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From my (still very limited) experience, the hallmark of venous lesions in MS patients is the stiffness of venous wall, it is not external compression. Neither is it alike varicose veins, thrombosis, atherosclerosis, or so. It is very strange, I am sitting in vascular sonography for years and I don't remember to see such a vein before scanning MS patients. Actually, the most similar pathology (as far as ultrasonographic picture is concerned) is May-Thurner syndrome in iliac veins.

Endovascular venous stenting in May-Thurner syndrome.Heijmen RH, Bollen TL, Duyndam DA, Overtoom TT, Van Den Berg JC, Moll FL.
Departments of Vascular Surgery, St. Antonius Hospital, Nieuwegein, The Netherlands.

BACKGROUND: Chronic pulsatile compression of the left common iliac vein between the crossing right common iliac artery and the lowest lumbar vertebral body may induce focal intimal proliferation of the vein (May-Thurner syndrome), resulting in impaired venous return and left iliofemoral thrombosis. Corrective surgical treatment requires extensive dissection. In this report, we describe our experience with endovascular venous stenting in May-Thurner syndrome. METHODS: Six patients with symptomatic May-Thurner syndrome were treated with percutaneous transluminal angioplasty and implantation of self-expanding stents. RESULTS Postprocedure phlebography revealed patent iliofemoral veins with unimpeded venous outflow and disappearance of collaterals in all patients. No procedure-related complications occurred. At follow-up (median, 12 months), 5 of 6 patients were free of symptoms. In one patient lower extremity edema was aggravated despite a patent stented segment of the left iliac vein. The patient continues to wear support stockings to compensate for continuing venous insufficiency. Color coded duplex scanning revealed patency at regular intervals in 5 patients. In one patient, occlusion of the stented venous segment with return of symptoms was detected at one month. Patency could not be restored despite catheter-directed thrombolytic therapy. After angioplasty, however, adequate collateral circulation was restored and symptoms resolved completely. CONCLUSIONS: Endovascular venous stenting in May-Thurner syndrome is technically feasible, and leads to reduction of symptoms in the majority of patients with high patency rates in the medium-term. This approach may prove to be a percutaneous alternative to surgical treatment.

PMID: 11292912 [PubMed - indexed for MEDLINE]

In one patient lower extremity edema was aggravated despite a patent stented segment of the left iliac vein. The patient continues to wear support stockings to compensate for continuing venous insufficiency. Color coded duplex scanning revealed patency at regular intervals in 5 patients. In one patient, occlusion of the stented venous segment with return of symptoms was detected at one month. Patency could not be restored despite catheter-directed thrombolytic therapy. After angioplasty, however, adequate collateral circulation was restored and symptoms resolved completely.

..... Four patients with May-Thurner syndrome underwent iliac vein angioplasty and stenting. Technical success was 100%. On clinical follow-up, the patients with May-Thurner syndrome have had improvement/resolution of their symptoms. There have been no complications from either therapy. May-Thurner syndrome is a clinical entity of left iliac vein compression by the right iliac artery, resulting in isolated left lower extremity swelling and may be a precipitating factor for iliofemoral deep venous thrombosis. Magnetic resonance imaging is the best modality for diagnosis of this entity as it can rule out the presence of pelvic masses and deep venous thrombosis while simultaneously demonstrating the anatomy characteristic of this syndrome.

OBJECTIVE: May-Thurner syndrome is characterized by left common iliac obstruction secondary to compression of the left iliac vein by the right common iliac artery against the fifth-lumbar vertebra. This anatomic variant results in an increased incidence of left-sided deep venous thrombosis (DVT). Furthermore, while a preponderance of left-sided DVT has been demonstrated in women during pregnancy and oral contraceptive use, patients are not typically screened for this condition after developing a left-sided DVT. As anticoagulation alone is ineffective for DVT treatment in the setting of May-Thurner anatomy, more aggressive treatment is warranted. Failure to diagnosis this condition predisposes these women to the unnecessary risks of recurrent DVT and post-thrombotic syndrome. METHODS: We present the occurrence of 7 adolescent patients with previously undiagnosed May-Thurner syndrome who presented with DVT after the initiation of oral contraceptive steroids (OCP) use. All 7 patients elected to proceed with mechanical thrombolysis/catheter based thrombolysis followed by endovascular stenting and were postoperatively treated with 6 months of warfarin. RESULTS: Mean patient age was 18.3 +/- 3.3 years (range, 16-24 years). Mean time to presentation after initiation of OCP was 5 weeks (range, 2-10 weeks). Mean time to intervention was 16.8 days (range, 10-24 days). All patients were treated with mechanical thrombectomy. Our rate of intraoperative clot resolution was 100%. All 7 patients were treated with self expanding nitinol stents after angioplasty of the iliac vein stenosis with resolution of the stenotic segment. Primary stent patency is 100% (7/7). Mean follow-up time is 13 +/- 13.84 months (range, 6-42 months). There have been no long-term complications related to surgical treatment or anticoagulation. All 7 patients have experienced resolution of left leg swelling and pain and have no evidence of post-thrombotic syndrome or DVT recurrence to date. CONCLUSIONS: Women on OCPs presenting with left-sided iliofemoral DVT should be screened for hypercoagulable disorders and underlying May-Thurner anatomy. Treatment of May-Thurner syndrome should include thrombolysis/thrombectomy and anticoagulation for current DVT in addition to angioplasty and stenting of the underlying obstruction.

PMID: 19135831 [PubMed - indexed for MEDLINE]

A note from Dr. Simka, regarding his impression of the difference in MS venous stenosis, after studying the veins with ultrasound:

Quote:
From my (still very limited) experience, the hallmark of venous lesions in MS patients is the stiffness of venous wall, it is not external compression. Neither is it alike varicose veins, thrombosis, atherosclerosis, or so. It is very strange, I am sitting in vascular sonography for years and I don't remember to see such a vein before scanning MS patients. Actually, the most similar pathology (as far as ultrasonographic picture is concerned) is May-Thurner syndrome in iliac veins.

Terry wrote:
Cheer,
Did Dr. Dake comment about the veins? I know you said they were small. Anything else?

cheerleader wrote:A note from Dr. Simka, regarding his impression of the difference in MS venous stenosis, after studying the veins with ultrasound:

From my (still very limited) experience, the hallmark of venous lesions in MS patients is the stiffness of venous wall, it is not external compression. Neither is it alike varicose veins, thrombosis, atherosclerosis, or so. It is very strange, I am sitting in vascular sonography for years and I don't remember to see such a vein before scanning MS patients. Actually, the most similar pathology (as far as ultrasonographic picture is concerned) is May-Thurner syndrome in iliac veins.

AC