May-Thurner syndrome is a condition that results from narrowing of the left
common iliac vein lumen due to pressure from the right common iliac artery as
it crosses anterior to it. We describe a very rare case in which a previously
asymptomatic patient presented with May-Thurner syndrome

Bangeholm, A.

Esmaeili, E.

Jordan, R.

Loukas, M.

Shah, R.

Tubbs, R.S.

English

Via Medica Journals

Folia Morphol. Vol. 67, No. 3, pp. 214–217Copyright © 2008 Via MedicaISSN 0015–5659www.fm.viamedica.plC A S E   R E P O R T214Address for correspondence: Dr. M. Loukas, MD, PhD, Ass. Prof., Department of Anatomical Sciences, St. George’s University, School ofMedicine, Grenada, West Indies, tel: 473 444 4175 x2556, fax: 473 444 2887, e-mail: edsg2000@yahoo.com, mloukas@sgu.eduA case of May-Thurner syndromeM. Loukas1, R. Shah1, E. Esmaeili1, A. Bangeholm1, R.S. Tubbs2, R. Jordan11Department of Anatomical Sciences, St. George’s University, Grenada, West Indies2Department of Cell Biology and Section of Pediatric Neurosurgery, University of Alabama at Birmingham,Birmingham, AL, USA[Received 23 December 2007; Accepted 2 May 2008]May-Thurner syndrome is a condition that results from narrowing of the leftcommon iliac vein lumen due to pressure from the right common iliac artery asit crosses anterior to it. We describe a very rare case in which a previouslyasymptomatic patient presented with May-Thurner syndrome. (Folia Morphol2008; 67: 214–217)Key words: common iliac artery, common iliac vein, May-ThurnersyndromeINTRODUCTIONMay-Thurner syndrome is a rare vascular constric-tion that was first described in 1908 by McMurrich [1]and further elaborated on by May and Thurner in1956 [10]. May-Thurner syndrome is described ascompression of the left common iliac vein (LCIV) bythe right common iliac artery (RCIA) as it travels fromthe aortoiliac bifurcation to the right inguinal region [9].Typically, this crossing over is considered to be ana-tomically normal. However, in some patients thecompression of the vein between the vertebral bodyposteriorly and the artery anteriorly causes thicken-ing of the inner wall of the vein, leading to intimalhyperplasia and thus to stenosis [10]. This compres-sion may present symptomatically or be an inciden-tal finding. Following the development and wide-spread use of cross-sectional imaging with comput-ed tomography, compression of the LCIV has becomemore frequently encountered in asymptomatic pa-tients and is usually readily identifiable with intrave-nously administered contrast material [7]. While theprevalence of the disorder is unknown, in patientsundergoing evaluation for lower extremity venousdisorders the condition is found in 2–5% of patients [3]and is most often seen in women between the se-cond and fourth decades of life [5]. Knowledge ofthese variations is necessary to avoid misdiagnosisof symptomatic patients. We describe a very rare casein which a previously asymptomatic patient present-ed with May-Thurner syndrome.CASE REPORTA 35-year-old Caucasian female with no prior ill-ness other than hypertension was scheduled for hys-terectomy to remove multiple uterine fibroids. Threedays before the scheduled operation the patient wasadmitted to the Emergency Room complaining ofsevere lower left leg pain and swelling.Physical examination revealed a painful left calfand swelling of the lower extremity over 48 hours.The patient’s height and weight were 162 cm and51 kg respectively. The left calf was measured at15 inches and the right calf at 14 inches. The swell-ing extended distally from the left knee to the an-kle. There was marked tenderness with palpationof the left calf. A blood pressure cuff was appliedto both legs up to 160 mm Hg. There was no dis-comfort on the right side but marked discomfortin the left lower extremity. Pulses were intact andequal to those of the lower extremities. No vari-cose veins were evident but venous insufficiencywas noted.215M. Loukas et al., May-Thurner syndromeComputed tomography of the pelvis and lowerlimb was performed and large fibroids of the uteruswere noticed. Ultrasonographic examination wasperformed and was negative for deep vein throm-bosis. In addition, an ascending venogram was per-formed and complete occlusion of the central por-tion of the left common iliac vein was noted asa result of compression from the overlying left com-mon iliac artery. Measurements obtained with thepatient in the supine position revealed a 6-mm Hgpressure gradient across the stenosis. The mean di-ameter at the origin of the left common iliac veinwas 3.2 mm, whereas the mean diameter of the rightcommon iliac vein at the same level was 11.9 mm.The mean percentage stenosis of the left commoniliac vein due to compression by the right commoniliac artery was 70% (Fig. 1). The