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Iliac vein compression syndrome: Case report and review of the literature
Iliac vein compression syndrome: Case report and review of the literature D o n a l d L e a Akers, Jr., M D , B r i a n C r e a d o , M D , and R o b e r t L. H e w i t t , M D ,
New Orleans, La. Iliac vein compression syndrome is a clinical condition that occurs as a result o f compression o f the left iliac vein between the right iliac arte12¢ and the fifth lumbar vertebrae. Patients usually have marked edema o f the left leg. We report a case o f a 16-year-old man who sought medical attention with significant left lower leg edema and four previous episodes o f left leg cellulitis. Evaluation demonstrated venous hypertension as a result o f left iliac vein compression. The patient underwent surgical correction; his symptoms resolved. Details and management o f the case are presented and discussed. A review o f the current literature regarding this condition also is included. (J Vase Surg 1996;24:477-81.
Iliac vein compression s y n d r o m e is a clinical condition that may occur despite a normal orientation between the left iliac vein and the right iliac artery. T h e left iliac vein is usually located posterior to the right iliac artery, b u t in rare situations can be c o m pressed between the iliac artery and the fifth lumbar vertebrae. This anatomic anomaly was first described by M c M u r r i c h in I908.1 I n 1965 C o c k e t t and T h o mas 2 described a series o f patients w h o had iliac vein compression syndrome. S y m p t o m s included left leg edema, pain, varicosities, stasis changes, venous ulceration, and venous claudicarion. I f this condition is n o t recognized, l o n g - t e r m complications including iliofemoral thrombosis may occur and lead to severe l o n g - t e r m disability. A l t h o u g h the diagnosis is rare, the actual incidence is u n k n o w n . This s y n d r o m e m o s t often affects w o m e n in the second to fourth decade o f life, w h o comprised 85% o f the patients in one series) We report an unusual case o f a y o u n g m a n w h o was f o u n d to have iliac vein compression syndrome. This report will describe the evaluation, treatment, and o u t c o m e and will review the literature concerning this anatomic anomaly.
From the Department of Surgery, and the Department of Pediatrics (Dr. Creado), Tulane University School of Medicine. Presented at the Twentieth Annual Meeting of The Southern Association for Vascular Surgery, Naples, Fla., Jan. 24-27, 1996. Reprint requests: Donald Lea Akers, Jr., MD, Department of Surgery; Tulane University School of Medicine, 1430 Tulane Ave., New Orleans, LA 70112. Copyright © i996 by The Society for Vascular Surgery and International Society for CardiovascularSurgery, North American Chapter. 0741-5214/96/$5.00 + 0 24/6/75485
CASE R E P O R T
A 16-year-old man initially had a chief complaint of recurrent episodes ofcellulitis of the left leg and chronic left leg edema. Over the preceding 6 months, he had had four episodes of cellulifis. The edema, which had developed in conjunction with the first episode of cellulitis, improvcd after treatment of the cellulitis but never completely resolved. Moreover, the residual swelling was exacerbated by each subsequent episode. The patient's medical history was unremarkable. On physical examination he was noted to have 2+ pitting edema of the left leg, and thc diameter of the left calfwas 2 cm greater than that of the right. He had equal pulses bilaterally at the femoral, popliteal, dorsalis pedis, and posterior tibial arteries. The left leg was slightly warmer than the right lcg, but was not tender. The remainder of the physical examination was unremarkable. Venous duplex examination suggested chronic vcnous insufficiency with significant reflux of the left leg and no evidence of any acute or chronic deep venous thrombosis. No suggestion of obstruction of venous return was found. A diagnosis of chronic venous insufficiency was made, and compression stockings were prescribed. Three months after his initial visit, the patient returned with an episode of cellulitis, which required hospitalization and the administration of intravenous antibiotics. During this hospital stay, a venogram demonstrated extrinsic compression of the left iliac vein (Fig. 1). With the patient in the supine position, pressures were measured in the venous system, which demonstrated a gradient of 8 cm H20 across this stenosis, A diagnosis ofiliac vein compression syndrome was established. After the resolution of his cellulitis, the patient underwent surgery for correction of the vein compression. Exploration of the retroperitoneum demonstrated the left iliac vein to be significantly compressed by the right iliac artery (Fig. 2). The junction between the inferior vena cava and the left iliac vein was opened to examine the lumen for thc presence of venous webs; however, none were found. 477
478
Akers, Creado, and Hewitt
JOURNAL OF VASCULARSURGERY September 1996
Fig. 1. Inferior vena cava venogram obtained through a left common femoral vein approach demonstrates area of compression of left common iliac vein. Area of compression corresponds to course of right common iliac artery. Numbers represent pressures obtained (in cm H20 ) with patient supine. An 8-cm gradient was present across lesion. Several adhesive bands on the surface of the left iliac vein then were lysed, which resulted in a reduction of the compression. The right iliac artery then was transected and positioned behind the left iliac vein to remove the source of compression (Fig. 3). The patient tolerated the procedure well and was maintained on heparin after surgery until converted to Coumadin. The patient was discharged on the fifth day after surgery. The patient has done well after surgery and had complete resolution of his leg edema when examined 3 months later. He continues to wear compression stocldngs and took Coumadin for 6 months. At 1 year after surgery, he has had no recurrence of his edema or cellulitis.
