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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2023. | This topic last updated: Aug 08, 2022.
INTRODUCTION
An overview of the types and etiologies of ICVO, clinical features, diagnosis, and approach
to treatment is reviewed here. Endovenous techniques for treatment of iliocaval venous
obstruction are reviewed separately. (See "Endovenous intervention for iliocaval venous
obstruction" and "May-Thurner syndrome", section on 'Treatment'.)
ILIOCAVAL ANATOMY
The central veins are systemic veins located within the thorax or abdomen. These are
distinguished from the somatic veins (eg, azygos/hemiazygos, body wall veins,
superficial/deep veins of the extremities) and visceral veins (eg, portal, hepatic, mesenteric,
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Overview of iliocaval venous obstruction
The central veins in the abdomen are located inferior to the diaphragmatic caval opening
at the level of the eighth thoracic vertebra and include the intrahepatic and infrahepatic
inferior vena cava (IVC) and the common, external, and internal iliac veins. These veins
arise from the confluence and regression of three paired embryonic veins [1]. While the
majority of left-sided cardinal veins regress, the right-sided supra and subcardinal veins
develop into the inferior vena cava, except for the short hepatic caval segment, which
develops from hepatic sinusoids. A double IVC (0.2 to 3 percent) may occur if the left
supracardinal vein persists, and left-sided IVC (<0.5 percent) may occur if the left
supracardinal vein persists. Variations of the inferior vena cava can arise related to
aberrations in development ( figure 1).
The external iliac vein is a continuation of the common femoral vein. The internal iliac veins
together with the external iliac vein join together to form the common iliac veins. The
common iliac veins join to form the inferior vena cava, which receives flow from the
lumbar, gonadal, renal, suprarenal, phrenic, renal, and hepatic vein before passing
through the caval hiatus of the diaphragm to empty into the right atrium ( figure 2). The
iliocaval system also has many developmental variations ( figure 1 and figure 3).
The iliac veins are generally located posterior and to the right of the iliac arteries. The
inferior vena cava is located to the right of the aorta. The common iliac veins at their
confluence are in close association with the fifth lumbar vertebral body ( figure 4).
Compression of the left iliac vein by the overlying right iliac artery forms the basis of May-
Thurner syndrome. (See "May-Thurner syndrome".)
Other structures can also compress the veins (eg, tumor, anomalous ureter) ( figure 1).
INCIDENCE/PREVALENCE
classification [CEAP] 5 ( table 1)) may affect 1 to 5 percent while active ulcers (CEAP 6)
may affect up to 1 percent of the adult population, respectively [9,10].
In many patients, iliac vein compression may be the trigger for developing acute deep vein
thrombosis (DVT) and chronic venous insufficiency in patients with certain risk factors. One
computed tomography (CT) surveillance study reported that 24 percent of patients with no
history of lower extremity DVT or any other associated symptoms had at least 50 percent
obstruction of the left common iliac vein [11]. However, in the absence of symptoms,
treatment is not advised. (See 'Management' below.)
The most common nonthrombotic cause of ICVO is May-Thurner syndrome (MTS), due to
partial or complete obstruction of the iliac vein by the overlying common iliac artery. Right-
sided MTS or even distal inferior vena cava (IVC) compression by the aortic bifurcation is
rare but has been reported [12]. Similarly, anatomic changes following arterial repair (eg,
abdominal aortic aneurysm [AAA]), which occur more commonly in the iliofemoral
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Overview of iliocaval venous obstruction
segment after open or endovascular abdominal aortic repair, can lead to ICVO [13-17].
The presence of an endoluminal foreign body (eg, IVC filter) may contribute to ICVO. These
devices lie in direct contact with the wall of the veins, and their constant movement related
to breathing causes endothelial injury. Central venous lines are often implicated. (See
"Central venous catheters: Overview of complications and prevention in adults", section on
'Central venous obstruction'.)
Thrombotic obstruction — Acute thrombosis of the central veins (ie, deep vein
thrombosis) can occur in any venous segment and from a variety of causes. (See "Overview
of the causes of venous thrombosis".)
thrombosis [30], thrombus embolization into inferior vena cava filters during catheter-
directed thrombolysis for proximal deep venous thrombosis [31], Budd-Chiari syndrome
[32], and venous aneurysmal disease [23]. (See "Overview of the causes of venous
thrombosis".)
CLINICAL FEATURES
Regardless of the inciting cause, the clinical features of iliocaval venous obstruction (ICVO)
are those of chronic venous insufficiency with pain, extremity heaviness, and edema, or
acute lower extremity deep vein thrombosis (DVT) with acute limb swelling and pain.
Clinical manifestations of chronic venous insufficiency and acute DVT are discussed in
detail separately. (See "Clinical presentation and diagnosis of the nonpregnant adult with
suspected deep vein thrombosis of the lower extremity" and "Clinical manifestations of
lower extremity chronic venous disease" and "Post-thrombotic (postphlebitic) syndrome".)
