Iliocaval Venous Compression Due to Aneurysm of the Abdominal Aorta: Report of Ten Cases J. Combe, MD, J. Besancenot, MD, P. Milteret, MD, G. Camelot, MD, Besanqon, France
Ten patients with symptomatic venous compression secondary to aneurysm of the infrarenal abdominal aorta are reported. Compression was responsible for edema of the lower extremities in seven cases, and, in three instances, for venous thromboembolic disease. The incidence of venous complications secondary to aneurysm (8.8% in our series) is close to that of urologic complications (10%), but their respective pathogeneses are different. Mechanical compression (nine patients) was the predominant mechanism and was due to retroperitoneal hematoma (two patients) and left-sided (three patients) or right-sided (four patients) development of the aneurysm. Noninvasive imaging, including computed tomographic scan and sonography, have replaced the more conventional invasive methods of diagnosis. The large diameter of the aneurysms generally found in these cases mandates rapid surgical treatment in order to avoid rupture and aortocaval fistula. Because of venous collateral circulation, caution must be exercised when working o n the left side of the aorta above the aneurysm and at the level of the lilac vessels. Treatment consists of the inclusion prosthetic replacement. The insertion of a Greenfield filter is needed only when pulmonary embolism occurs or in the case of recent or life-threatening caval thrombosis. (Ann Vasc Surg 1990;4:20-25) KEY WORDS: Abdominal aorta; aneurysms; inferior vena cava; thromboembolic venous disease; retroperitoneal fibrosis.
venous compression which form the basis of this report.
Rupture into the inferior vena cava is the most widely recognized venous complication of abdominal aortic aneurysm [1,2]. Other types of complications involving the venous system are less common. In the last ten years we have encountered I0 cases of aneurysm of the abdominal aorta complicated by
P A T I E N T S AND M E T H O D S Between 1978 and 1987, 112 aneurysms of the infrarenal abdominal aorta were seen in the Vascular Surgery Unit of the University Hospital in Besanqon, France. Ten patients (eight men and two women) had a symptomatic venous complication. Ages of the patients ranged from 61 to 86 years, the mean being 74.1 years. Seven patients had associated coronary artery disease, and five of these patients had a past history of myocardial infarction.
From the Service de Chirurgie Vasculah'e, H~pital Jean Mingoz, Besanqon, l~)'ance. Presented at the Annual Meeting of the Socidtd de Chirurgie Vasculaire de Langue Franqaise, May 20-21, 1988, La Grande Motte, France. Reprint requests: J. Combe, MD, Service de Chirurgie Vasculaire, HOpital Jean Mingoz, Boulevard Fleming, 25000 Besanqon, France,
20
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ILIOCAVAL VENOUS C O M P R E S S I O N
21
Three patients had hemodynamically significant carotid artery lesions, two o f which had required surgical treatment. Five patients had peripheral arterial disease. Clinical findings
An aneurysm was palpable in seven instances. More than one aneurysm was found in four patients; two had aneurysms of the thoracic aorta and two had multiple aneurysms. T w o aneurysms ruptured retroperitoneally. In one other case acute thrombosis o f the aneurysm occurred. In two cases the patient had recurrent pulmonary embolism associated with iliofemoral venous thrombosis; in one case the patient had phlebitis in his left leg and in seven cases the patients had edema without venous obstruction. Of these patients, edema was noted in the lower leg in three, and in the thigh and lower leg in four. Edema was located on the left side in five cases and the right side in two cases. In one case edema involved the pelvis with associated perineal, hemorrhoidal, and parietal varices secondary to portacaval and cavocaval collaterality. Venous signs led to the discovery o f the aortic aneurysm in six cases. Complementary investigations
Iliocavograms, sonograms, and computed tomographic (CT) scans were obtained in six patients. They contributed to the understanding of the mechanism of venous compression. The left lilac vein was involved in six cases: in two instances the obstruction was complete, and in four instances the vein showed extrinsic compression and was horizontalized. In all instances backflow occurred through the left internal iliac vein, attesting to venous stasis. The inferior vena cava was involved in five cases: in one case obstruction was complete while in four cases a smooth encroachment was noted on the left border (Figs. 1,2). Lateral views of cavograms showed that the compression also involved the anterior aspect o f the infrarenal aorta because o f the right-sided development of the aneurysm (Figs. 3,4). In three cases there were multiple sites of compression of the venous system: in two instances, the compression involved the lilac veins. In one patient with multiple aneurysms multiple compression sites included the left lilac, left femoral (Fig. 5) and popliteal veins. Collateral venous pathways through the internal iliac, iliolumbar, and azygorenal veins were demonstrated by phlebocavograms. Lateral spinal collateral pathways were usually more developed on the left except in one case of thrombosis of the vena cava (Fig. 6).