DISCUSSION The formation o f bands at the m o u t h o f the left c o m m o n iliac vein was first described by McMurrich in 1908.1 In 1965 Cockett and Thomas 2 coined the term "iliac vein compression syndrome" to describe the clinical symptoms associated with this anatomic finding. These authors observed that in their practice venous problems were identified more frequently in the left leg than in the right. They identified a subgroup o f patients who had an isolated area of obstruction at the m o u t h of the left c o m m o n iliac vein that resulted in chronic left leg symptoms. Surgical correction o f the lesion resulted in the resolution of the symptoms o f venous obstruction. Since that initial report, several additional reports have addressed iliac
vein compression syndrome. 3-7 The basic principal in the treatment o f this lesion is to remove the obstructive disease. The anatomic anomaly that results in iliac vein compression syndrome occurs when the left iliac vein is compressed between the right iliac artery and the fifth lumbar vertebra. This anatomic variant results in a decrease in the lumen of the left iliac vein and has been associated with the formation o f venous bands. In an autopsy series, Nexus et al. 8 found bands at the m o u t h o f the left iliac vein in 22% o f dissections; he suggested that this was a normal anatomic variant and was not necessarily related to significant venous disease. This opinion is valid insofar as the true incidence ofiliac vein compression syndrome is rare, with fewer than 100 cases presented in the literature. The develo p m e n t o f deep venous thrombosis and postphlebitic syndrome, however, does have a left side predominance, which suggests that the incidence o f this process may be higher than is currently appreciated) Iliac vein compression syndrome is most often found in w o m e n during their second to the fourth decade o f life. It usually first appears as progressive leg edema with no significant history o f thrombotic problems. 9 The symptoms can range from venous claudication to mild complaints that are consistent with chronic venous insufficiency. Physical examination can demonstrate mild to severe edema, chronic
JOURNAL OF VASCULAR SURGERY
Volume 24, Number 3
Akers, Creado, and Hewitt 479
Fig. 2. Initial operative exposure of bifurcation of aorta and inferior vena cava. Right common iliac artery can be seen in its course across left iliac vein, and corresponding compression of vein is noted.
Fig. 3. Rightcommoniliacarteryhasnowbeentransposedbehindleftiliacvein. Note complete resolution of compression of vein. leg skin changes, development ofvaricosities, significant venous collateral vessels, and ulceration. The initial assessment should begin with a noninvasive evaluation, usually a duplex examination. In the
absence of deep venous thrombosis, however, the findings are usually nonspecific. Results o f impedance plethysmography are often normal in the early stages o f the disease and are likewise usually o f little benefit.
