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Considerations in the diagnosis and therapy for deep vein thrombosis
American Journal of Emergency Medicine (2007) 25, 860.e1 – 860.e4
www.elsevier.com/locate/ajem
Case Report Considerations in the diagnosis and therapy for deep vein thrombosis Venous thromboembolism represents a significant clinical problem, affecting patients of all age groups, nationalities, and socioeconomic strata. May-Thurner syndrome is an underreported clinical condition in which the left common iliac vein is compressed by the right common iliac artery with subsequent development of deep vein thrombosis. This syndrome most often affects young to middle-aged women, and patients usually present with left leg symptoms. This has the potential to cause long-term chronic insufficiency. We report a case of extensive iliofemoral deep venous thrombosis due to May-Thurner syndrome and review the current options for diagnosis and therapy. Despite advances in diagnosis and treatment, venous thromboembolism remains as a potentially life-threatening disorder affecting hospitalized patients as well as ostensibly healthy individuals [1]. Deep venous thrombosis (DVT) tops the differential diagnosis list for unilateral lower extremity edema. A lesser-known entity, May-Thurner syndrome can initiate DVT formation through compression of the left common iliac vein by the overlying right iliac artery, resulting in impeded venous blood flow from the left lower extremity. Early recognition of May-Thurner syndrome could prevent DVT formation and provide symptomatic relief. A 26-year-old woman presented with persistent progressive painless swelling of the left thigh of about 6 weeks’ duration. Physical examination revealed a swollen left leg to the level of the groin, with pitting edema and slight tenderness. Her left thigh was 6 cm larger in circumference than the right thigh, and there were dilated, engorged veins on the lower abdomen mainly on the left side, the direction of flow being below upward toward the umbilicus. Doppler ultrasonography confirmed the presence of a large thrombus extending from central femoral vein to the left iliac vein. The patient was a nonsmoker, was not on medications, and had no significant contributory factors. Computed tomographic (CT) scan was then arranged because the upper extent of the thrombus could not be confirmed by Doppler ultrasound, and the diagnosis of May-Thurner syndrome was considered. Dual-phase thin-section (section thickness, 1.25 mm) abdominal CT was performed at arterial (angiography) and venous (venography) phases with 64-slice multidetector row CT (Siemens, Erlangen, Germany). Three-dimensional volume rendering and transverse CT demonstrated normal 0735-6757/$ – see front matter D 2007 Elsevier Inc. All rights reserved.
arterial anatomy and compression of the left common iliac vein by the right common iliac artery, with extensive thrombus throughout the left iliac system (Fig. 1). No pelvic mass was noted. Subsequently, venography was performed. A 4F micropuncture sheath was placed into the left popliteal vein; left iliac venography was performed, which confirmed compression of the central left common iliac vein, with thrombus extending from the common femoral vein to the level of obstruction (Fig. 2A). A multisidehole infusion system (Craig-McNamara, Micro Therapeutics, Irvine, CA) was introduced through the vascular sheath, with its infusion length embedded in the entire thrombus burden. After 10 mg bolus of recombinant tissue plasminogen activator, an infusion was instituted at 1 mg/h, with heparin infusing via the side arm of the sheath at 42 U/h. Intravenous heparin was delivered by an infusion at 500 U/h. Venography was performed the next day, which revealed partial resolution of the thrombus (Fig. 2B), with the remaining thrombus removed using a Trellis mechanical thrombectomy device (AngioJet, Possis Medical, Inc, Minneapolis, Minn) (Fig. 2C). The underlying left common iliac vein lesion was treated with angioplasty (Fig. 3A) and placement of a stent (16 90 mm Wallstent, Boston Scientific, Natick, Mass) (Fig. 3B). After completion of endovascular therapy, the patient was prescribed anticoagulation therapy with oral warfarin for a minimum of 6 months. She will be followed up by means of clinic visits, and stent patency will be assessed by duplex ultrasonography performed at 1, 3, 6, and 12 months and then yearly thereafter. Compression of the left iliac vein between the right common iliac artery and the fifth lumbar vertebra was described first by McMurrich [2] in 1908 and later in much more detail in a large autopsy study by May and Thurner [3], who also recognized the clinical implications of the iliac bspursQ leading to acute DVT. On the basis of autopsies, May and Thurner found a 22% prevalence of a spur—the name they gave to the intravenous endothelial changes seen at the point of compression near the mouth of the left common iliac vein. Cockett and Thomas [4] coined the term iliac vein compression syndrome in 1965 and called attention to the obstructive symptoms in affected patients, who are often seen without clinical signs of previous DVT. A clinical suspicion of venous thrombosis should always be confirmed by objective tests because patients with minimal leg symptoms may have extensive venous thrombosis, whereas the classic symptoms and signs of pain,
860.e2
Fig. 1 Axial CT venogram image demonstrates stenosed left common iliac vein (arrow) with crossing right common iliac artery immediately anterior and medial to it. Normal-caliber contrastenhanced right common iliac vein is seen lateral to this.