Among patients with clinical features of acute deep vein thrombosis, particularly involving
the proximal extremity, we suggest evaluating for ICVO in patients with risk factors for
May-Thurner syndrome and in those with persistent or recurrent symptoms following an
adequate course of anticoagulation. (See "May-Thurner syndrome".)
DIAGNOSIS
Although iliocaval venous obstruction (ICVO) may be suspected based upon clinical history
and physical examination, the diagnosis requires imaging or physiologic studies
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Overview of iliocaval venous obstruction
demonstrating obstruction of these central veins. The initial test for ICVO is a venous
duplex ultrasound (VDUS). Advanced venous imaging may be useful for helping to
determining an etiology, if this is not apparent. Intravascular ultrasound (IVUS), which may
be the best imaging modality for defining the intraluminal pathology, is generally reserved
for those in whom treatment is pursued.
Duplex ultrasound — Venous duplex ultrasound allows functional, anatomic, and dynamic
evaluation of the status of the deep veins of the involved extremity. However, duplex
ultrasound may be technically challenging when evaluating the proximal extremity veins,
particularly in patients with a high body mass index (ie, BMI ≥40) [33]. Nevertheless, duplex
remains the initial and most reliable imaging study for patients with clinical features of
ICVO ( image 1 and image 2). Venous duplex ultrasound detects occlusion of the
distal iliac veins, which, if present, is highly suggestive of more proximal occlusion.
To evaluate the common femoral vein, a 4 to 7 MHz linear array transducer is commonly
used, while a 2 to 3 MHz should be used to evaluate the iliac veins and inferior vena cava
(IVC). The angle of insonation should be kept at <60°. The contralateral side will function as
a control if IVC thrombosis/occlusion is not present.
To establish the diagnosis of iliocaval venous stenosis, we use the following parameters
[34]:
A combination of monophasic flow in the common femoral vein at rest and continuous
flow during the Valsalva maneuver may offer the highest diagnostic value for ICVO [35].
Venous duplex ultrasound can also be used in B-mode to determine the degree of vein
diameter reduction by comparing the vessel diameter at the smallest lumen area to that of
normal vein. Peak vein velocity (PVV) can be measured in the post-stenotic vein and
compared with the prestenotic segment; a PVV gradient >2.0 mmHg is considered
significant [34].
For patients who present with chronic lower extremity symptoms, chronic venous
insufficiency is established with venous duplex ultrasound demonstrating chronic changes
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Overview of iliocaval venous obstruction
and deep venous reflux. In a study published by the author, common femoral vein reflux
>2.5 seconds was found in significantly more patients with iliac vein stenosis >50 percent
by intravascular ultrasound compared with those who had reflux <2.5 seconds (80 [24 of
30] versus 25 percent [6 of 24]) [36]. Likewise, a >50 percent stenosis was found in
significantly more patients with reflux >1 second compared with <1 second (61.4 versus 30
percent).
Venography and intravascular ultrasound — For patients with ICVO, IVUS may be the
most sensitive diagnostic test and is typically performed during therapeutic venography to
confirm ICVO prior to proceeding with angioplasty and stenting. As an example, with May-
Thurner syndrome, the exact morphology and degree of the lesion "spur" within the
common iliac vein are best appreciated using IVUS. (See "Endovenous intervention for
iliocaval venous obstruction", section on 'Procedural imaging' and "May-Thurner
syndrome".)
MANAGEMENT
system are provided separately. (See "Endovenous intervention for iliocaval venous
obstruction".)
Nonthrombotic ICVO
Thrombotic ICVO — For patients with thrombotic ICVO, the initial treatment is
therapeutic anticoagulation per venous thromboembolism (VTE) guidelines; however, while
anticoagulation reduces propagation of thrombus, it does little to resolve acute clot.
Available data support endovenous treatment for reducing the incidence of post-phlebitic
syndrome and related sequelae for those with severe symptoms related to proximal
thrombus (ie, ICVO) [41-45]. (See "Overview of the treatment of proximal and distal lower
extremity deep vein thrombosis (DVT)".)
The decision to proceed with further treatment is determined by the clinical history and
risk factors associated with iliocaval thrombosis (eg, risk factors for May-Thurner, known
IVC filter). When indicated, treatment is aimed at decreasing the volume of thrombus with
catheter-directed thrombolysis if not contraindicated ( table 2), then evaluating for
underlying intrinsic venous stenosis and, if present, angioplasty and stenting of the
diseased iliocaval segment. Appropriate expertise and institutional resources must be
available to provide this intervention. If such resources are not available, anticoagulation
with interval follow-up vascular imaging is a reasonable alternative. (See "Endovenous
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Overview of iliocaval venous obstruction
Adjunctive vein ablation — For patients presenting with symptoms and signs of chronic
venous insufficiency because of venous outflow obstruction, ablation of superficial veins
may help relieve severe symptoms associated with combined superficial and deep venous
reflux. (See "Overview of lower extremity chronic venous disease", section on 'With deep
venous reflux' and "Overview of lower extremity chronic venous disease", section on 'With
superficial venous reflux' and "Approach to treating symptomatic superficial venous
insufficiency" and "Approach to treating symptomatic superficial venous insufficiency",
section on 'Candidates for venous intervention'.)