JOURNAL OF VASCULARSURGERY
480
Akers, Creado, and Hewitt
Taheri et al.,3 however, found that exercise venous plethysmography does have a high diagnostic success rate. Direct venous pressure measurements also may provide important information about possible outflow obstruction. Nicolaides and Zukowsld 1° demonstrated a relationship between increased ambulatory pressure and venous ulceration. Arm-foot pressure differentials have been used by Raju 11 to determine the significance of possible outflow obstruction. He found that a gradient of greater than 4 mm H g was strongly suggestive of significant disease. Recently, computed tomographic scans have been suggested as a test that may provide useful information when extrinsic compression is the cause of the obstruction. The role of this method, however, in the primary evaluation of the patient who has iliac vein compression is still unclear. 12 Venography remains the goldstandard diagnostic test because it will demonstrate an area of compression where the right iliac artery crosses the left iliac vein (Fig. 1). Venous collateral vessels from the left iliac system to the right iliac system often can be identified. Obtaining transvenous pressure measurements is essential in confirming the diagnosis. Nexus et al. s and Cockett et al.2 stated that a significant gradient exists when the pressure differential is greater than 2 mm Hg. Rigas 5 states that a resting supine gradient of 2 cm H20 is considered clinically significant. In symptomatic patients who have a significant gradient, an operative approach should be offered. Although the management of chronic venous insufficiency begins with conservative treatment with compressive therapy, a more aggressive surgical approach is recommended in patients who have iliac vein compression syndrome. Taheri et al. 3 argue that progressive symptoms will continue to develop in these patients, so the anatomic anomaly should be corrected as soon as it is identified. Other authors agree that the lesion should be addressed as soon as it is identified because the disease process is progressive in nature. 4,5,9 Several surgical approaches have been used to treat this condition. In those patients who have an isolated defect at the mouth of the left common iliac vein, direct surgical repair is advocated.3 Early operative approaches focused on removing the external compression. 2,s If no evidence of any intraluminal webs or bands is found and the iliac vein achieves normal diameter after the release of the bands, this approach may be adequate. Ifintraluminal webs or bands are present or cannot be ruled out by the preoperative evaluation, the operative repair includes open exploration of the inferior vena cava and the left iliac vein, resection of existing bands or webs, and then transposition of the left iliac artery to a position that is posterior to the vein. 3'9 Intraluminal
September 1996
disease in the iliac vein is found in 25% of these patients. An alternative to the division of the iliac artery had once been proposed by Trimble, 4 who placed a silicon elastic bridge over the iliac vein to prevent the iliac artery from compressing it; however, this technique is no longer in use (personal communication, January 1996.). If the left iliac vein has been severely damaged or if there is a significant thromboric process, a left femoral vein-to-right femoral vein bypass grafting procedure (Palma procedure) can be performed with the greater saphenous vein from the right leg. An arteriovenous fistula is created in conjunction with the bypass to assist with long-term patency. When a Palma procedure is performed, the arteriovenous fistula is usually ligated 6 weeks after the bypass grafting procedure is performed. After surgery, the patient was given heparin, and later was converted to Coumadin. After surgery, patients should be maintained on anticoagulation medication for a minimum of 6 months. In addition, the patient should be encouraged to continue with leg compressive therapy for life. Long-term resuits for the treatment of iliac vein compression syndrome have been good. O f 80 patients reported by variousauthors, 68 (85%) have had significant improvement) -6'9 It should be noted that these results encompass the several aforementioned surgical approaches. Nonetheless, the basic tenet of each procedure was to remove the constrictive effect of the fight iliac artery, which led to successful outcomes in most patients. No significant long-term complications developed from these operative repairs. Several patients did have subsequent thrombosis of their left iliac venous system. In this group of patients, crossfemoral saphenous vein venous bypass was used to relieve their symptoms. One final method recently used to treat iliac vein compression involves balloon angioplasty of the iliac vein followed by stent placement. n To date, a single patient has been treated in this fashion, with a patent system demonstrated at 6 months. Although this method offers the potential of avoiding operative intervention, its role in the treatment of this syndrome still remains to be defined. CONCLUSION Iliac vein compression syndrome is an unusual cause of left leg venous disease. This anatomic anomaly can cause significant long-term chronic venous insufficiency. The diagnosis requires a high index of suspicion if the lesion is to be treated before chronic problems develop. The current recommended treatment of this lesion requires surgical correction of the compressive phenomenon. Longterm results indicate that the majority of patients can achieve significant relief from their symptoms.