tenderness, and swelling of the leg can be caused by nonthrombotic disorders. Despite the nonspecificity of clinical features, history and physical examination are important components of the diagnostic process because they may uncover an alternative cause of the patient’s symptoms and because they allow patients to be classified as having a high, intermediate, or low probability for venous
Case Report thrombosis [5]. With a simple clinical scoring system that included 3 main components (symptoms and signs at presentation, presence or absence of risk factors, and presence or absence of a possible alternative diagnosis), Wells and associates [5] showed that approximately 80% of patients with high clinical probability have venous thrombosis, whereas only 5% of patients with low clinical probability have venous thrombosis. When combined with the results of noninvasive tests, these pretest probabilities can be used to both simplify and reduce costs of the diagnostic process. The patient with symptomatic chronic left common iliac compression will typically present with symptoms, many of which are similar to those found in patients with DVT. Swelling, pain in the distal lower extremity, engorged varicose veins, and even venous stasis skin changes can all be seen. Inability to wear a tight-fitting shoe may be the initial complaint. Difficulty in performing physical exercise such as running can be seen secondary to the discomfort of having one leg swollen compared with the unaffected right one. Unlike DVT, whose onset is generally acute, MayThurner syndrome is expected to present in a more chronic fashion. There is a female predominance with this syndrome, and it is observed more frequently between the second and fourth decades of life [4]. Approximately 50% to 60% of patients presenting with left-sided
Fig. 2 A, Venogram via left popliteal access demonstrates complete occlusion of the left femoral vein with development of venous collaterals. B, Repeat venogram after overnight thrombolysis shows restoration of flow in the left external and common iliac veins, with filling defects representing residual thrombus. C, Pharmomechanical thrombectomy device deployed in the left femoral and iliac veins, with proximal and distal occlusive balloons inflated.
Case Report
860.e3
Fig. 3 A, Balloon angioplasty of proximal left common iliac vein stenosis. B, Venogram after stent deployment shows normal-caliber left common iliac vein and absence of thrombus.
iliofemoral DVT have common iliac vein intraluminal webs from extrinsic compression [6]. Therefore, iliac vein compression syndrome is relatively common, and there should be a high index of suspicion, particularly in a young woman who presents with acute iliofemoral thrombosis of the left leg. The condition arises as the aorta travels left of the inferior vena cava as it descends through the abdomen such that when it bifurcates, the right common iliac artery must cross over the left common iliac vein near the bifurcation of each central vessel [7]. Because an artery has a much thicker wall and is under much greater pressure than a vein, when pushed together the vein becomes the compressed vessel. If the vein is sufficiently compressed against the pelvic rim, the increased pressure can cause edema in the left lower extremity [8]. The triad of Virchow [9] describes an increased risk of venous thrombosis with stasis, hypercoagulability, and vessel intimal injury; the first of which is present with any venous obstruction. There is evidence that intimal injury may also take place in the form of a spur when the compression occurs over time. Despite many collateral vessels throughout the pelvis, significant com-
