occlusive thrombus and facilitate guide-wire passage through apparently
impossible occlusions. Venography and IVUS demonstrate the occlusive, echo-dense thrombus that obliterates
the lumen (Figures56.10, 56.11). e initial venograms
will show very little of the residual caval and iliac segments. Following overnight thrombolysis, using a bilateral
popliteal approach, the venogram will reveal additional
venous anatomy. e procedure progresses very methodically in caval reconstructions. Serial angioplasty precedes simultaneous deployment of kissing self-expanding
stents (Figures 56.12, 56.13). e long-term patency of
large-caliber (12- to 16-mm) self-expanding stents placed
in the common iliac segment is acceptable and compares
Figure56.10 A venogram of a May- urner lesion and thromboses of the
iliac veins. e image is taken with the patient prone on the angio table.
Note the retroperitoneal and transpelvic collaterals.
32,33
31
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Figure56.11 Intravascular ultrasound (IVUS) Volcano Eagle Eye 6F
catheter image of a severe and chronic iliac occlusion where the residual
lumen has been obliterated. It is usually necessary to used thrombolytic
therapy to facilitate wire traversal of such lesions.
favorably to surgical thrombectomy, alone, and bypass
33
surgery.
Neglen and Raju reported early experience with
cannulation of totally occluded segments and technical
success of stenting as 98% and 97%, respectively, in the
treatment of ninety-four consecutive patients with sus-
12
pected iliac vein obstruction.
In this series, the reported
primary, assisted primary, and secondary patency rates at
1year were 82%, 91%, and 92%, respectively.
e clinical impact of correcting the deep venous
obstructive lesions in symptomatic patients can be measured in terms of quality of life as pain and swelling diminish when the venous hypertension is reduced by restoration
of axial ow. In 2002, Raju etal. reported on the clinical
impact of the venous stents in managing chronic venous
12
insu ciency.
is was the rst mention in the literature of the e ect of stenting on the healing of venous stasis ulcers. Stasis dermatitis and ulceration was present in
69/304 (23%) limbs treated with stenting with or without
saphenous ablation. ey reported that the cumulative
recurrence-free ulcer healing rate was 63% at 24months.
Furthermore, the rate of healing was not in uenced by concomitant treatment of saphenous re ux. e reduction of
pain and swelling a er intervention were both statistically
signi cant (P < 0.001).
IVC occlusion, in combination with iliac obstruction,
can lead to severe venous hypertension when collateral
circulation is inadequate. e IVC syndrome can include
lower extremity swelling, stasis dermatitis and ulceration,
varicosities, and loss of sensation and strength in the legs.
Pain can be felt in the lower back, pelvis, or inguinal region
in addition to the discomfort and heaviness in one or both
limbs. It is most common to discover caval obstruction con ned to the infrarenal cava. In patients in whom we have
suspected an early thrombosis in infancy, the entire IVC
was discovered to be very narrow, as if minimally recanalized following thrombosis.
Figure56.12 ese images show the baseline cavagram and the result of overnight thrombolysis. Additional anatomy is revealed by infusing a
thrombolytic agent for 12–18 hours via multi–side hole catheters advanced from a popliteal approach. In the second image, note the lling defects
and the tram-track sign revealing the residual thrombus.
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Figure56.13 ree images showing the sequence of a baseline cavagram followed by stages of the reconstruction. Following bilateral popliteal catheter
placement for thrombolysis, eventually a wire can be passed into the suprarenal cava. In this case, both wires pass through a previously occluded caval
lter. Initial caval dilatation starts with small-diameter balloons and progresses to kissing 10- to 12- mm balloons. e third image shows the double
barrel stents traversing the lter.
F O C A L I S S U E S F O R
ENDOVASCULAR THERAPY
A. IVUS: IVUS is an important tool in endovenous
therapy. It has application in two main areas: (1) assessing the nonthrombosed common iliac segment and (2)in
the follow-up examination of with signs and symptoms
of restenosis. In the rst instance, IVUS has proven to be
the best way to image and evaluate the iliac stenosis in the
11
May- urner syndrome.