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Akers, Creado, and Hewitt 481
REFERENCES 1. McMurrich JP. The occurrence of congenital adhesionsin the common iliac veins and their relation to thrombosis of the femoral and iliac veins. Am J Med Sci 1908;135:342-6. 2. Cockett FB, Thomas LM. The iliaccompressionsyndrome. Br J Surg 19'65;52:816-25. 3. Taheri SA, WilliamsJ, Powell S, et al. Iliocaval compression syndrome. Am J Surg 1987;154:169-72. 4. Trimble C, Bernstein EF, Pomerantz M, Eiseman g. A prosthetic bridging deviceto relieveiliacvenous compression. Surg Forum 1972;23:249-51. 5. Rigas A, Vomvoyannis A, Tsardakas E. Iliac compression syndrome: report of ten cases. J Cardiovasc Surg (Torino) 1970;11:389-92. 6. Reasbeck PG, Reasbeck JC. Iliac compression syndrome: a myth, a rarity or a condition frequently missed? N Z Med J 1983;96:383-5. 7. AkersDL, Markowitz IM, KersteinMD. Iliacvein bypasswith
8.
9.
10. 11. 12.
autogenous saphenous vein for iliac vein compression syndrome. Am Surg i987;53:675-8. Nexus D, Fletcher EWL, Cockett FB, Thomas ML. Compression and band formation at the mouth of the left common iliac vein. Br J Surg 1968;55:369-74. Lalka SG. Management of chronic obstructive venous disease of the lower extremity. In: Rutherford RB, editor. Vascular surgery. Philadelphia:W. B. Saunders, 1995:1862-82. Nicolaides AN, Zukowski AJ. The value of dynamic venous pressure measurements. World J Surg 1986;10:919-24. Raju S. New approaches to the diagnosis and treatment of venous obstruction. J Vase Surg 1986;4:42-54. Berger A, Jaffe JW, York TN. Iliac compression syndrome treated with stent placement, J Vase Surg 1995;21:510 -4.
Submitted Jan. 31, 1996; accepted June 1, 1996.
Important Notice Effective October 1, 1996, all new manuscript submissions should be sent to the new editorial office (Journal of Vascular Surgery, Editorial Office, Toronto Hospital, Eaton 5-312, Toronto, Ontario, Canada, M5G 2C4) to the attention of K. Wayne Johnston, MD, and Robert B. Rutherford, MD. Manuscripts received before October 1, 1996, and those currently in the process of review will remain the responsibility of Editors Calvin B. Ernst, MD, and James C. Stanley, MD.
New Orleans, La. Iliac vein compression syndrome is a clinical condition that occurs as a result o f compression o f the left iliac vein between the right iliac arte12¢ and the fifth lumbar vertebrae. Patients usually have marked edema o f the left leg. We report a case o f a 16-year-old man who sought medical attention with significant left lower leg edema and four previous episodes o f left leg cellulitis. Evaluation demonstrated venous hypertension as a result o f left iliac vein compression. The patient underwent surgical correction; his symptoms resolved. Details and management o f the case are presented and discussed. A review o f the current literature regarding this condition also is included. (J Vase Surg 1996;24:477-81.
Iliac vein compression s y n d r o m e is a clinical condition that may occur despite a normal orientation between the left iliac vein and the right iliac artery. T h e left iliac vein is usually located posterior to the right iliac artery, b u t in rare situations can be c o m pressed between the iliac artery and the fifth lumbar vertebrae. This anatomic anomaly was first described by M c M u r r i c h in I908.1 I n 1965 C o c k e t t and T h o mas 2 described a series o f patients w h o had iliac vein compression syndrome. S y m p t o m s included left leg edema, pain, varicosities, stasis changes, venous ulceration, and venous claudicarion. I f this condition is n o t recognized, l o n g - t e r m complications including iliofemoral thrombosis may occur and lead to severe l o n g - t e r m disability. A l t h o u g h the diagnosis is rare, the actual incidence is u n k n o w n . This s y n d r o m e m o s t often affects w o m e n in the second to fourth decade o f life, w h o comprised 85% o f the patients in one series) We report an unusual case o f a y o u n g m a n w h o was f o u n d to have iliac vein compression syndrome. This report will describe the evaluation, treatment, and o u t c o m e and will review the literature concerning this anatomic anomaly.
