Decreased incidence of left common iliac vein compression in patients with abdominal aortic aneurysms
Article Outline
Objective
Compression of the left common iliac vein (LCIV) by the right common iliac artery is an anatomic variant that may increase the risk for LCIV thrombosis. The incidence of LCIV compression in patients with abdominal aortic aneurysms (AAA) is unknown, however. The aim of this descriptive anatomic study was to determine (1) the incidence of LCIV compression in patients with and without AAA and (2) if endovascular AAA repair acutely alters the incidence of LCIV compression and, hence, the risk of LCIV thrombosis.
Method
A retrospective analysis of medical records and helical computed tomography (CT) scans was conducted in 100 AAA patients and 100 non-AAA patients (n = 200). Medical records were reviewed for symptoms and risk factors for deep vein thrombosis, and data were reported according to the Joint Society Reporting Standards for acute lower-extremity venous thrombosis. The minor diameters of the aorta, inferior vena cava, and common iliac arteries and veins were measured. For AAA patients, measurements were obtained from preoperative and 30-day postoperative CT scans.
Results
The mean age of the study cohort was 38 years (range, 17 to 85 years) for non-AAA subjects and 73 years (range, 51 to 89 years) for AAA subjects. The mean acute lower-extremity venous thrombosis risk factor score was low for both patient groups (non-AAA, 0.82 ± 0.12; AAA, 2.63 ± 0.14). Mean compression of the LCIV was 37.8% (range, 0% to 74.8%) for non-AAA patients but only 27.3% (range, 0% to 74.2%; P < .0006) for AAA patients. Of non-AAA patients with venous compression, the right common iliac artery was the compressing structure in 87% of cases. However, of AAA patients with venous compression, the left common iliac artery was the compressing structure in 76% of cases. There was no statistically significant change in the degree of compression of the LCIV before and after endovascular repair (27.3% vs 25.1%, respectively) nor was there a change in the structure that compressed the LCIV.
Conclusion
Patients with AAA were found to have more tortuous iliac arteries that led to less anatomic compression of the LCIV compared with nonaneurysmal patients. Furthermore, the left common iliac artery was found to compress the LCIV in most of the AAA patients, and the right iliac artery was found to compress the LCIV in most non-AAA patients. Endovascular AAA repair did not acutely alter these anatomic findings. Patients with AAA may therefore be at lower risk of developing LCIV thrombosis owing to the nature of their anatomy.
Compression of the left common iliac vein (LCIV) between the overlying right common iliac artery and the lumbar vertebrae is an anatomic variant commonly known as May-Thurner syndrome, or Cockett syndrome in Europe. The presence of this anatomic variant has classically been associated with an increased risk of developing left iliofemoral deep vein thrombosis (DVT).1, 2 In support of this, Virchow3 reported in 1851 that pelvic vein thrombosis was five times as likely to occur on the left side as on the right side, suggesting that this observation was due to compression of the overlying artery.
Nearly a century later, in 1943, Ehrich and Krumbhaar4 found obstructive lesions at the mouth of the LCIV in 24% of cadavers. In addition, May and Thurner,1 who became widely known for their findings, reported that 22% of 430 cadavers had compression of the LCIV by the right common iliac artery against the fifth lumbar vertebra. They believed that this venous compression and the associated chronic pulsations of the right common iliac artery induced endothelial irritation that resulted in “spur” formation in the thin-walled LCIV.
Although LCIV compression is thought to be associated with chronic left lower-extremity edema or left iliofemoral DVT, or both, as imaging technology has become more sophisticated and widespread in the last decade, additional information on the true incidence of this anatomic variant is beginning to change the way we view the presence of this anatomy. In a 2004 study measuring compression of the LCIV in an asymptomatic patient population, we reported that 24% of patients had >50% LCIV compression, and 66% of patients had >25% LCIV compression.5 It is therefore possible that this anatomic variant is more common than previously appreciated, even in asymptomatic patients, and may represent an anatomic variant that is not necessarily associated with pathology.
Patients with abdominal aortic aneurysms (AAA) represent a unique patient population with respect to the presence of this anatomic variant given their significant arterial pathology. It is unknown, however, if asymptomatic patients with AAA present with similar anatomic findings of LCIV compression. In addition, the incidence of LCIV compression and DVT in patients after endovascular AAA repair has not been well studied. Therefore, the aims of this descriptive anatomic study were to determine the incidence of LCIV compression in asymptomatic patients with AAA compared with patients without AAA and determine if endovascular repair of AAA acutely alters the incidence and degree of LCIV compression, and hence, the risk of left lower-extremity DVT following surgery.