pression can produce symptomatic edema. Diagnosis is confirmed by Doppler ultrasound and CT venogram. The therapeutic goals for treating the patient with acute iliofemoral DVT include prevention of PE, restoration of unobstructed blood flow through the thrombosed segment, prevention of recurrent thrombosis, and preservation of the venous valve function. Success in the achievement of these clinical goals will minimize the morbidity and mortality of PE and will diminish the sequelae of the postthrombotic syndrome. One of every 3 to 4 patients with symptomatic proximal DVT of the lower extremities will develop postthrombotic sequelae [10,11]. This syndrome usually appears within 1 year after the index thrombosis [10,11]. Clinical presentation may vary from minor signs, including skin discoloration, venous ectasia, discomfort, and swelling, to severe manifestations, such as chronic pain, intractable edema, or leg ulcer [12,13]. Postthrombotic sequelae have a substantial negative impact on quality of life and have considerable socioeconomic consequences for both the individual patient and the health care system [14]. The current standard of care for DVT includes systemic anticoagulation with heparin followed by therapy with
860.e4
Case Report
warfarin sodium [15]. Such a regimen, however, does not promote lysis to reduce the thrombus load nor does it contribute to restoration of the venous valve function. Anticoagulation alone, therefore, does not protect the limb from postthrombotic syndrome, which can occur from months to years after the acute thrombotic event and is more prevalent after iliofemoral DVT [16]. Historically, multiple surgical treatment options have been advocated, but the advent of plasminogen activators to promote lysis of intravascular thrombi provides a less invasive strategy to restore venous patency in patients with acute DVT, as described in our case [17]. Catheter-directed thrombolytic therapy and/or stent placement is currently the first-line treatment for acute extensive iliofemoral DVT [18-20]. In summary, history of persistent left lower extremity swelling with or without DVT in a woman between the second and fourth decades of life without an obvious cause is highly suggestive of May-Thurner syndrome, and this possibility should be investigated. It is relatively common, and there should be a high index of suspicion. This diagnosis is confirmed with CT venography, which demonstrates the iliac vein compression. Symptoms indicate intervention for treatment, symptom relief, and long-term sequelae. Whereas anticoagulation with heparin and warfarin remains as the cornerstone of care, adjuvant therapy with thrombolytic and mechanical interventional therapies can be very helpful in a select group of patients with venous thromboembolic disease. Endovascular treatment with stent placement is an alternative to direct surgical repair of the compressed left common iliac vein. Graham M. Roche-Nagle MD Mary C. Barry MD Department of Vascular Surgery St Vincent’s University Hospital Dublin 4, Ireland E-mail address: [email protected] Ronan Ryan MD David P. Brophy MD Department of Interventional Radiology St Vincent’s University Hospital Dublin 4, Ireland doi:10.1016/j.ajem.2007.02.012
References [1] Bosson JL, Labarere J, Sevestre MA, Belmin J, Beyssier L, Elias A, et al. Deep vein thrombosis in elderly patients hospitalized in subacute care facilities: a multicenter cross-sectional study of risk factors, prophylaxis, and prevalence. Arch Intern Med 2003;163: 2613 - 8.
[2] McMurrich JP. The occurrence of congenital adhesions in the common iliac veins and their relation to the thrombosis of the femoral and iliac veins. Am J Med Sci 1908;135:142 - 7. [3] May R, Thurner J. The cause of the predominantly sinistral occurrence of thrombosis of the pelvic veins. Angiology 1957;8:419 - 27. [4] Cockett FB, Lea Thomas M. The iliac compression syndrome. Br J Surg 1965;52:816 - 21. [5] Wells PS, Hirsh J, Anderson DR, Lensing AWA, Foster G, Kearon C, et al. Accuracy of clinical assessment of deep-vein thrombosis. Lancet 1995;345:1326 - 30. [6] Mickley V, Schwagierek R, Rilinger N, Gorich J, Sunder-Plassmann L. Left iliac venous thrombosis caused by venous spur: treatment with thrombectomy and stent implantation. J Vasc Surg 1998; 28:492 - 7. [7] Gray H. Anatomy of the human body. 20th ed. Philadelphia (Pa)7 Lea & Febiger; 1918. [8] Baron HC, Shams J, Wayne M. Iliac vein compression syndrome: a new method of treatment. Am Surg 2000;66:653 - 5. [9] Virchow R. Uber die Erweiterung kleiner Gefasse. Arch Pathol Anat 1851;3:427. [10] Prandoni P, Lensing AW, Cogo A, Cuppini S, Villalta S, Carta M, et al. The long-term clinical course of acute deep venous thrombosis. Ann Intern Med 1996;125:1 - 7. [11] Brandjes DP, Bqller HR, Heijboer H, Huisman MV, de Rijk M, Jagt H, et al. Randomised trial of effect of compression stockings in patients with symptomatic