Fig. 1. Cavogram, anteroposterior view, showing compression of vena cava and of left common lilac vein by a large infrarenal aneurysm developing anteriorly and on left.
Factors predisposing to venous complications included: diameter of the aneurysm superior to 6 cm in nine cases; right-sided development of the aneurysm in four cases; associated lilac artery a n e u r y s m venous compression in three cases; retroperitoneal
Fig. 2. Cavogram, anteroposterior view, showing concentric compression of infrarenal vena cave due to aortic aneurysm developing to the right.
22
ILIOCA VAL VENOUS C O M P R E S S I O N
ANNALS OF VASCULAR SURGERY
Fig. 3. Cavogram, lateral view, showing anterior compression of infrarenai vena cava by aortic aneurysm developing on right (same patient as in Figure 2).
Fig. 5. Sonogram, longitudinal plane, showing associated femoral artery aneurysm responsible for compression of femoral vein.
Fig. 4. Aortogram showing aneurysm of infrarenal aorta developing on right (same patient as in Figure 2).
Fig. 6. Iliocavogram showing thrombosis of inferior vena cava with collateral circulation developed on right.
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ILIOCA VAL V E N O U S C O M P R E S S I O N
44 months. At the time of this writing seven patients are alive and have no arterial symptoms; edema has regressed completely in five instances and partially in two. One patient has residual edema due to extended iliocaval thrombosis.
DISCUSSION
Fig. 7. Computed tomography showing inflammatory aneurysm wroth perianeurysmal fibrosis affecting inferior vena cava and left ureterohydronephrosis.
hematoma in two cases; and major retroperitoneal fibrosis (Fig. 7) in one case. There were two instances of associated ureteral complications: compression of the ureter by a common iliac artery aneurysm and ureteral stenosis secondary to retroperitoneal fibrosis. Treatment Six patients were treated by heparin followed by oral anticoagulant therapy, and two patients underwent partial interruption of the inferior vena cava because of repeated pulmonary embolization, one by a Mobin Uddin device, the other by Greenfield filter. Nine patients had operations. In seven patients, the aneurysms were incised and a graft was inserted. Five patients had an aortoiliac bifurcation graft while an aortoaortic tube graft and an aortofemoral bifurcation graft were inserted in one case each. Two patients were treated by exclusion of their aneurysm associated with an axillary bifemoral bypass.
RESULTS One patient, operated on for retroperitoneal rupture, died in the immediate postoperative period of myocardial infarction. Two patients died 18 months after operation, one of congestive heart failure with pulmonary edema, the other of rupture of an aneurysm of the abdominal aorta. One patient had occlusion of the left limb of his aortoiliac bifurcation graft and was treated by a femorofemoral crossover bypass. Follow-up ranged from three to
Although rarely mentioned, venous complications of aneurysms of the abdominal aorta are not uncommon. In our experience, they represent slightly less than 9% of all aortic aneurysms. This incidence is approximately that of urologic complications, which are more widely recognized [3]. In 1951 Herschowitz, cited by Snider [4], reported the case of inferior vena caval compression by aortic aneurysm in a 70-year-old man with lower limb edema who died when his aneurysm ruptured into the duodenum. In 1962 Natali and Stuhl published two cases of caval compression due to aneurysm [5]. One of these patients presented with hemorrhagic varices of the lower limbs and the perineum. Mechanical compressions, either related to the size or the location of the aneurysm, were predominant in our series. They were seen in the case of aneurysms of greater than 6 cm or those developing to the right (Figs. 2-4). This particular form of aneurysm predisposes to aortocaval or aortoduodenal fistulas and to initial caval compression syndromes [6-9]. In most cases aneurysmal compression involves the left common iliac vein and the origin and the left border of the vena cava (Fig. I). In aneurysms developing to the right, anteroposterior cavograms show regular narrowing while the lateral cavograms show anterior compression of the infrarenal vena cava. Noninvasive investigations, including sonography (Fig. 8) and CT scan, are usually remarkably demonstrative of these aspects [10,1 I]. Multiple level compressions can be found when the aortic aneurysm is associated with iliac artery aneurysm. Often the compression due to the iliac aneurysm is greater than that of the aortic aneurysm. Associated ureteral compression can be responsible for initial renal insufficiency with oligoanuria of mechanical origin [12]. Mechanical compression by retroperitoneal hematoma is not uncommon. Snider [4] and Gertner [13] reported cases of chronic rupture which progressed for two to four weeks. Retroperitoneal fibrosis, often an extension of perianeurysmal inflammation [14], can also be responsible for venous compression. The aneurysm is not always palpable or demonstrable by CT scan [15]. Retroperitoneal fibrosis often involves both the venous and urinary tract systems, which explains the frequency of associated urologic manifestations [3,7,12]. Infection has also been suggested as a possible cause of
24
ILIOCA VAL VENOUS COMPRESSION
Fig. 8. Sonogram, longitudinal view, showing large infrarenal aneurysm associated with parietal thrombosis and extrinsic compression of vena cava and thrombosis of left common lilac vein.
