Case Presentation: A 24-year-old female with past medical history significant for sickle cell trait presented 2 weeks status post cesarean section with 3 days of progressive left leg pain and swelling in her left lower extremity. She is a mother of 4, a nonsmoker, and denies history of venous thromboembolism and family history of hypercoagulability. She received an intramuscular injection of medroxyprogesterone following her cesarean section. The patient was received in a wheelchair due to significant pain on ambulation. The patient notes numbness to her entire left foot, denies chest pain, shortness of breath, abdominal pain, nausea, vomiting, constipation, diarrhea, black or bloody stool, urinary symptoms, dizziness, lightheadedness, syncope, fever, or chills. Her abdomen showed a well healed incision from her cesarean section. Her left lower extremity appeared erythematous and tense on palpation. Tenderness to palpation was noted in the region of the gastrocnemius and popliteal fossa. Labs revealed normal lactate and creatine kinase reducing concern for compartment syndrome or acute ischemia. Labs were significant for leukocytosis with neutrophilia and low bicarbonate. Ultrasound showed extensive thrombosis of the left lower extremity extending from the external iliac vein through the paired calf veins. Angiography illustrated a May-Thurner anatomical variant. Pharmacochemical thrombectomy was performed to reduce clot burden and venous thrombolysis with tissue plasminogen activator infusion was done to clear remaining thrombus. The following day a stent was placed in the left common iliac vein to treat stenosis secondary to MTS. The patient will continue dual antiplatelet and oral anticoagulant therapy as outpatient.
Discussion: May-Thurner syndrome (MTS) is an anatomical variant that causes compression of the left common iliac vein against bony structures in the iliocaval region. The most common variant seen is the right common iliac artery overlying and causing compression of the left common iliac vein leading to outflow obstruction. With partial obstruction, this condition may be asymptomatic; however, progression can occur leading to deep vein thrombosis (DVT). Compression is also associated with intimal hyperplasia which increases risk for venous stasis and thrombosis. Incidence of MTS is estimated to be 20-25% of the general population, although 2-5% of patients present symptomatically. Risk factors for symptomatic MTS include female gender especially those who are postpartum, multiparous, or using oral contraceptives, scoliosis, dehydration, hypercoagulable disorders, and cumulative radiation exposure.
Conclusions: This case illustrates a patient presenting with DVT secondary to MTS. The patient had stasis of the blood resulting from venous obstruction, vessel wall injury in the form of intimal hyperplasia of the left common iliac vein, and hyper-coagulability resulting from her medroxyprogesterone injection and recent pregnancy meeting each of Virchow’s triad risk factors for venous thrombosis. The anatomical variant associated occurs high into the pelvis which can make visualizing with ultrasound challenging; however, this patient had extensive thrombosis making identification of DVT with US possible. The gold standard for diagnosis involves contrast venography, MRI, or intravascular ultrasound. Stenosis is recommended to prevent future DVT recurrence and additional complications including pulmonary emboli, chronic venous stasis, and iliac vein rupture.