Whereas the phlebogram will
generally demonstrate widening of the transverse diameter
of the common iliac segment, and decrease in the intensity
of contrast, IVUS will clearly reveal the severity of the AP
narrowing causing high venous resistance (Figures56.14,
56.15). e presence of collaterals has previously thought to
be necessary for diagnosis of a hemodynamically signi cant
iliac lesion. Information from IVUS has shown that not
all signi cant narrowings are accompanied by collaterals,
which can be demonstrated phlebographically in the supine
position.
B. RESTENOSIS: Restenosis is important issue in
stenting. Untreated restenosis can lead to rethrombosis.
Whereas early rethrombosis (<30days) is usually due to
inadequate anticoagulation or in ow and out ow issues,
late loss of patency is most o en due to intimal hyperplasia and subsequent thrombosis. When patients present
with recurrent symptoms of limb edema or discomfort,
the intensity is generally much less than the initial clinical
presentation. e routine duplex exam will generally show
patency of the stents. e wave form will remain phasic.
Intimal hyperplasia, or in-stent restenosis, is best imaged
with IVUS. Before we had access to IVUS, we would redilate stents in patients with recurrent pain or edema. e
symptoms and signs resolved. As little as 30–35% luminal decrease by intimal hyperplasia can cause recurrence
Figure56.14 An excellent example of how compression of the le
common iliac vein results in widening of the transverse diameter and
narrowing of the anteroposterior lumen. On the venogram, this causes
decrease in the intensity of contrast. is is the classic appearance of a
May- urner compression on venography.
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Figure56.15 IVUS image the iliac compression seen in Figure56.14.
e AP diameter is “pancaked,” and the echogenic rim indicates
brotic thickening of the vein wall. is slit-like appearance shows
why the contrast is less dense and why the ow velocity increases at the
May- urner lesion.
of symptoms. In 2004, Neglen and Raju reported their
observations of restenosis in venous stents and concluded
that risk factors included a history of venous thrombosis,
a positive test for thrombophilia, and longer stent systems
34
extending below the inguinal ligament.
Gender and side
had no signi cance. A er 42months of observation in 324
limbs treated with stenting, 23% had no sign of luminal
narrowing on phlebography, 61% showed greater than 20%
narrowing, and 15% showed greater than 50% narrowing. e value of identifying restenosis is in maintaining
long-term patency of the stents. eir study showed that
reintervention optimizes long-term patency. At 3years, primary, primary assisted, and secondary patency were 75%,
90%, and 93%, respectively.
C. ANTICOAGULATION: Once ow is reestablished with stents, anticoagulation is important in patients
with thrombophilia and those with signi cant residual
distal thrombus and vein wall irregularity from previous
DVT. Both conditions are risk factors for recurrent DVT
despite good iliac ow. However, in patients with normal
distal veins, the presence of a single or double iliac stent
does not require long-term anticoagulation, per se. e
use of anticoagulation and antiplatelet agents varies among
clinicians. Low molecular weight heparin is used to bridge
subtherapeutic international normalized ratio (INR) levels,
particularly in patients who must travel more than 2 hours
to return home. Plavix, 75 mg/d, is started prior to stenting and continued for 30 d.Patients not on warfarin also
take 80 mg aspirin. It should be noted that rethrombosis of
a metallic stent is a matter of urgency. In our experience, it is
much more di cult, and sometimes not possible, to reopen
chronic in-stent thrombosis. Unlike organized thrombus
in native veins, the old thrombus in occluded stents is very
hard to traverse.
D. STENTS: Self-expanding metallic stents are used
in venous stenting. e 12- to 14-mm Wallstent (Boston
Scienti c, Natick, MA) has been used more than other
stents because of the good long-term patency rates, the
visibility under uoroscopy, and the ability to reposition.