For patients with superficial venous reflux, correction of ICVO appears to be important to
decrease reflux recurrence after venous ablation procedures, and managing superficial
reflux, when present, appears to be important for symptom relief following iliac stenting.
In a retrospective review conducted over a decade at a single institution, ICVO was found
in 207 patients [46]. Among them, 121 were treated with endovenous laser ablation (EVLA)
in addition to iliac stent placement and 86 patients were treated with EVLA alone. The
incidence of pain, edema, and ulceration was significantly reduced in the stent plus EVLA
group compared with EVLA alone. The primary iliac vein patency rate was 93.3 percent at
four years' follow-up. In the EVLA-alone group, there was a high rate of superficial venous
reflux recurrence.
Role of open surgery — The use of open surgical techniques to manage iliocaval venous
obstruction, which requires a specific set of open surgical skills, has decreased significantly
in the era of minimally invasive vascular treatments primarily due to the often significant
operative dissection, morbidity, and high rates of rethrombosis associated with open
surgery [47,48].
For selected patients with thrombotic ICVO who are candidates for intervention, but in
whom thrombolytic therapy is contraindicated ( table 2), guidelines from the Society for
Vascular Surgery (SVS) provide a recommendation for open surgical venous thrombectomy
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Overview of iliocaval venous obstruction
[41]. An open cutdown via a common femoral venotomy can be used to evacuate gross
thrombus and to uncover any stenotic venous lesion [41,49-51]. (See "Endovenous
intervention for iliocaval venous obstruction", section on 'Options for reducing thrombus
burden'.)
For stenotic iliac vein lesions (eg, May-Thurner syndrome), the main components of open
surgery are full dissection of the right iliac artery separating it from the underlying left iliac
vein and open iliac vein thrombectomy with possible patch angioplasty of the left iliac vein
[52]. An arteriovenous fistula is often created to assist long-term patency of the bypass
grafts or reconstructed veins, and the fistula is ligated in six weeks.
Surgical options following failed endovascular therapy for an occluded iliac vein include
saphenofemoral crossover bypass, cross-pelvic venous bypass (Palma-Dale procedure),
femorofemoral or ilio-ilial prosthetic bypass, and femorocaval and aortic elevation
[47,48,51,53-57]. (See "Techniques used for open iliocaval venous reconstruction".)
Following open venous surgery, patients usually receive long-term anticoagulation and
compression stockings [58].
For patients with femoral venous catheters, catheter removal may be warranted. (See
"Catheter-related upper extremity venous thrombosis in adults", section on 'Catheter
management'.)
disease that can be due to one of several etiologies that may contribute to chronic
venous hypertension and chronic venous insufficiency, or with acute venous
occlusion typically leading to extensive deep vein thrombosis (DVT). (See
'Introduction' above and 'Incidence/prevalence' above.)
● Etiologies leading to ICVO are divided into those that are initially nonthrombotic but
that may lead to thrombosis depending on the severity of venous outflow obstruction
and those that are predominantly thrombotic. Nonthrombotic etiologies are caused
by either intrinsic venous stenosis or extrinsic compression. The presence of an
endoluminal foreign body (eg, inferior vena cava filter) can also impede flow.
Thrombotic obstruction can be related to inherited or acquired thrombophilia. (See
'Pathophysiology and etiologies' above and 'Iliocaval anatomy' above.)
● ICVO can present with symptoms of chronic venous hypertension and chronic venous
insufficiency, or more acutely with limb swelling and pain, which can be bilateral. For
patients with any of the following clinical features, we suggest evaluation for ICVO.
• Known prior history central venous instrumentation (eg, central vein catheter,
inferior vena cava filter).
(angioplasty/stenting).
● Open surgical treatment (open venous angioplasty, venous bypass) is associated with
worse outcomes compared with percutaneous angioplasty/stenting and is rarely
needed to manage ICVO. However, if thrombolysis is contraindicated, percutaneous
mechanical thrombectomy alone or an open cutdown via a common femoral
venotomy can be used to evacuate thrombus to uncover the lesion prior to
angioplasty and stenting. (See "Endovenous intervention for iliocaval venous
obstruction", section on 'Percutaneous mechanical thrombectomy' and 'Role of open
surgery' above.)
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