proximal-vein thrombosis. Lancet 1997;349:759 - 62. [12] Bernardi E, Prandoni P. The post-thrombotic syndrome. Curr Opin Pulm Med 2000;6:335 - 42. [13] Kahn SR, Hirsch A, Shrier I. Effect of postthrombotic syndrome on health-related quality of life after deep venous thrombosis. Arch Intern Med 2002;162:1144 - 8. [14] Bergqvist D, Jendteg S, Johansen L, Persson U, Odegaard K. Cost of long-term complications of deep venous thrombosis of the lower extremities: an analysis of a defined patient population in Sweden. Ann Intern Med 1997;126:454 - 7. [15] Strandness Jr DE, Langlois Y, Cramer M, et al. Long-term sequelae of acute venous thrombosis. JAMA 1983;250:1289 - 92. [16] Hull RD, Raskob GE, Rosenbloom D, Hull RD, Raskob GE, Rosenbloom D, et al. Heparin for 5 days as compared with 10 days in the initial treatment of proximal venous thrombosis. N Engl J Med 1990;322:1260 - 4. [17] Mewissen MW, Seabrook GR, Meissner MH, Cynaman J, Labropoulos N, Haughton SH. Catheter-directed thrombolysis for lower extremity deep venous thrombosis: report of a national multicenter registry. Radiology 1999;211:39 - 49. [18] Patel NH, Stookey KR, Ketcham DB, Cragg AH. Endovascular management of acute extensive iliofemoral deep venous thrombosis caused by May-Thurner syndrome. J Vasc Interv Radiol 2000;11: 1297 - 302. [19] O’Sullivan GJ, Semba CP, Bittner CA, Kee ST, Lopez SJ, Powel BW, et al. Endovascular management of iliac vein compression (MayThurner) syndrome. J Vasc Interv Radiol 2000;11:823 - 36. [20] Hurst DR, Forauer AR, Bloom JR, Greenfield LJ, Wakefield TW, Williams DM. Diagnosis and endovascular treatment of iliocaval compression syndrome. J Vasc Surg 2001;34:106 - 13.
www.elsevier.com/locate/ajem
Case Report Considerations in the diagnosis and therapy for deep vein thrombosis Venous thromboembolism represents a significant clinical problem, affecting patients of all age groups, nationalities, and socioeconomic strata. May-Thurner syndrome is an underreported clinical condition in which the left common iliac vein is compressed by the right common iliac artery with subsequent development of deep vein thrombosis. This syndrome most often affects young to middle-aged women, and patients usually present with left leg symptoms. This has the potential to cause long-term chronic insufficiency. We report a case of extensive iliofemoral deep venous thrombosis due to May-Thurner syndrome and review the current options for diagnosis and therapy. Despite advances in diagnosis and treatment, venous thromboembolism remains as a potentially life-threatening disorder affecting hospitalized patients as well as ostensibly healthy individuals [1]. Deep venous thrombosis (DVT) tops the differential diagnosis list for unilateral lower extremity edema. A lesser-known entity, May-Thurner syndrome can initiate DVT formation through compression of the left common iliac vein by the overlying right iliac artery, resulting in impeded venous blood flow from the left lower extremity. Early recognition of May-Thurner syndrome could prevent DVT formation and provide symptomatic relief. A 26-year-old woman presented with persistent progressive painless swelling of the left thigh of about 6 weeks’ duration. Physical examination revealed a swollen left leg to the level of the groin, with pitting edema and slight tenderness. Her left thigh was 6 cm larger in circumference than the right thigh, and there were dilated, engorged veins on the lower abdomen mainly on the left side, the direction of flow being below upward toward the umbilicus. Doppler ultrasonography confirmed the presence of a large thrombus extending from central femoral vein to the left iliac vein. The patient was a nonsmoker, was not on medications, and had no significant contributory factors. Computed tomographic (CT) scan was then arranged because the upper extent of the thrombus could not be confirmed by Doppler ultrasound, and the diagnosis of May-Thurner syndrome was considered. Dual-phase thin-section (section thickness, 1.25 mm) abdominal CT was performed at arterial (angiography) and venous (venography) phases with 64-slice multidetector row CT (Siemens, Erlangen, Germany). Three-dimensional volume rendering and transverse CT demonstrated normal 0735-6757/$ – see front matter D 2007 Elsevier Inc. All rights reserved.