From the Department of Surgery, and the Department of Pediatrics (Dr. Creado), Tulane University School of Medicine. Presented at the Twentieth Annual Meeting of The Southern Association for Vascular Surgery, Naples, Fla., Jan. 24-27, 1996. Reprint requests: Donald Lea Akers, Jr., MD, Department of Surgery; Tulane University School of Medicine, 1430 Tulane Ave., New Orleans, LA 70112. Copyright © i996 by The Society for Vascular Surgery and International Society for CardiovascularSurgery, North American Chapter. 0741-5214/96/$5.00 + 0 24/6/75485
CASE R E P O R T
A 16-year-old man initially had a chief complaint of recurrent episodes ofcellulitis of the left leg and chronic left leg edema. Over the preceding 6 months, he had had four episodes of cellulifis. The edema, which had developed in conjunction with the first episode of cellulitis, improvcd after treatment of the cellulitis but never completely resolved. Moreover, the residual swelling was exacerbated by each subsequent episode. The patient's medical history was unremarkable. On physical examination he was noted to have 2+ pitting edema of the left leg, and thc diameter of the left calfwas 2 cm greater than that of the right. He had equal pulses bilaterally at the femoral, popliteal, dorsalis pedis, and posterior tibial arteries. The left leg was slightly warmer than the right lcg, but was not tender. The remainder of the physical examination was unremarkable. Venous duplex examination suggested chronic vcnous insufficiency with significant reflux of the left leg and no evidence of any acute or chronic deep venous thrombosis. No suggestion of obstruction of venous return was found. A diagnosis of chronic venous insufficiency was made, and compression stockings were prescribed. Three months after his initial visit, the patient returned with an episode of cellulitis, which required hospitalization and the administration of intravenous antibiotics. During this hospital stay, a venogram demonstrated extrinsic compression of the left iliac vein (Fig. 1). With the patient in the supine position, pressures were measured in the venous system, which demonstrated a gradient of 8 cm H20 across this stenosis, A diagnosis ofiliac vein compression syndrome was established. After the resolution of his cellulitis, the patient underwent surgery for correction of the vein compression. Exploration of the retroperitoneum demonstrated the left iliac vein to be significantly compressed by the right iliac artery (Fig. 2). The junction between the inferior vena cava and the left iliac vein was opened to examine the lumen for thc presence of venous webs; however, none were found. 477
478
Akers, Creado, and Hewitt
JOURNAL OF VASCULARSURGERY September 1996
Fig. 1. Inferior vena cava venogram obtained through a left common femoral vein approach demonstrates area of compression of left common iliac vein. Area of compression corresponds to course of right common iliac artery. Numbers represent pressures obtained (in cm H20 ) with patient supine. An 8-cm gradient was present across lesion. Several adhesive bands on the surface of the left iliac vein then were lysed, which resulted in a reduction of the compression. The right iliac artery then was transected and positioned behind the left iliac vein to remove the source of compression (Fig. 3). The patient tolerated the procedure well and was maintained on heparin after surgery until converted to Coumadin. The patient was discharged on the fifth day after surgery. The patient has done well after surgery and had complete resolution of his leg edema when examined 3 months later. He continues to wear compression stocldngs and took Coumadin for 6 months. At 1 year after surgery, he has had no recurrence of his edema or cellulitis.
DISCUSSION The formation o f bands at the m o u t h o f the left c o m m o n iliac vein was first described by McMurrich in 1908.1 In 1965 Cockett and Thomas 2 coined the term "iliac vein compression syndrome" to describe the clinical symptoms associated with this anatomic finding. These authors observed that in their practice venous problems were identified more frequently in the left leg than in the right. They identified a subgroup o f patients who had an isolated area of obstruction at the m o u t h of the left c o m m o n iliac vein that resulted in chronic left leg symptoms. Surgical correction o f the lesion resulted in the resolution of the symptoms o f venous obstruction. Since that initial report, several additional reports have addressed iliac
vein compression syndrome. 3-7 The basic principal in the treatment o f this lesion is to remove the obstructive disease. The anatomic anomaly that results in iliac vein compression syndrome occurs when the left iliac vein is compressed between the right iliac artery and the fifth lumbar vertebra. This anatomic variant results in a decrease in the lumen of the left iliac vein and has been associated with the formation o f venous bands. In an autopsy series, Nexus et al. 8 found bands at the m o u t h o f the left iliac vein in 22% o f dissections; he suggested that this was a normal anatomic variant and was not necessarily related to significant venous disease. This opinion is valid insofar as the true incidence ofiliac vein compression syndrome is rare, with fewer than 100 cases presented in the literature. The develo p m e n t o f deep venous thrombosis and postphlebitic syndrome, however, does have a left side predominance, which suggests that the incidence o f this process may be higher than is currently appreciated) Iliac vein compression syndrome is most often found in w o m e n during their second to the fourth decade o f life. It usually first appears as progressive leg edema with no significant history o f thrombotic problems. 9 The symptoms can range from venous claudication to mild complaints that are consistent with chronic venous insufficiency. Physical examination can demonstrate mild to severe edema, chronic
JOURNAL OF VASCULAR SURGERY
Volume 24, Number 3
Akers, Creado, and Hewitt 479
Fig. 2. Initial operative exposure of bifurcation of aorta and inferior vena cava. Right common iliac artery can be seen in its course across left iliac vein, and corresponding compression of vein is noted.