venous thrombosis, for example in the case of an aneurysm due to Salmonella infection [16]. Venous compression is very often clinically silent because paraspinal venous collaterals develop. Typical symptoms include peripheral edema, generally bilateral, the importance of which can range from simple premalleolar edema to massive edema involving the root of the thigh and the perineum. Associated urinary signs, including hematuria, renal colic, uni- or bilateral ureterohydronephrosis, or anuria [12] are not infrequent and may be misleading. When the aneurysm is palpable, the cause of venous compression is readily suggested. Otherwise, sonography or CT scans are diagnostic [I0]. The prognostic significance of venous complications of aneurysms of the abdominal aorta must be underscored. The study of our 10 cases and of 15 other cases in the literature shows that venous compression often heralds rupture. Of these 25 cases, 16 aneurysms had a diameter of between 6 and 9 cm [17]. Ten aneurysms, two of small size and associated with retroperitoneal fibrosis [13-15], had ruptured. Rupture was retroperitoneal in four cases, into the duodenum in two cases, and into the inferior vena cava in four cases. Other acute complications included acute thrombosis of the aneurysm in two cases [18] and thrombosis of the inferior vena cava associated with femoral embolism in one case [19]. Onset of venous compression is an additional argument for rapid surgical treatment of aneurysm.
ANNALS OF VASCULARSURGERY
Retroperitoneal fibrosis can complicate surgery. In reality, however, retroperitoneal fibrosis rarely overruns the second lumbar vertebra [20] and the iliac bifurcation or external iliac artery. Gaining control of the neck of the aneurysm and the iliac arteries is generally easy. When the aneurysm is extensive, arterial control may be obtained by inserting an intravascular catheter with an inflatable balloon by the iliac or axillary route. In certain cases it may be necessary to implant the prosthetic graft on the supraceliac or lower thoracic aorta. When this is needed, a tunnel is created ventral to the pancreas, thus avoiding the retroperitoneal fibrosis. The aneurysm is then excluded by ligation of the iliac arteries and completed by embolization of the aneurysm whenever necessary. The presence of collateral circulation can be a factor of postoperative hemorrhage. Leitz and associates [8] have recommended against dissection of the iliac vessels and for anastomosis of the prosthetic graft directly to the femoral arteries. In truth, as underscored by Cayot [19], tunneling is equally dangerous. In our experience, venous collateral circulation was not a major problem as long as dissection was started at the distal pole of the aneurysm and continued along its left side proximally. Prevention of thromboembolic accidents in the case of venous compression warrants discussion. Rosenthal [21] and Brichon [22] recommend interrupting the vena cava by a clip concomitantly with treating the aneurysm. In our opinion, this is excessive. We believe the indications for interruption of the inferior vena cava include an aneurysm revealed by pulmonary embolism, thrombosis of the inferior vena cava, contraindications to anticoagulant therapy, and borderline cardiorespiratory status. Rather than the Adams-DeWeese device, we prefer to insert an endocaval filter percutaneously, prior to anesthesia induction and surgery. In all other cases, direct operation on the aneurysm reduces the venous stasis due to mechanical compression, making partial interruption o f the vena cava unnecessary if pre-, intra-, and postoperative prophylaxis of the thromboembolic disease is employed.
REFERENCES 1. DE BAKEY ME, COOLEY DA, MORRIS GC Jr, COLLINS H. Arteriovenous fistula involving the abdominal aorta: report of 4 cases with successful repair. Ann Surg 1958;147:646-657. 2. CHEVALIER JM, ROY P, BONDEUX JP, BRUNEAU L. Rupture spontan6e d'un an6vrysme de l'aorte abdominale dans la veine cave inf6rieure. J Chir 1976;111:69-74. 3. CHAMPAULT G, KIEFFER E, MARAVAL M, NATALI J. Les aspects urologiques des an~vrysmes de l'aorte abdominale. Ann Urol 1976;10:83-90. 4. SNIDER RL, PORTER JM, EIDEMILLER LR. Inferior vena caval obstruction caused by expansion of an abdominal
VOLUME 4 No 1 - 1990
5.