arterial anatomy and compression of the left common iliac vein by the right common iliac artery, with extensive thrombus throughout the left iliac system (Fig. 1). No pelvic mass was noted. Subsequently, venography was performed. A 4F micropuncture sheath was placed into the left popliteal vein; left iliac venography was performed, which confirmed compression of the central left common iliac vein, with thrombus extending from the common femoral vein to the level of obstruction (Fig. 2A). A multisidehole infusion system (Craig-McNamara, Micro Therapeutics, Irvine, CA) was introduced through the vascular sheath, with its infusion length embedded in the entire thrombus burden. After 10 mg bolus of recombinant tissue plasminogen activator, an infusion was instituted at 1 mg/h, with heparin infusing via the side arm of the sheath at 42 U/h. Intravenous heparin was delivered by an infusion at 500 U/h. Venography was performed the next day, which revealed partial resolution of the thrombus (Fig. 2B), with the remaining thrombus removed using a Trellis mechanical thrombectomy device (AngioJet, Possis Medical, Inc, Minneapolis, Minn) (Fig. 2C). The underlying left common iliac vein lesion was treated with angioplasty (Fig. 3A) and placement of a stent (16 90 mm Wallstent, Boston Scientific, Natick, Mass) (Fig. 3B). After completion of endovascular therapy, the patient was prescribed anticoagulation therapy with oral warfarin for a minimum of 6 months. She will be followed up by means of clinic visits, and stent patency will be assessed by duplex ultrasonography performed at 1, 3, 6, and 12 months and then yearly thereafter. Compression of the left iliac vein between the right common iliac artery and the fifth lumbar vertebra was described first by McMurrich [2] in 1908 and later in much more detail in a large autopsy study by May and Thurner [3], who also recognized the clinical implications of the iliac bspursQ leading to acute DVT. On the basis of autopsies, May and Thurner found a 22% prevalence of a spur—the name they gave to the intravenous endothelial changes seen at the point of compression near the mouth of the left common iliac vein. Cockett and Thomas [4] coined the term iliac vein compression syndrome in 1965 and called attention to the obstructive symptoms in affected patients, who are often seen without clinical signs of previous DVT. A clinical suspicion of venous thrombosis should always be confirmed by objective tests because patients with minimal leg symptoms may have extensive venous thrombosis, whereas the classic symptoms and signs of pain,
860.e2
Fig. 1 Axial CT venogram image demonstrates stenosed left common iliac vein (arrow) with crossing right common iliac artery immediately anterior and medial to it. Normal-caliber contrastenhanced right common iliac vein is seen lateral to this.
tenderness, and swelling of the leg can be caused by nonthrombotic disorders. Despite the nonspecificity of clinical features, history and physical examination are important components of the diagnostic process because they may uncover an alternative cause of the patient’s symptoms and because they allow patients to be classified as having a high, intermediate, or low probability for venous
Case Report thrombosis [5]. With a simple clinical scoring system that included 3 main components (symptoms and signs at presentation, presence or absence of risk factors, and presence or absence of a possible alternative diagnosis), Wells and associates [5] showed that approximately 80% of patients with high clinical probability have venous thrombosis, whereas only 5% of patients with low clinical probability have venous thrombosis. When combined with the results of noninvasive tests, these pretest probabilities can be used to both simplify and reduce costs of the diagnostic process. The patient with symptomatic chronic left common iliac compression will typically present with symptoms, many of which are similar to those found in patients with DVT. Swelling, pain in the distal lower extremity, engorged varicose veins, and even venous stasis skin changes can all be seen. Inability to wear a tight-fitting shoe may be the initial complaint. Difficulty in performing physical exercise such as running can be seen secondary to the discomfort of having one leg swollen compared with the unaffected right one. Unlike DVT, whose onset is generally acute, MayThurner syndrome is expected to present in a more chronic fashion. There is a female predominance with this syndrome, and it is observed more frequently between the second and fourth decades of life [4]. Approximately 50% to 60% of patients presenting with left-sided
Fig. 2 A, Venogram via left popliteal access demonstrates complete occlusion of the left femoral vein with development of venous collaterals. B, Repeat venogram after overnight thrombolysis shows restoration of flow in the left external and common iliac veins, with filling defects representing residual thrombus. C, Pharmomechanical thrombectomy device deployed in the left femoral and iliac veins, with proximal and distal occlusive balloons inflated.