Fig. 3. Rightcommoniliacarteryhasnowbeentransposedbehindleftiliacvein. Note complete resolution of compression of vein. leg skin changes, development ofvaricosities, significant venous collateral vessels, and ulceration. The initial assessment should begin with a noninvasive evaluation, usually a duplex examination. In the
absence of deep venous thrombosis, however, the findings are usually nonspecific. Results o f impedance plethysmography are often normal in the early stages o f the disease and are likewise usually o f little benefit.
JOURNAL OF VASCULARSURGERY
480
Akers, Creado, and Hewitt
Taheri et al.,3 however, found that exercise venous plethysmography does have a high diagnostic success rate. Direct venous pressure measurements also may provide important information about possible outflow obstruction. Nicolaides and Zukowsld 1° demonstrated a relationship between increased ambulatory pressure and venous ulceration. Arm-foot pressure differentials have been used by Raju 11 to determine the significance of possible outflow obstruction. He found that a gradient of greater than 4 mm H g was strongly suggestive of significant disease. Recently, computed tomographic scans have been suggested as a test that may provide useful information when extrinsic compression is the cause of the obstruction. The role of this method, however, in the primary evaluation of the patient who has iliac vein compression is still unclear. 12 Venography remains the goldstandard diagnostic test because it will demonstrate an area of compression where the right iliac artery crosses the left iliac vein (Fig. 1). Venous collateral vessels from the left iliac system to the right iliac system often can be identified. Obtaining transvenous pressure measurements is essential in confirming the diagnosis. Nexus et al. s and Cockett et al.2 stated that a significant gradient exists when the pressure differential is greater than 2 mm Hg. Rigas 5 states that a resting supine gradient of 2 cm H20 is considered clinically significant. In symptomatic patients who have a significant gradient, an operative approach should be offered. Although the management of chronic venous insufficiency begins with conservative treatment with compressive therapy, a more aggressive surgical approach is recommended in patients who have iliac vein compression syndrome. Taheri et al. 3 argue that progressive symptoms will continue to develop in these patients, so the anatomic anomaly should be corrected as soon as it is identified. Other authors agree that the lesion should be addressed as soon as it is identified because the disease process is progressive in nature. 4,5,9 Several surgical approaches have been used to treat this condition. In those patients who have an isolated defect at the mouth of the left common iliac vein, direct surgical repair is advocated.3 Early operative approaches focused on removing the external compression. 2,s If no evidence of any intraluminal webs or bands is found and the iliac vein achieves normal diameter after the release of the bands, this approach may be adequate. Ifintraluminal webs or bands are present or cannot be ruled out by the preoperative evaluation, the operative repair includes open exploration of the inferior vena cava and the left iliac vein, resection of existing bands or webs, and then transposition of the left iliac artery to a position that is posterior to the vein. 3'9 Intraluminal
September 1996
disease in the iliac vein is found in 25% of these patients. An alternative to the division of the iliac artery had once been proposed by Trimble, 4 who placed a silicon elastic bridge over the iliac vein to prevent the iliac artery from compressing it; however, this technique is no longer in use (personal communication, January 1996.). If the left iliac vein has been severely damaged or if there is a significant thromboric process, a left femoral vein-to-right femoral vein bypass grafting procedure (Palma procedure) can be performed with the greater saphenous vein from the right leg. An arteriovenous fistula is created in conjunction with the bypass to assist with long-term patency. When a Palma procedure is performed, the