In contrast to the right common iliac vein, which ascends almost vertically to the inferior vena cava, the left common iliac vein traverses diagonally from left to right to enter the inferior vena cava. Along this course, it goes under the right common iliac artery, which<unk>  compress it against the lumbar spine and limit the flow of blood out of the left leg. There are case reports of the inferior vena cava being compressed by the iliac arteries or right-sided compression syndromes, but the vast majority are on the left side. While this is the suspected cause of the syndrome, the left iliac vein is frequently seen to be compressed in asymptomatic patients, and considered an anatomic variant- a 50% luminal compression of the left iliac vein occurs in a quarter of healthy individuals. Compression becomes clinically significant only if it causes appreciable hemodynamic changes in venous flow or venous pressure, or if it leads to acute or chronic DVT. In addition to compression, the vein develops intraluminal fibrous spurs from the effects of the chronic pulsatile compressive force from the artery. The narrowed turbulent channel predisposes the patient to thrombosis. The compromised blood flow often causes collateral blood vessels to form. These are most often horizontal transpelvis collaterals, connecting both internal iliac veins, thus creating outflow through the right common iliac vein. Sometimes vertical collaterals are formed, most often paralumbar, which can cause neurological symptoms, like tingling and numbness. This compressed, narrowed outflow channel causes stasis of the blood, which is one element of Virchow's triad that precipitates deep vein thrombosis.
May–Thurner syndrome
Van Wyk and Grumbach syndrome
Helsmoortel-Van der Aa syndrome
Wells-Jankovic syndrome
Jeavons syndrome
Crome syndrome
Bogart–Bacall syndrome
Keutel syndrome