Methods
The medical records and helical abdominal computed tomography (CT) scans of 100 patients evaluated in the emergency department for abdominal pain between November 1999 and April 2000 and of 100 patients who underwent endovascular AAA repair between April 2000 and December 2004 were analyzed retrospectively. The selection of patients in each group was consecutive, with the exception that CT scans obtained without contrast and CT scans of poor quality owing to motion artifact were excluded. This study was completed according to the guidelines set forth and approved by the Institutional Review Board (# 0339-014) of the Northwestern University Feinberg School of Medicine.
Medical records were reviewed for demographic data including gender, age, hypertension, congestive heart failure, cerebral vascular disease, diabetes mellitus, smoking status, and anticoagulant medications. Risk factors for DVT were also collected and reported according to the Joint Society Reporting Standards for acute lower-extremity venous thrombosis.6 These risk factors included a history of DVT, immobilization, postoperative state, age, malignancy, type of malignancy, New York Heart Association (NYHA) classification of cardiac disease, limb trauma, hypercoagulable disorder, hormone therapy, pregnancy, postpartum state, and obesity. A mean acute lower-extremity venous thrombosis risk factor score was calculated for patients with and without AAA from a maximum possible score of 28.
Owing to the retrospective nature of this study, data were obtained for the acute lower-extremity venous thrombosis risk factor score in 99 of 100 patients with AAA, except in the NYHA cardiac disease category, for which data was obtained from 81 of 100 patients. In patients without AAA, data was obtained for the acute lower-extremity venous thrombosis risk factor scores in 90 of 100 patients, except in the obesity category, for which data were obtained from 54 of 100 patients.
A Lightspeed QXI CT scanner (GE, Milwaukee, Wisc) with a spatial resolution of 0.584 mm was used in all cases. Images were taken in the supine position during maximum inspiration and scanning parameters included 1-mm to 2-mm axial images in AAA patients and 5-mm images in non-AAA patients. Images were obtained with a rotation speed of 0.8 seconds and table speed of 7.5 to 15 mm/s. A single 125 mL to 150 mL bolus of nonionic contrast material was injected with a power injector through an arm vein at 2 to 4 mL/s.
CT scan measurements were made with GE PACS Centricity Workstations with digitally enlarged images and digitally calibrated measurement tools. Measurements of the minor diameter at the area of maximum size of the aorta, inferior vena cava, and common iliac arteries and veins were made for the segment of vessel most in the plane of the image (center line of flow). Measurements of the LCIV were made at the site of crossing of the compressing structure (right or left common iliac artery) and distal (caudal) to it. The percent compression of the LCIV was determined by dividing the diameter of the LCIV at the point of maximal compression by the diameter of the uncompressed distal (caudal) LCIV. The same researcher obtained all measurements to avoid inter-interpreter variance. This method of measurement was validated in our prior publication comparing this method with area measurements.5
Endovascular AAA repair was performed at Northwestern Memorial Hospital by one of four different operating surgeons (J. S. M., M. D. M., M. K. E., M. R. K.). The operating surgeon determined the device type to be used after assessment of anatomic measurements from CT scans obtained with intravenous contrast. Endovascular graft sizes were determined according to standard anatomic guidelines from the corresponding companies. Endovascular grafts included the Excluder (W. L. Gore & Assoc, Flagstaff, Ariz), AneuRx (Medtronic, Santa Rosa, Calif), and Zenith (Cook, Bloomington, Ind). Anatomic measurements were obtained from preoperative and 30-day postoperative CT scans to assess the effect of the endovascular device on acute anatomic changes.
Results are expressed as mean ± standard error of the mean. Differences between two groups were analyzed with the Student t test or the Mann-Whitney rank sum test. Correlations between pairs of variables were analyzed using the Spearman rank order correlation test. All statistical analyses were performed with SigmaStat (SPSS, Chicago, Ill). Statistical significance was assumed at P < .05.
