Case Studies & Discussion: Venous Compression Syndromes

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On Sunday morning, Christopher M. Harnain, MD, MBA, RPVI, interventional radiologist from Weill Cornell Medicine in New York, presented a session on venous compression syndromes, detailing their pathophysiology, diagnostic approaches, and management strategies. The session included case studies to illustrate different syndromes, such as nutcracker syndrome, May-Thurner syndrome, thoracic outlet syndrome, and popliteal venous compression syndrome.

Dr Harnain defined renal vein compression, aka nutcracker syndrome, as a compression of the left renal vein (LRV) between the aorta and superior mesenteric artery. Symptoms of nutcracker syndrome include hematuria, proteinuria, left flank pain, and venous origin pelvic pain. It is diagnosed with ultrasound (pre- to post-compression ratio >2.25 in the renal vein, systolic velocity ratio >5); computed tomography (CT)/magnetic resonance venography (“beak sign" and aortomesenteric angle <39°); and venography and IVUS (renocaval pressure gradient >3 mm Hg). Treatment approaches include weight gain, ACE inhibitors, and aspirin (conservative); left renal vein transposition, renal auto-transplantation, or gonadal vein transposition (surgical); and renal vein stenting (endovascular; high technical success but concerns about migration).  

He then described iliac vein compression, aka May-Thurner syndrome, as compression of the left common iliac vein by the right common iliac artery that leads to venous stasis and intimal injury, increasing deep vein thrombosis (DVT) risk. It is diagnosed with ultrasound (small-caliber iliac vein, thick echogenic walls, continuous flow at compression site) and IVUS to confirm the severity of compression. Treatment for symptomatic May-Thurner syndrome is Iliac vein stenting.  

The third venous compression syndrome that Dr Harnain defined was thoracic outlet syndrome, aka Paget-Schroetter syndrome, which is a chronic compression of the subclavian vein at the thoracic outlet, often from repetitive overhead arm motion. Symptoms include unilateral arm swelling, hand cyanosis, and prominent chest wall collaterals. It is diagnosed utilizing ultrasound (subclavian vein thrombosis with compression during arm movement) and IVUS, which identifies venous narrowing with arm abduction. Treatment for this syndrome is thrombectomy followed by venoplasty or decompression surgery for acute cases; long-term management includes surgical decompression, repeat venogram, and anticoagulation.  

The last syndrome, popliteal venous compression syndrome, is defined as compression of the popliteal vein, often associated with popliteal artery entrapment, caused by an aberrant gastrocnemius muscle, aneurysms, cysts, or muscle slings. Symptoms include varicose veins, venous insufficiency, and a DVT risk. It is diagnosed with ultrasound and MRI (compression of the popliteal vein with knee extension and plantar flexion), and treatment includes. Release of the medial head of the gastrocnemius muscle in severe cases (surgery) and a conservative option of compression therapy for mild symptoms.  

In summary, Dr Harnain indicated that venous compression syndromes can affect multiple anatomical locations, leading to significant morbidity if untreated. Diagnosis relies on imaging techniques such as duplex ultrasound, venography, IVUS, and cross-sectional imaging to confirm hemodynamically significant compression. Treatment is individualized based on severity and symptoms, ranging from conservative management to endovascular and surgical interventions. Endovascular techniques, such as stenting and thrombectomy, are increasingly used, but long-term outcomes and risks (eg, stent migration) require further study. Decompressive surgery remains a key option for certain syndromes, particularly in cases of chronic vascular compression leading to recurrent symptoms.