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Overview of iliocaval venous obstruction

Overview of iliocaval venous obstruction
Literature review current through: Jan 2024.
This topic last updated: Aug 08, 2022.

INTRODUCTION — Iliocaval venous obstruction (ICVO) is a clinicopathologic condition of the systemic veins of the abdomen that can be due to one of several etiologies and that may contribute to venous obstruction, hypertension, or extensive lower extremity deep vein thrombosis (DVT). ICVO is increasingly encountered in daily practice due to the use of cross-sectional imaging and an overall increased awareness of the condition. Increased use of inferior vena cava filters may also be a contributing factor.

Understanding the pathophysiology of the possible etiologies of iliocaval venous obstruction will help the clinician develop a better understanding of available treatment options and the best way to achieve desirable anatomic and functional outcomes.

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, pulmonary veins, and coronary sinus).

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 — Iliocaval venous obstruction (ICVO) is an underrecognized venous outflow condition [2-9]. It likely contributes to the prevalence of venous hypertension and venous insufficiency, particularly among patients with symptoms of advanced venous disease such as venous ulcers or post-thrombotic syndrome. While the incidence and prevalence of ICVO is not known for certain, it might be estimated from the prevalence of these and other associated conditions. Healed venous ulcers (Clinical-Etiologic-Anatomic-Pathophysiologic 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.)

PATHOPHYSIOLOGY AND ETIOLOGIES — Understanding the pathophysiology of iliocaval venous obstruction (ICVO) may help clinicians develop a better understanding of treatments and how to achieve desirable anatomical and functional outcomes. The predominant pathophysiologic mechanisms by which central vein obstruction occurs are vein wall injury with subsequent neointimal hyperplasia causing venous stenosis, which can lead to thrombosis; endoluminal obstruction related to an endoluminal device; or thrombosis alone. In many cases, the etiology of obstruction is multifactorial. The various etiologies leading to ICVO are most simply divided into those that are predominantly thrombotic and those that are initially nonthrombotic but that may lead to thrombosis depending on the severity of the obstruction.

Nonthrombotic obstruction — Anatomic or pathologic conditions impeding venous outflow can be due to extrinsic compression (eg, tumor, aneurysm, anatomic anomalies) or intrinsic vein stenosis, which may be related to an intraluminal device or due to hemodynamic abnormalities. Such partial or complete impedance to iliocaval venous outflow can lead to extensive deep vein thrombosis (DVT) of the ipsilateral extremity (ie, thrombotic ICVO). (See 'Thrombotic ICVO' 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 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'.)

In addition, compression/stenosis from a misplaced/displaced IVC filter (eg, prophylactic filter, therapeutic filter placement) is also a relatively common etiology of ICVO [18]. IVC filters can also thrombose. (See "Placement of vena cava filters and their complications".)

Other causes of nonthrombotic obstruction include compression by tumor (malignant or benign) [19,20] or by renal [21] or hepatic [22] cysts, and venous aneurysmal disease [23]. Congenital anomalies of the vena cava, such as inferior vena cava agenesis, may be associated with obstruction (figure 1) [24]. IVC stenosis following liver transplant has also been reported [25,26]. These stenoses are primarily technical and usually occur in the early postoperative period. Size mismatch between the donor vein and IVC, hematoma at the anastomotic site, kinking, or early intimal hyperplasia are the main reasons for developing IVC stenosis after liver transplant.

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 is associated with a significant increase in inflammatory markers, including type 1 collagen deposition, which decreases the normal elasticity of the vein wall, reducing the normal diameter in the acute phase [27]. Subsequently, intraluminal scarring and fibrosis further decreases vein elasticity in the chronic phase. Even with partial recanalization, in spite of full anticoagulation, some degree of impedance to venous outflow is present. Among those with thrombotic ICVO, up to 50 percent of patients may develop post-thrombotic symptoms (eg, limb swelling, heaviness, venous ulceration) [28]. (See "Post-thrombotic (postphlebitic) syndrome", section on 'Clinical features' and "Post-thrombotic (postphlebitic) syndrome".)

Other thrombotic etiologies include inherited thrombophilia, acquired hypercoagulable conditions [29], recent surgery, immobilization, testicular tumors [19], catheter-related 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".)

ICVO is an underrecognized cause of chronic venous hypertension and venous insufficiency, particularly among patients with more severe clinical manifestations of chronic venous disease such as skin changes or venous ulcers (Clinical-Etiological-Anatomical-Pathological [CEAP] clinical classifications 3 to 6 (table 1)) [2-9]. In a study of patients only with CEAP (table 1) classification 5 or 6 venous ulcers, 37 percent of imaging studies demonstrated obstruction of at least 50 percent, and 23 percent had obstruction of >80 percent [10]. Thus, for patients with chronic venous insufficiency, we evaluate for ICVO in those with a known history of prior central venous instrumentation (eg, inferior vena cava filter) and in those with moderate-to-severe symptoms of chronic venous insufficiency (ie, CEAP 3 to 6).