Results
The mean age of patients with AAA was 73 years (85% men, 15% women) and that of patients without AAA was 38 years (38% men, 62% women) (Table I). Three patients with AAA had a history of proven venous thrombosis. No patients without AAA had a history of acute lower-extremity venous thrombosis or pulmonary embolism, but one patient did have a history of thrombosis of the portal vein. No patient in either group had a history of a thrombophilic disorder. The mean acute lower-extremity venous thrombosis risk factor scores for patients with and without AAA were 2.63 ± 0.14 (range, 0 to 6) and 0.82 ± 0.12 (range, 1 to 8), respectively, from a maximum possible score of 28. These low scores provided additional support that the patients included in this study were truly asymptomatic.
Table I. Patient demographics
| Patients without AAA (%) | Patients with AAA (%) | |
|---|---|---|
| Gender | ||
| Men | 38 (38) | 85(85) |
| Women | 62(62) | 15(15) |
| Age | 38±1.4(17-85) | 71±0.8(51-89) |
| Hypertension | 22 | 78 |
| Coronary artery disease | 1 | 54 |
| Congestive heart failure | 2 | 8 |
| Cerebrovascular disease | 1 | 17 |
| Diabetes mellitus | 5 | 16 |
| Current smoker | 15 | 21 |
| Previous smoker | 6 | 53 |
| Aspirin | 5 | 77 |
| Warfarin | 0 | 11 |
| Clopidogrel | 0 | 9 |
Table II summarizes the results of the CT scan analysis in each patient group. No significant difference was noted in size between the right and left common iliac arteries in patients with AAA before and after repair and in patients without AAA. No significant difference was found between the right common iliac vein and the uncompressed left common iliac vein caudal to the area of compression in patients with AAA before and after repair and in patients without AAA.
Table II. Computed tomography scan measurements
| Patients without AAA | Patients with AAA | ||
|---|---|---|---|
| Preoperative | Postoperative | ||
| Aortic diameter (cm) | |||
| Minor axis | 1.6±0.3⁎ | 5.3±0.1 | 5.3±0.1 |
| Minor axis, range | 1.1-2.2 | 2.7-11.0 | 2.5-10.8 |
| IVC (mm) | 16.3±0.4 | 17.5±0.3 | 18.0±0.3 |
| RCIA (mm) | 9.1±0.2⁎ | 14.9±0.4 | 15.8±0.4 |
| LCIA (mm) | 9.1±0.2⁎ | 14.3±0.3 | 15.4±0.3 |
| RCIV (mm) | 12.7±0.3⁎ | 14.0±0.2 | 14.1±0.2 |
| LCIV (mm) | 12.1±0.3⁎ | 13.7±0.3 | 13.6±0.3 |
| Aortic bifurcation to lumbar vertebra distance (mm) | 3.27±0.2† | 9.33±0.5 | 8.97±0.5 |
| Overall mean compression (%) | 37.8±1.7‡ | 27.4±1.9 | 25.1±1.8 |
| Range of mean compression (%) | 0.0-74.8 | 0.0-72.4 | 0.0-66.9 |
⁎ P < .001 vs AAA pre-op and AAA post-op. |
† P < .001 vs AAA pre-op and AAA post-op. |
‡ P < .0006 vs AAA pre-op and P < .0000005 post-op. |
Mean compression of the LCIV in non-AAA patients was 37.8% ± 1.7% (range, 0% to 74.8%; median, 39.6%) (Fig 1, Fig 2, A). However, mean venous compression of the LCIV for AAA patients preoperatively was only 27.3% ± 1.9% (range, 0% to 74.2%; median, 25.4%; P < .0006 vs non-AAA) (Fig 1, Fig 2, A). There was no statistically significant change in the degree of compression of the LCIV before and after endovascular repair (27.3% vs 25.1%, respectively). It should be noted that in all cases of postoperative LCIV compression, the endovascular stent-graft extended distal to the location of LCIV compression. Further analysis of the degree of LCIV compression in patients without AAA demonstrated that 25% of patients had >50% compression (Table III). In patients with AAA, however, only 10% had >50% compression. CT scans of AAA patients after endovascular repair revealed a similar pattern.
Fig 1.
A, Individual results of percent mean compression of the left common iliac vein in patients without abdominal aortic aneurysms (AAA). B, Results of those with AAAs.
Fig 2.
A, Mean percentage of compression of the left common iliac vein in patients without abdominal aortic aneurysms (AAA) and in patients with AAA before and after endovascular AAA repair, B, Structure most often compressing the left common iliac vein in patients with and without AAA.