mean distance fromthe posterior border of the right common iliac ar-tery to the nearest lumbar vertebra was 4.5 mm.The femoral vein was grossly patent and duplicat-ed. The clinical history and imaging findings werediagnostic for May-Thurner syndrome, although wewere unable to detect the presence or absence ofintimal hypertrophy.After the occluded vein had been identified,a guide wire and a catheter were inserted into theleft common iliac vein. A percutaneous translumi-nal angioplasty of the left common iliac vein andexternal iliac vein was performed with a 10 ¥ 4 ¥¥ 80 Cordis balloon. Furthermore, an endovasculartandem stent (10 ¥ 40 SMART), was placed intothe left common and external iliac veins. The pa-tient tolerated the procedure well and no immedi-ate symptomatic complications were noticed. Thepatient was discharged the same day. The patientindicated that she had had a laparoscopy ten yearspreviously and that she suffered from chronic hy-pertension. She is currently on a diuretic (Lasix) andlow molecular weight heparin (Lovenox).DISCUSSIONIn 1957 May and Thurner examined 430 cadav-ers and documented the decrease in venous flowthat resulted from intimal change in the LCIV. Sincethen the syndrome has been variously termed May--Thurner syndrome, iliac vein compression syndrome,Cockett syndrome or iliocaval compression syndrome[5, 10, 18].The syndrome may present clinically as left low-er extremity edema, varicosities, venous stasis chang-es, venous claudication, pain or venous ulceration.Some cases have been described where the syn-drome is found in adolescent-aged females [15].However, the majority of the cases are in womenbetween the second and fourth decades of life [5].Recent imaging data indicate that compressionof the LCIV at the arterial crossover point may bepresent in 66% of the general population withoutany venous symptoms [7]. Intraluminally, the meanluminal stenosis of the LCIV due to compression bythe artery has been reported to be as high as 68% [12].Patients who are within this age group and presentwith a history of persistent left lower extremity swell-ing with or without deep venous thrombosis withno other obvious causes should have May-Thurnersyndrome excluded.Figure 1. A left iliac vein venogram. Note the compression point at which the left iliac vein is not filled with contrast medium. In the samefigure the shadow of the vein has been outlined with a dotted line.216Folia Morphol., 2008, Vol. 67, No. 3The study of choice has typically been contrastvenography, which shows compressions of the iliacvein with spur. Intravenous ultrasound has also beenused in diagnosis. According to the literature, venog-raphy is less sensitive than IVUS at 66% and 90%,respectively [16]. Once the condition has been iden-tified, traditional therapy involves anticoagulationor surgical correction of the vein compression, ei-ther by a vein patch repair or by a venous crossoverbypass graft. More recently, interventional radiolo-gical techniques such as intraluminal stent place-ment have been used [11].Anticoagulation therapy in symptomatic patientsas a sole treatment has not been very effective. Ithas prevented migration of the thrombi, althoughwithout managing or reducing the mechanical ob-struction caused by the intimal hyperplasia. Recenttreatment utilizing intraluminal venous stents hasbeen associated with greater success, as it deals withthrombus formation and the mechanical obstruc-tion [6, 8, 13, 14].Anatomically, the point of origin of the commoniliac arteries varies according to the level of aorticbifurcation. The abdominal aorta bifurcates intoright and left common iliac arteries anterolateral tothe fourth lumbar vertebral body or upon the discbetween the fourth and the fifth in 75% of cases [4].The arteries continue to diverge as they descend todivide at the level of the sacroiliac joint into exter-nal and internal iliac arteries. The length of the indi-vidual arteries also varies. The common iliac arterycan be as short as 1.2 cm or as long as 11 cm. Theusual length is 3.5–7.5 cm in 72% of cases. Of theremaining 28%, 14% were shorter than 3.5 cm and14% were longer then 7.5 cm [2, 4].The common iliac veins are formed by the unionof the external and internal iliac veins anterior tothe sacroiliac joint, ascending obliquely to end onthe right side of the 5th lumbar vertebra, uniting atan acute angle with the contralateral vessel to formthe inferior vena cava. The left common iliac vein islonger than right common iliac vein and more ob-lique. It lies first medial then posterior to the rightcommon iliac artery [4]. The left common iliac veinreceives the iliolumbar, lateral sacral and mediansacral veins as tributaries. No valves are found inthese veins [17]. It has been reported that lowerextremity