Case Report
860.e3
Fig. 3 A, Balloon angioplasty of proximal left common iliac vein stenosis. B, Venogram after stent deployment shows normal-caliber left common iliac vein and absence of thrombus.
iliofemoral DVT have common iliac vein intraluminal webs from extrinsic compression [6]. Therefore, iliac vein compression syndrome is relatively common, and there should be a high index of suspicion, particularly in a young woman who presents with acute iliofemoral thrombosis of the left leg. The condition arises as the aorta travels left of the inferior vena cava as it descends through the abdomen such that when it bifurcates, the right common iliac artery must cross over the left common iliac vein near the bifurcation of each central vessel [7]. Because an artery has a much thicker wall and is under much greater pressure than a vein, when pushed together the vein becomes the compressed vessel. If the vein is sufficiently compressed against the pelvic rim, the increased pressure can cause edema in the left lower extremity [8]. The triad of Virchow [9] describes an increased risk of venous thrombosis with stasis, hypercoagulability, and vessel intimal injury; the first of which is present with any venous obstruction. There is evidence that intimal injury may also take place in the form of a spur when the compression occurs over time. Despite many collateral vessels throughout the pelvis, significant com-
pression can produce symptomatic edema. Diagnosis is confirmed by Doppler ultrasound and CT venogram. The therapeutic goals for treating the patient with acute iliofemoral DVT include prevention of PE, restoration of unobstructed blood flow through the thrombosed segment, prevention of recurrent thrombosis, and preservation of the venous valve function. Success in the achievement of these clinical goals will minimize the morbidity and mortality of PE and will diminish the sequelae of the postthrombotic syndrome. One of every 3 to 4 patients with symptomatic proximal DVT of the lower extremities will develop postthrombotic sequelae [10,11]. This syndrome usually appears within 1 year after the index thrombosis [10,11]. Clinical presentation may vary from minor signs, including skin discoloration, venous ectasia, discomfort, and swelling, to severe manifestations, such as chronic pain, intractable edema, or leg ulcer [12,13]. Postthrombotic sequelae have a substantial negative impact on quality of life and have considerable socioeconomic consequences for both the individual patient and the health care system [14]. The current standard of care for DVT includes systemic anticoagulation with heparin followed by therapy with
860.e4
Case Report
warfarin sodium [15]. Such a regimen, however, does not promote lysis to reduce the thrombus load nor does it contribute to restoration of the venous valve function. Anticoagulation alone, therefore, does not protect the limb from postthrombotic syndrome, which can occur from months to years after the acute thrombotic event and is more prevalent after iliofemoral DVT [16]. Historically, multiple surgical treatment options have been advocated, but the advent of plasminogen activators to promote lysis of intravascular thrombi provides a less invasive strategy to restore venous patency in patients with acute DVT, as described in our case [17]. Catheter-directed thrombolytic therapy and/or stent placement is currently the first-line treatment for acute extensive iliofemoral DVT [18-20]. In summary, history of persistent left lower extremity swelling with or without DVT in a woman between the second and fourth decades of life without an obvious cause is highly suggestive of May-Thurner syndrome, and this possibility should be investigated. It is relatively common, and there should be a high index of suspicion. This diagnosis is confirmed with CT venography, which demonstrates the iliac vein compression. Symptoms indicate intervention for treatment, symptom relief, and long-term sequelae. Whereas anticoagulation with heparin and warfarin remains as the cornerstone of care, adjuvant therapy with thrombolytic and mechanical interventional therapies can be very helpful in a select group of patients with venous thromboembolic disease. Endovascular treatment with stent placement is an alternative to direct surgical repair of the compressed left common iliac vein. Graham M. Roche-Nagle MD Mary C. Barry MD Department of Vascular Surgery St Vincent’s University Hospital Dublin 4, Ireland E-mail address: [email protected] Ronan Ryan MD David P. Brophy MD Department of Interventional Radiology St Vincent’s University Hospital Dublin 4, Ireland doi:10.1016/j.ajem.2007.02.012
References [1] Bosson JL, Labarere J, Sevestre MA, Belmin J, Beyssier L, Elias A, et al. Deep vein thrombosis in elderly patients hospitalized in subacute care facilities: a multicenter cross-sectional study of risk factors, prophylaxis, and prevalence. Arch Intern Med 2003;163: 2613 - 8.
