Management of May Thurner Syndrome in Pregnant Patients

Abstract

May Thurner Syndrome contributes to thromboembolic disease and can cause significant morbidity in pregnant patients secondary to exaggerated anatomic relationships and physiologic changes in the hematologic system favoring thrombogenesis. Because this condition is both underrecognized and underreported, management in pregnant and postpartum patients is based on expert opinion without any formal evidence-based guidance. Herein, we review five pregnancies in four patients with May Thurner Syndrome and general management strategies. Through collaborative and multidisciplinary care, patients with May Thurner Syndrome can be safely and successfully managed during pregnancy and the postpartum period with appropriate anticoagulation.

May-Thurner syndrome: a review

“…Failure to recognize MTS can lead to significant undertreatment, resulting in long-term morbidity. 5 CT, MRI, venography or intravascular ultrasound demonstrate flattening of the iliac vein beneath the artery. Importantly, this anatomy can be found incidentally in asymptomatic patients.…”

“…24 Compared to balloon angioplasty or thrombectomy alone, and especially compared to anticoagulation alone, long-term venous patency rates associated with stenting are higher, with a lower risk of re-thrombosis, more complete resolution of thrombus, and lower risk for PTS, with reduced PTS severity. 5,25 Figure 4 (A-D The results of angioplasty alone are traditionally below par when compared with stenting, irrespective of the post angioplasty result. 24 At this point, an IVUS can help assess the response to plain balloon angioplasty and confirm the landing zones for the stent if required.…”

“…1,2 MTS has an estimated incidence between 18-49%, it is an anatomical condition resulting from extrinsic venous compression of left common iliac vein (LCIV) and less common right common iliac vein (RCIV) by right common iliac artery (RCIA) and fifth lumbar vertebra (L5), (Figure 1) which over time produces vascular remodeling that can develop DVT, chronic venous insufficiency/associated sequelae. [3][4][5] RCIA is considered to cause this partial obstruction by direct mechanical compression of LCIV also, intimal hyperplasia in LCIV due to shear stress on anterior, posterior walls of LCIV secondary to pulsation of overlying RCIA contributes to venous obstruction and subsequent thrombosis. 6 An association of between 2-5% is estimated in patients with MTS and symptomatic venous disease of the lower limbs and 20% of patients who present thromboembolism, especially in those with recurrent thromboembolic disease, 7 this syndrome is usually diagnosed in patients with symptoms of chronic edema or DVT in the lower limbs.…”