Iliac vein compression (IVC) describes a mechanical narrowing of the large blood vessels located deep within the pelvis. These veins, the iliac veins, collect deoxygenated blood from the legs and return it toward the heart. When the internal diameter of an iliac vein is significantly reduced, blood flow is impeded, causing pressure to build up in the leg veins. This narrowing creates an environment where blood flow is sluggish, leading to a condition called venostasis. Venostasis greatly amplifies the likelihood of developing a deep vein thrombosis (DVT), a blood clot that can lead to severe swelling, pain, and chronic venous disease.
May-Thurner Syndrome: The Primary Anatomical Cause
The most recognized cause of iliac vein compression is May-Thurner Syndrome (MTS), an inherent variation in the relationship between the major pelvic blood vessels. This syndrome occurs because of an unusual crossing pattern where the rigid right common iliac artery passes directly over the softer left common iliac vein, pinning it against the bony structure of the fifth lumbar vertebra.
The constant, rhythmic pulse of the artery subjects the underlying vein wall to chronic trauma. This long-term mechanical stress irritates the inner lining of the vein, which is called the endothelium. In response to this recurring injury, the vein attempts to reinforce itself by developing scar tissue, a process known as fibrosis.
This fibrotic reaction leads to the formation of internal structures, often described as “spurs” or “webs,” that project into the vein’s lumen. These internal bands further obstruct blood flow, compounding the mechanical compression. While the anatomy that predisposes a person to MTS is found in approximately 20% to 30% of the population, only a small fraction of these individuals ever develop symptomatic venous disease.
The clinical importance of this anatomical arrangement is high. For individuals who develop DVT in the upper leg and pelvis, the underlying compression from MTS can be identified in up to 50% of left-sided cases. The resulting impediment to blood return can cause significant swelling, chronic pain, and eventually lead to the development of chronic venous insufficiency in the affected limb.
Acquired and Secondary Sources of External Pressure
Iliac vein compression can also be caused by various external forces that develop over time. These acquired sources of pressure are non-vascular and result from other structures or conditions within the abdominal and pelvic cavities. The soft, flexible nature of the iliac veins makes them susceptible to being squeezed by adjacent solid or enlarging masses.
Retroperitoneal Masses
Growths located in the space behind the abdominal lining, known as retroperitoneal masses, are a significant source of external pressure. These masses can include benign or malignant tumors, such as sarcomas, or significantly enlarged lymph nodes resulting from infection or cancer. These growths physically encase or displace the iliac vein, reducing its diameter and impeding flow.
Pregnancy
Pregnancy, particularly in the later stages, is a common and usually temporary cause of this type of compression. As the uterus expands to accommodate the growing fetus, it exerts substantial pressure on the major veins returning blood from the lower body. The enlarged uterus presses on the iliac veins, which can exacerbate a previously asymptomatic anatomical compression or cause new symptoms.
Post-Treatment Scarring
Other sources of acquired compression stem from inflammatory or scarring processes in the pelvic region. Patients who have undergone pelvic surgery or extensive radiation therapy may develop dense fibrotic tissue. This post-treatment scarring, sometimes referred to as retroperitoneal fibrosis, can contract and harden around the iliac vein, causing a fixed stenosis that severely restricts blood flow.
Contributing Factors That Amplify Risk
While the physical compression is the direct cause of the mechanical narrowing, several systemic or behavioral factors significantly increase the risk of it becoming symptomatic. These factors primarily interact with the slowed blood flow created by the compression, tipping the balance toward clot formation.
Hypercoagulable States
Hypercoagulable states refer to an abnormal increase in the blood’s natural clotting tendency. These can be genetic, such as an inherited condition like Factor V Leiden, or acquired through certain diseases. When a clotting disorder is present alongside a compressed vein where blood is already pooling, the risk of developing a DVT rises substantially.
Hormonal Influences
Hormonal influences are another group of contributing factors, disproportionately affecting women. The use of oral contraceptives or hormone replacement therapy introduces synthetic hormones that promote a hypercoagulable state. For a person with an existing, non-symptomatic iliac vein compression, this hormonal change can be the trigger that leads to the formation of a deep vein thrombosis.
Increased External Pressure and Immobility
Conditions that increase the pressure within the abdomen also exacerbate the underlying compression by squeezing the veins from the outside. Examples include severe obesity, chronic constipation that strains the abdomen, or excessive fluid accumulation in the abdominal cavity. Similarly, prolonged periods of immobility, such as during long-haul flights, extended bed rest following surgery, or a sedentary lifestyle, slow blood flow further, allowing the existing compression to become a greater risk for clot formation.