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 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]:

Post-stenotic turbulence as indicated by the mosaic color flow appearance (noisy signal)

An abnormal Doppler signal at the area of stenosis

Sluggish and/or no spontaneous flow, as well as very poor augmentation

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 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).

CT and MR venography — Venography using cross-sectional imaging (image 3) such as computed tomography (CT) with a venous phase or magnetic resonance (MR) venography is sensitive for estimating the location and degree of ICVO, identification of thrombus and other anatomic variations that may exist, and the presence of venous collaterals.

An additional benefit of using MR imaging is the ability to detect anatomic factors or certain pathological conditions of the abdominal, pelvic, and spinal structures that may be contributing to venous compression, such as lumbar vertebral degeneration, bulging or protruding intervertebral discs, osteophytes, or spondylolisthesis [37]. However, several factors, such as cost, contrast volume, and availability of the equipment, need to be considered when choosing these modalities [38,39].

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

Approach to venous intervention — Whether to proceed with a venous intervention depends upon the severity of symptoms and the presence or absence of thrombus (ie, nonthrombotic iliocaval venous obstruction [ICVO], thrombotic ICVO) [40]. (See 'Pathophysiology and etiologies' above.)

Techniques for endovenous intervention including thrombolysis (pharmacologic, mechanical, or both), when needed, angioplasty and stenting in the iliocaval venous system are provided separately. (See "Endovenous intervention for iliocaval venous obstruction".)

Nonthrombotic ICVO

Asymptomatic – For asymptomatic patients with incidentally identified venous stenosis of the iliac veins or inferior vena cava on imaging performed for other reasons, no treatment is necessary. Such patients are counseled regarding potential future symptoms.

Mild symptoms – For patients with only mild symptoms (Clinical-Etiologic-Anatomic-Pathophysiologic [CEAP] 1 through 3) (table 1), in the absence of thrombus (ie, deep vein thrombosis [DVT]), treatment is conservative. Compression stockings are often sufficient for controlling symptoms of venous insufficiency.

Severe symptoms – For patients with moderate-to-severe symptoms such as swelling, pain, skin discoloration, or ulceration (CEAP clinical classes 3 to 6 (table 1)), treatment is targeted toward reducing the severity of the stenotic venous lesion using angioplasty/stenting. (See "Endovenous intervention for iliocaval venous obstruction".)

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 intervention for iliocaval venous obstruction", section on 'Thrombolysis' and "Endovenous intervention for iliocaval venous obstruction", section on 'Angioplasty/stenting'.)

For those in whom thrombolysis is contraindicated, selected patients may be candidates for percutaneous mechanical thrombectomy or open surgical thrombectomy. (See "Endovenous intervention for iliocaval venous obstruction", section on 'Percutaneous mechanical thrombectomy' and 'Role of open surgery' below.)

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 [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].

Etiology-specific treatment — In addition to addressing the venous disease, other treatment may be needed, depending upon the specific etiology (eg, tumor management).

For patients with femoral venous catheters, catheter removal may be warranted. (See "Catheter-related upper extremity venous thrombosis in adults", section on 'Catheter management'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Superficial vein thrombosis, deep vein thrombosis, and pulmonary embolism" and "Society guideline links: Chronic venous disorders".)

SUMMARY AND RECOMMENDATIONS

Iliocaval venous obstruction (ICVO) is an underrecognized multifaceted venous 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).

Moderate-to-severe symptoms of chronic venous insufficiency (Clinical-Etiology-Anatomy-Pathophysiology [CEAP] 3 to 6).

Persistent or recurrent symptoms following adequate course of anticoagulation for acute DVT, particularly if the proximal extremity is affected.

Risk factors for May-Thurner syndrome. (See "May-Thurner syndrome".)

The severity of the clinical symptoms determines whether to proceed with intervention for all potential underlying etiologies. In the absence of symptoms, treatment is not advised. (See 'Approach to venous intervention' above and 'Adjunctive vein ablation' above.)

For patients with only mild symptoms, conservative treatment is recommended; compression therapy is usually sufficient to relieve symptoms.

For patient with moderate-to-severe symptoms and nonthrombotic ICVO, treatment is targeted toward reducing the severity of the stenotic venous lesion (angioplasty/stenting).

For patients with thrombotic ICVO, treatment begins with therapeutic anticoagulation. The likelihood of uncovering a treatable venous lesion is based upon clinical features and risk factors that support treatment, which must be weighed against the risk of bleeding associated with thrombolysis. The appropriate expertise and institutional resources must be available to undertake thrombolysis. After successful thrombolysis, the underlying venous stenosis is treated with 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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Topic 15223 Version 11.0

References

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