Table III. Compression data
| Patients with AAA | |||
|---|---|---|---|
| Patients without AAA n (%) | Preoperative n (%) | Postoperative n (%) | |
| No compression | 3(3) | 12(12) | 14(14) |
| Overall mean compression | |||
| >25% | 73(73) | 52(52) | 50(50) |
| >50% | 25(25) | 10(10) | 7(7) |
| >60% | 9(9) | 6(6) | 2(2) |
| >70% | 3(3) | 1(1) | 0 |
No significant correlation was found between the mean acute lower-extremity venous thrombosis risk factor score and degree of LCIV compression for patients with or without AAA (AAA, P = .908; non-AAA, P = .360), and there was no correlation between the size of the right or left common iliac arteries and degree of LCIV compression. Furthermore, there was no significant correlation between the degree of LCIV compression and sex of the patient, and only a very weak correlation between degree of compression and age of the patient for both patient groups (AAA r = 0.197, P = .0498; non-AAA r = –0.252, P = .0114).
Interestingly, the structure most often compressing the LCIV against the vertebral body was markedly different in patients with and without AAA (Fig 2, B). In AAA patients with LCIV compression, the left common iliac artery was the compressing structure in 76% of cases (Fig 3, A), and in non-AAA patients with LCIV compression, the right common iliac artery was the compressing structure in 87% of cases (Fig 3, B). There was no change in the structure that compressed the LCIV after endovascular repair. In an attempt to identify a variable that could predict the degree of LCIV compression or the artery performing the compression, the distance between the aortic bifurcation and lumbar vertebra was measured for all patients (Table II). However, no correlation was found to exist between this measurement and the degree of LCIV compression or the structure performing the compression.
Fig 3.
A, Axial computed tomography (CT) image in a patient with an abdominal aortic aneurysm (AAA) illustrates compression of the left common iliac vein (LCIV) by the left common iliac artery. B, CT image in a patient without an AAA illustrates compression of the LCIV by the right common iliac artery. Black arrow, left common iliac vein.
Acute DVT developed ≤10 days after surgery in three patients who underwent endovascular AAA repair. Left and right iliofemoral vein DVT were detected in two patients each, and a left posterior tibial DVT was detected in one patient. An additional patient developed a left gastrocnemius vein thrombus 4 years after endovascular repair. No patients without AAA developed DVT.
Discussion
May-Thurner syndrome, also known as iliac vein compression syndrome or Cockett syndrome, is a well-known anatomic variant characterized by compression of the LCIV by the overlying right common iliac artery. In 1908, McMurrich7 examined 107 cadavers and described adhesions in the LCIV in 32%, which he speculated were congenital in origin. May and Thurner1 conducted an autopsy series of 430 cadavers in 1957 and described a “spur-like formation” in the LCIV of 22% of cases. As a result of histologic examination and because no spurs were found in the fetuses examined, the spurs were thought to develop during the patient’s lifetime. It was postulated that the mechanical compression of the LCIV by the pulsatile right common iliac artery induced endothelial irritation, resulting in proliferation of the LCIV wall and the development of a spur composed of fibrous tissue.1 The authors theorized that the presence of a spur altered the flow of blood and caused venous stasis, thereby increasing the likelihood of DVT in the left lower extremity.
Patients with DVT caused by May-Thurner syndrome typically present with persistent left leg edema, and some patients have signs of venous hypertension. Symptoms typically appear in women aged 20 to 40 years and are precipitated by pregnancy or prolonged immobilization. In a 2002 study using magnetic resonance imaging, Wolpert et al8 reported LCIV compression in 37% of patients with left lower-extremity edema. In 2004, Chung et al9 reported LCIV compression by the right common iliac artery in 61% of patients with left-sided DVT.9 The progression of symptoms in May-Thurner syndrome was described by Kim et al10 as a sequence of three stages: stage I, asymptomatic iliac vein compression; stage II, formation of a venous spur; and stage III, development of LCIV DVT.10
The incidence of LCIV compression has also been studied in an asymptomatic population. We conducted a retrospective study of asymptomatic patients with normal arterial anatomy and reported5 that nearly one quarter of all patients had >50% compression. These findings were consistent with autopsy studies of the early 20th century that found LCIV compression in 22% to 32% of cases.1, 4, 7 These findings suggest that iliac vein compression is a common anatomic variant that may not necessarily be associated with chronic left-lower extremity venous congestion or iliofemoral DVT. Rather, this anatomic variant combined with other risk factors for venous thrombosis, such as immobility, trauma, and cancer, may place the patient at an increased risk of developing venous thrombosis.