arteriovenous fistula is usually ligated 6 weeks after the bypass grafting procedure is performed. After surgery, the patient was given heparin, and later was converted to Coumadin. After surgery, patients should be maintained on anticoagulation medication for a minimum of 6 months. In addition, the patient should be encouraged to continue with leg compressive therapy for life. Long-term resuits for the treatment of iliac vein compression syndrome have been good. O f 80 patients reported by variousauthors, 68 (85%) have had significant improvement) -6'9 It should be noted that these results encompass the several aforementioned surgical approaches. Nonetheless, the basic tenet of each procedure was to remove the constrictive effect of the fight iliac artery, which led to successful outcomes in most patients. No significant long-term complications developed from these operative repairs. Several patients did have subsequent thrombosis of their left iliac venous system. In this group of patients, crossfemoral saphenous vein venous bypass was used to relieve their symptoms. One final method recently used to treat iliac vein compression involves balloon angioplasty of the iliac vein followed by stent placement. n To date, a single patient has been treated in this fashion, with a patent system demonstrated at 6 months. Although this method offers the potential of avoiding operative intervention, its role in the treatment of this syndrome still remains to be defined. CONCLUSION Iliac vein compression syndrome is an unusual cause of left leg venous disease. This anatomic anomaly can cause significant long-term chronic venous insufficiency. The diagnosis requires a high index of suspicion if the lesion is to be treated before chronic problems develop. The current recommended treatment of this lesion requires surgical correction of the compressive phenomenon. Longterm results indicate that the majority of patients can achieve significant relief from their symptoms.
JOURNALOF VASCULARSURGERY Volume 24, Number 3
Akers, Creado, and Hewitt 481
REFERENCES 1. McMurrich JP. The occurrence of congenital adhesionsin the common iliac veins and their relation to thrombosis of the femoral and iliac veins. Am J Med Sci 1908;135:342-6. 2. Cockett FB, Thomas LM. The iliaccompressionsyndrome. Br J Surg 19'65;52:816-25. 3. Taheri SA, WilliamsJ, Powell S, et al. Iliocaval compression syndrome. Am J Surg 1987;154:169-72. 4. Trimble C, Bernstein EF, Pomerantz M, Eiseman g. A prosthetic bridging deviceto relieveiliacvenous compression. Surg Forum 1972;23:249-51. 5. Rigas A, Vomvoyannis A, Tsardakas E. Iliac compression syndrome: report of ten cases. J Cardiovasc Surg (Torino) 1970;11:389-92. 6. Reasbeck PG, Reasbeck JC. Iliac compression syndrome: a myth, a rarity or a condition frequently missed? N Z Med J 1983;96:383-5. 7. AkersDL, Markowitz IM, KersteinMD. Iliacvein bypasswith
8.
9.
10. 11. 12.
autogenous saphenous vein for iliac vein compression syndrome. Am Surg i987;53:675-8. Nexus D, Fletcher EWL, Cockett FB, Thomas ML. Compression and band formation at the mouth of the left common iliac vein. Br J Surg 1968;55:369-74. Lalka SG. Management of chronic obstructive venous disease of the lower extremity. In: Rutherford RB, editor. Vascular surgery. Philadelphia:W. B. Saunders, 1995:1862-82. Nicolaides AN, Zukowski AJ. The value of dynamic venous pressure measurements. World J Surg 1986;10:919-24. Raju S. New approaches to the diagnosis and treatment of venous obstruction. J Vase Surg 1986;4:42-54. Berger A, Jaffe JW, York TN. Iliac compression syndrome treated with stent placement, J Vase Surg 1995;21:510 -4.
Submitted Jan. 31, 1996; accepted June 1, 1996.
Important Notice Effective October 1, 1996, all new manuscript submissions should be sent to the new editorial office (Journal of Vascular Surgery, Editorial Office, Toronto Hospital, Eaton 5-312, Toronto, Ontario, Canada, M5G 2C4) to the attention of K. Wayne Johnston, MD, and Robert B. Rutherford, MD. Manuscripts received before October 1, 1996, and those currently in the process of review will remain the responsibility of Editors Calvin B. Ernst, MD, and James C. Stanley, MD.