6.
7,
8.
9, 10.
11.
12.
13.
ILIOCA VAL VENOUS COMPRESSION
aortic aneurysm. Report of a case and review of the literature. Surge~ 1974;75:613-616, STUHL L, NATALI J, ROUFFIAT J, THIROLO1X J. L'opacification radiologique des an6vrysmes de l'aorte abdominale par vole veineuse. Presse M~d 1962;70:21(13-2106. CHOMETTE G. Compressions et obstructions de la veine cave inf6rieure. Aspects anatomopathologiques. In: KIEFFER E (ed), Chirurgie de la veine cave inf6rieure et de ses branches. Paris: Expansion Scientifique Fran~:aise, 1985, pp 132-140. MAZEMAN E, RIQUET D, BAILLEUL JP, BISERTE J. DUVAL G, An6vrysmes aortoiliaques et obstructions ur4t6rales. A propos de 3 nouvelles observations, Ann Urol 1980;14:358-362. LEITZ KH, FREYSCHMIDT J, BORST HG. Ven6se komplikationen beim abdominalen aorten anevrysma. Vasa 1976;5:196-198. GOULD SE. Pathology of the heart and blood vessels. 3d Ed. Springfield: CC Thomas, 1968. MELLIERE D, BECQUEMIN JP, MEUNIER S, KOEHN EM. Bilan d'extension des phl6bites iliaques ou iliocaves. Apport de la tomodensitom6trie. J Mal Vasc 1982;8:55-61. PINOT J J, KASBAR1AN M. Tomodensitom6trie de la veine cave inf6rieure. In: KIEFFER E. (Ed), Chirurgie de la veine cave inf6rieure et de ses.branches. Act. Chir. Vasc. Paris: Expansion Scientifique Frangaise, 1985, pp 25-37. JACQUOT C, D'AUZAC DE MALARTINE C. MAGDELEINAT P, BARIETY R. Anurie par fibrose r6tropdriton6ale p6rian6vrysmale. Presse MOd 1983;12:1145-1148. GERTNER MH, HARGROVE WC, ROBERTS B. A rup-
14. 15. 16.
17. 18.
19.
20. 21. 22.
II II II
25
tured abdominal aortic aneurysm presenting as inferior vena caval obstruction. Surgery 1978;83:605-608. WALKER DI, BLOOR K, WILLIAMS G, GILLIE I. Inflammatory aneurysms of the abdominal aorta. Brit J Surg 1972 ;59:609--614. BENO1T G, GILLOT C, AUZEPY P, RICHARD C. Fibrose r6trop6riton6ale p6rian6vrysmale. Presse MOd 1983; 12:2466-2467. DEVOLFE C, BARRAL X, LESCOEUR N, NINET J, DESCOTES J, PASQUIER J, An6vrysmes infectieux de l'aorte abdominale et septic6mie ~ Salmonella. J Mal Vasc 1982;7:339-344. TAYLOR LM, PORTER JM. Donn4es de base concernant les an6vrysmes de I'aorte abdominale. Ann Chir Vasc 1986; 1:502-504, BRIDGES KG, DONNELY MD. Acute occlusion of an abdominal aortic aneurysm complicated by bilateral lower extremity venous thrombosis. A case report. Cardiovasc Dis B,II Texas Heart lnst 1981;8:93-101. CAYOT H, DAVID M. FREYS M, CORTET P, VIARD H, Erosion vert6brale, embolie p6riph6rique et compression de la veine cave inf6rieure. Trois complications rares d'un andvrysme de l'aorte abdominale. Lyon Chir 1979;75:t22124. M1TCHINSON J. The pathology of idiopathic retroperitoheal fibrosis, J Clin Pathol 1970;23:681-689. ROSENTHAL D. COSSMAN D, MARSUMOTO G, GALLOW AD, Prophylactic interruption of the inferior vena cava, Am J Surg 1979;137:389-394. BRICHON PY, MAGNE JL, BOUCHET C, VIGNEAU B, DUFOUR C, COMBES P, LEBAS JL, GUtD1CELLI H. Les andvrysmes rompus de l'aorte abdominale sous r6nale. Apropos de 75 cas. Chirurgie 1984;110:531-537.