Little is known, however, about the incidence and degree of LCIV compression in asymptomatic patients with AAA, a patient population more prone to tortuous and enlarged or aneurysmal iliac arteries. It is also unknown whether endovascular AAA repair alters the degree of LCIV compression, and to our knowledge, no other study has examined this. Our data revealed that patients with AAA had statistically significant decreased mean compression of the LCIV compared with patients without aneurysmal disease, and endovascular repair of AAA did not alter the degree of compression after 30 days. The decreased incidence of LCIV compression in patients with AAA may be due to the presence of arterial pathology causing the arteries to become tortuous and less likely to trap the inferior vena cava bifurcation and common iliac veins against the vertebral column. Furthermore, aneurysmal dilatation may displace the normal position of the inferior vena cava and common iliac veins. Surprisingly, we also found that the compressing structure markedly differed in the two patient populations. Again, the anatomic differences because of the arterial pathology of AAA patients may be causing this significant difference.
The incidence of DVT in patients with AAA after endovascular repair has not been extensively studied. We observed thrombotic events in 4% of patients after endovascular AAA repair. This is consistent with Eagleton et al,11 who reported a 6% incidence of DVT after endovascular AAA repair.11 In our study, the development of thrombotic events was not related to the degree of LCIV compression nor did the endografts change the degree of compression at 30 days postoperatively. It is possible that the thrombotic events developed secondary to manual compression of the common femoral artery after endovascular therapy. Although our study showed that endovascular AAA repair did not appear to alter the risk of acute DVT due to LCIV compression, it should be noted that this is a retrospective analysis, and detection of postoperative thrombotic events were made by clinical findings. Interpretation of this data, therefore, should be made with caution.
CT scans were used in this study to determine the degree of LCIV compression. This method of measurement was validated by our prior study using multiplanar line of flow reconstructions and by several other studies.5, 9, 12 Chung et al9 reported that spiral CT angiography can be used to evaluate LCIV stenosis or obstruction by structures, including the common iliac arteries, in patients presenting with acute DVT.9 In a comparison of the incidence of LCIV compression in symptomatic patients as visualized by CT venography and by contrast venography, Oguzkurt et al12 also reported that CT venography can be used to demonstrate LCIV compression.12
Our study has some limitations. First, this was a retrospective study and thus subject to the inherent problems associated with retrospective analyses. Second, the sample size was small (n = 200). A larger sample size would have revealed more conclusive data on the risk of DVT formation. Third, venous-phase CT scans were not available in all cases, and in these patients, measurements were obtained on arterial phase. Finally, because this is a retrospective study, it was not possible to control for the hydration status of patients. This could overestimate the degree of compression of the LCIV in a dehydrated patient; however, we would expect all segments of the vein (proximal and distal) to decrease to a similar degree, thereby only minimally if at all affecting the percentage of compression.
Conclusion
Our study demonstrates that compression of the LCIV is more common than previously expected in patients with and without AAA, but patients with AAA have less compression of the LCIV compared with patients without AAA. Furthermore, the structure compressing the LCIV is markedly different in these patient populations. Because of the high incidence of compression in these asymptomatic patient populations and the low incidence of DVT in the general population13 and in the AAA population,11 the mere presence of compression may not increase the likelihood of DVT without the presence of other risk factors such as thrombophilic disorders, endothelial injury, and stasis. Therefore, on the basis of our findings, some degree of compression of the LCIV is a normal anatomic variant whose presence alone does not place a patient at increased risk for DVT.
Author contributions
We would like to thank Wendy Meadows and Mary Evans for their assistance with chart review.
References
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- . Computed tomography findings in 10 cases of iliac vein compression (May-Thurner) syndrome . Eur J Radiol . 2005;55:421–425
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This study was supported by the Northwestern University Medical Student Summer Research Program (NCM).Competition of interest: none.
PII: S0741-5214(06)00998-0
doi:10.1016/j.jvs.2006.05.046
© 2006 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