[2] McMurrich JP. The occurrence of congenital adhesions in the common iliac veins and their relation to the thrombosis of the femoral and iliac veins. Am J Med Sci 1908;135:142 - 7. [3] May R, Thurner J. The cause of the predominantly sinistral occurrence of thrombosis of the pelvic veins. Angiology 1957;8:419 - 27. [4] Cockett FB, Lea Thomas M. The iliac compression syndrome. Br J Surg 1965;52:816 - 21. [5] Wells PS, Hirsh J, Anderson DR, Lensing AWA, Foster G, Kearon C, et al. Accuracy of clinical assessment of deep-vein thrombosis. Lancet 1995;345:1326 - 30. [6] Mickley V, Schwagierek R, Rilinger N, Gorich J, Sunder-Plassmann L. Left iliac venous thrombosis caused by venous spur: treatment with thrombectomy and stent implantation. J Vasc Surg 1998; 28:492 - 7. [7] Gray H. Anatomy of the human body. 20th ed. Philadelphia (Pa)7 Lea & Febiger; 1918. [8] Baron HC, Shams J, Wayne M. Iliac vein compression syndrome: a new method of treatment. Am Surg 2000;66:653 - 5. [9] Virchow R. Uber die Erweiterung kleiner Gefasse. Arch Pathol Anat 1851;3:427. [10] Prandoni P, Lensing AW, Cogo A, Cuppini S, Villalta S, Carta M, et al. The long-term clinical course of acute deep venous thrombosis. Ann Intern Med 1996;125:1 - 7. [11] Brandjes DP, Bqller HR, Heijboer H, Huisman MV, de Rijk M, Jagt H, et al. Randomised trial of effect of compression stockings in patients with symptomatic proximal-vein thrombosis. Lancet 1997;349:759 - 62. [12] Bernardi E, Prandoni P. The post-thrombotic syndrome. Curr Opin Pulm Med 2000;6:335 - 42. [13] Kahn SR, Hirsch A, Shrier I. Effect of postthrombotic syndrome on health-related quality of life after deep venous thrombosis. Arch Intern Med 2002;162:1144 - 8. [14] Bergqvist D, Jendteg S, Johansen L, Persson U, Odegaard K. Cost of long-term complications of deep venous thrombosis of the lower extremities: an analysis of a defined patient population in Sweden. Ann Intern Med 1997;126:454 - 7. [15] Strandness Jr DE, Langlois Y, Cramer M, et al. Long-term sequelae of acute venous thrombosis. JAMA 1983;250:1289 - 92. [16] Hull RD, Raskob GE, Rosenbloom D, Hull RD, Raskob GE, Rosenbloom D, et al. Heparin for 5 days as compared with 10 days in the initial treatment of proximal venous thrombosis. N Engl J Med 1990;322:1260 - 4. [17] Mewissen MW, Seabrook GR, Meissner MH, Cynaman J, Labropoulos N, Haughton SH. Catheter-directed thrombolysis for lower extremity deep venous thrombosis: report of a national multicenter registry. Radiology 1999;211:39 - 49. [18] Patel NH, Stookey KR, Ketcham DB, Cragg AH. Endovascular management of acute extensive iliofemoral deep venous thrombosis caused by May-Thurner syndrome. J Vasc Interv Radiol 2000;11: 1297 - 302. [19] O’Sullivan GJ, Semba CP, Bittner CA, Kee ST, Lopez SJ, Powel BW, et al. Endovascular management of iliac vein compression (MayThurner) syndrome. J Vasc Interv Radiol 2000;11:823 - 36. [20] Hurst DR, Forauer AR, Bloom JR, Greenfield LJ, Wakefield TW, Williams DM. Diagnosis and endovascular treatment of iliocaval compression syndrome. J Vasc Surg 2001;34:106 - 13.