Stent migration is rare, but can occur with any stent if it is
undersized and the vein expands. Tandem Wallstents will
not interlock as the SmartStent (Cordis, New Brunswick,
NJ) will. e foreshortening of the Wallstent requires experience, and there are time when a stent that does not foreshorten is ideal. Asingle, high-grade focal stenosis requires
a su ciently long stent to prevent the stent from slipping
(like a watermelon seed) to either side. In our experience,
long-term success of these interventions is also related to
establishing continuity of ow within the deep system of
the entire lower extremity. Poor in ow from the tibiopopliteal segments, or the femoral may compromise long term
patency as much as poor-out ow caused by under-stenting
the iliac compression. Stents must extend into the IVC to
completely treat the iliac compression. Otherwise, the compression persists and the stent can thrombose (Figure56.16).
Pitfalls include the following situations. Visualizing
the IVC with contrast alone can give a false estimate of
the vein diameter. Above the thrombotic occlusion or
stenosis, a normal vein may not expand with contrast
injection due to low volume. Placement of an undersized stent can result in migration (Figure56.17). Avery
tight, focal lesion should be treated with a longer stent.
Trying to match the length of the lesion too closely can
result in the stent slipping above or below the lesion during deployment (Figure 56.18). Adequate apposition
to the vein wall, above or below the lesion, will prevent
this problem. e ends of the self-expanding stents can
be sharp. Adequate overlap of 15–20mm at the interface
Figure56.16 CT showing stent position too low in the iliac vein. It is
below the right iliac artery, which can still compress the vein. Stents
must be extended into the IVC by 1–2 centimeters. Failure to do so can
result in early thrombosis of thestent.
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Figure56.17 CT image of a stent that migrated to the right atrium.
e stent was placed in the suprarenal IVC on the preceding day.
Before IVUS, the diameter of the IVC could be underestimated with
low-volume contrast imaging. e stent migrated to the heart and
caused a tapenade. e percutaneous removal required a 16-Fr sheath
in the jugular vein, a 20-mm goose-neck snare, a femoral catheter, a
multidisciplinary team and determination. e 22-year-old patient
made a full recovery.
of stents during tandem deployment is important to prevent a bare area. is gap can be a site for restenosis. More
importantly, it prevents possible perforation of the vein
wall (Figure 56.19). In all instances, one must be prepared to address the complication. Snares can be use to
retrieve a stent, and covered stents can be used to prevent
e x s a n g u i n a t i o n .
E. OCCLUDED VENOUS STENTS: Reopening
a chronically occluded venous stent can be very di cult.
It is much harder than reestablishing ow in a chronically
occluded native vessel. If a stent thromboses, immediate
intervention is recommended. Lysis of acute thrombus can
restore patency. Chronic thrombus can be traversed, but
there is no good way to debulk organized thrombus within
the stent lumen. Apilot lumen may be achieved with rotational atherectomy using the JetStream 3 (Pathway Medical
Technologies, Kirkland, WA) is will permit placement
of the wire for dilatation. Cutting balloons and angioplasty
may expand the channel, but we lack endovascular tools to
“clean out” the stent. Placement of a new stent, within the
lumen, may provide adequate ow. It is, however, hard to
expand the inner stent when there is a circumferential layer
of organized thrombus. ere is a high risk of rethrombosis with a narrow lumen. Most of the iliac stent failures
have been due to failure to place the stent high enough in
the cava. e double barrel or kissing stent con guration
requires extension of the two stents well above the bifurcation to maintain patency. Also, simultaneous balloon
dilatation is recommended to avoid compressing a stent
(Figure56.20).
Figure56.18 Deployment of a self-expanding stent in a very tight lesion
can result in “watermelon seed” slippage, as seen in this image. Short
tight lesions require longer stents to prevent this complication.
Figure56.19 Dramatic contrast image of an iatrogenic caval tear and
retroperitoneal extravasation. e two stents are not su ciently
overlapped. Care is taken not to oversize dilating balloons and to
perform kissing balloon technique in the parallel caval stents. An
uneven force was applied to the cava and stents and resulted in this
perforation, which was treated e ectively with a coveredstent.
ENDOVASCULAR MANAGEMENT OF ILIOCAVAL THROMBOSIS • 477
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