deep venous thrombosis occurs three toeight times more frequently on the left than on theright side [14]. With venous compression occurringin May-Thurner syndrome, the incidence of throm-bi formation grows.Owing to the impendence of blood flow from thestenosis, collateral pathways are utilized. Thomas etal. described these collaterals and classified them intothree groups according to the site of the blockage:the external iliac vein (group 1), the common iliac vein(group 2) and both the common and the external iliacveins (group 3) [19]. They observed that all the collat-eral veins were normal channels but were enlarged bythe increased blood flow. In some instances they car-ried the blood in the reverse direction. In the specificcase of the common iliac vein being obstructed, as inour case, the collateral veins run from the internal iliacvein on the side of obstruction through the parame-trial and pre-sacral plexuses to the opposite internaliliac vein, and frequently through the ascending lum-bar vein on the side of the obstruction. Occasionallythe ovarian veins and internal and external vertebralplexuses act as collaterals [19].This specific vascular malformation may come toclinical attention in the symptomatic patient, but itwould be interesting to study whether the syndromeis acquired or congenital. If congenital, early signsmight be seen in children. This case report indicatesthe potential and the need for continued explora-tion of this region of the human body.REFERENCES1. Ahmed H, Hagspiel K (2001) Intravascular ultrasono-graphic findings in May-Thurner syndrome (iliac veincompression syndrome). J Ultrasound Med, 20: 251––256.2. Bergman R (1988) Compendium of human anatomicvariations. Cardiovascular system. Urban & Schwarzen-berg, Baltimore, pp. 84, 92.3. Billakanty S, Burket M, Grubb B (2006) May-Thurnersyndrome: a vascular abnormality encountered duringelectrophysiologic study. PACE, 29: 1310–1311.4. Clemente C (1985) Gray’s anatomy. Chapter 8. The ar-teries. 30th ed. Lea & Febiger, Philadelphia, pp. 748–760.5. Cockett FB, Thomas ML (1965) The iliac compressionsyndrome. Br J Surg, 52: 816–821.6. Grunwald M, Goldberg M, Hoffman L (2004) Endovas-cular management of May-Thurner syndrome. AJR, 183:1523–1524.7. Kibbe M, Ujiki M, Goodwin A, Eskandari M, Yao J,Matsumura J (2004) Iliac vein compression in an as-ymptomatic patient population. J Vasc Surg, 39: 937–943.8. Lamont JP, Pearl GJ, Patetsios P, Warner MT, Gable DR,Garrett W, Grimsley B, Smith BL, Shutze WP (2002) Pro-spective evaluation of endoluminal venous stents in thetreatment of the May-Thurner syndrome. Ann VascSurg, 16: 61–64.9. Liu J, Bonn J, Needleman L, Chiou HJ, Gardiner GA Jr,Goldberg BB (1999) Feasibility of three-dimensionalintravascular ultrasonography: preliminary clinical stud-ies. J Ultrasound Med, 18: 489–495.217M. Loukas et al., May-Thurner syndrome10. May R, Thurner J (1957) The cause of the predominantlysinistral occurrence of thrombosis of the pelvic veins.Angiology, 8: 419–427.11. Oderich G, Treiman G, Schneider P, Bhirangi K (2000)Stent placement for treatment of central and peri-pheral venous obstruction: a long-term multi-institution-al experience. J Vasc Surg, 32: 760–769.12. Oguzkurt L, Tercan F, Pourbagher M, Kizilkilic O, Turkoz R,Boyvat F (2005) Computed tomography findings in 10cases of iliac vein compression (May-Thurner) syndrome.Eur J Radiol, 55: 421–425.13. O’Sullivan GJ, Semba CP, Bittner CA, Kee ST, Razavi MK,Sze DY, Dake MD (2000) Endovascular management ofiliac vein compression syndrome. J Vasc Interv Radiol,11: 823–836.14. Patel NH, Stookey KR, Ketcham DB, Cragg AH (2000)Endovascular management of acute extensive iliofe-moral deep venous thrombosis caused by May--Thurner syndrome. J Vasc Interv Radiol, 11: 1297–1302.15. Raffini L, Raybagkar D, Cahill A, Kaye R, Blumenstein M,Manno C (2006) May-Thurner syndrome (iliac vein com-pression) and thrombosis in adolescents. Pediatr BloodCancer, 47: 834–838.16. Raju S, Neglen P (2006) High prevalence of nonthrom-botic iliac vein lesions in chronic venous disease: a per-missive role in pathogenicity. J Vasc Surg, 44: 136–143.17. Standring S (2005) Gray’s anatomy. Chapter 108. Truepelvis, pelvic floor and perineum. 39th ed. Elsevier,Churchill, Livingstone, Edinburgh, pp. 1360–1363.18. Taheri SA, Williams J, Powell S, Cullen J, Peer R,Nowakowski P, Boman L, Pisano S (1987) Iliocaval com-pression syndrome. Am J Surg, 154: 169–172.19. Thomas M, Fletcher W, Cockett, Negus D (1967) Venouscollaterals in external and common iliac vein obstruc-tion. 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A case of May-Thurner syndrome

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A case of May-Thurner syndrome

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