Ten patients with symptomatic venous compression secondary to aneurysm of the infrarenal abdominal aorta are reported. Compression was responsible for edema of the lower extremities in seven cases, and, in three instances, for venous thromboembolic disease. The incidence of venous complications secondary to aneurysm (8.8% in our series) is close to that of urologic complications (10%), but their respective pathogeneses are different. Mechanical compression (nine patients) was the predominant mechanism and was due to retroperitoneal hematoma (two patients) and left-sided (three patients) or right-sided (four patients) development of the aneurysm. Noninvasive imaging, including computed tomographic scan and sonography, have replaced the more conventional invasive methods of diagnosis. The large diameter of the aneurysms generally found in these cases mandates rapid surgical treatment in order to avoid rupture and aortocaval fistula. Because of venous collateral circulation, caution must be exercised when working o n the left side of the aorta above the aneurysm and at the level of the lilac vessels. Treatment consists of the inclusion prosthetic replacement. The insertion of a Greenfield filter is needed only when pulmonary embolism occurs or in the case of recent or life-threatening caval thrombosis. (Ann Vasc Surg 1990;4:20-25) KEY WORDS: Abdominal aorta; aneurysms; inferior vena cava; thromboembolic venous disease; retroperitoneal fibrosis.
venous compression which form the basis of this report.
Rupture into the inferior vena cava is the most widely recognized venous complication of abdominal aortic aneurysm [1,2]. Other types of complications involving the venous system are less common. In the last ten years we have encountered I0 cases of aneurysm of the abdominal aorta complicated by
P A T I E N T S AND M E T H O D S Between 1978 and 1987, 112 aneurysms of the infrarenal abdominal aorta were seen in the Vascular Surgery Unit of the University Hospital in Besanqon, France. Ten patients (eight men and two women) had a symptomatic venous complication. Ages of the patients ranged from 61 to 86 years, the mean being 74.1 years. Seven patients had associated coronary artery disease, and five of these patients had a past history of myocardial infarction.
From the Service de Chirurgie Vasculah'e, H~pital Jean Mingoz, Besanqon, l~)'ance. Presented at the Annual Meeting of the Socidtd de Chirurgie Vasculaire de Langue Franqaise, May 20-21, 1988, La Grande Motte, France. Reprint requests: J. Combe, MD, Service de Chirurgie Vasculaire, HOpital Jean Mingoz, Boulevard Fleming, 25000 Besanqon, France,
20
VOLUME 4N o 1 - 1990
ILIOCAVAL VENOUS C O M P R E S S I O N
21
Three patients had hemodynamically significant carotid artery lesions, two o f which had required surgical treatment. Five patients had peripheral arterial disease. Clinical findings
An aneurysm was palpable in seven instances. More than one aneurysm was found in four patients; two had aneurysms of the thoracic aorta and two had multiple aneurysms. T w o aneurysms ruptured retroperitoneally. In one other case acute thrombosis o f the aneurysm occurred. In two cases the patient had recurrent pulmonary embolism associated with iliofemoral venous thrombosis; in one case the patient had phlebitis in his left leg and in seven cases the patients had edema without venous obstruction. Of these patients, edema was noted in the lower leg in three, and in the thigh and lower leg in four. Edema was located on the left side in five cases and the right side in two cases. In one case edema involved the pelvis with associated perineal, hemorrhoidal, and parietal varices secondary to portacaval and cavocaval collaterality. Venous signs led to the discovery o f the aortic aneurysm in six cases. Complementary investigations
Iliocavograms, sonograms, and computed tomographic (CT) scans were obtained in six patients. They contributed to the understanding of the mechanism of venous compression. The left lilac vein was involved in six cases: in two instances the obstruction was complete, and in four instances the vein showed extrinsic compression and was horizontalized. In all instances backflow occurred through the left internal iliac vein, attesting to venous stasis. The inferior vena cava was involved in five cases: in one case obstruction was complete while in four cases a smooth encroachment was noted on the left border (Figs. 1,2). Lateral views of cavograms showed that the compression also involved the anterior aspect o f the infrarenal aorta because o f the right-sided development of the aneurysm (Figs. 3,4). In three cases there were multiple sites of compression of the venous system: in two instances, the compression involved the lilac veins. In one patient with multiple aneurysms multiple compression sites included the left lilac, left femoral (Fig. 5) and popliteal veins. Collateral venous pathways through the internal iliac, iliolumbar, and azygorenal veins were demonstrated by phlebocavograms. Lateral spinal collateral pathways were usually more developed on the left except in one case of thrombosis of the vena cava (Fig. 6).
Fig. 1. Cavogram, anteroposterior view, showing compression of vena cava and of left common lilac vein by a large infrarenal aneurysm developing anteriorly and on left.
Factors predisposing to venous complications included: diameter of the aneurysm superior to 6 cm in nine cases; right-sided development of the aneurysm in four cases; associated lilac artery a n e u r y s m venous compression in three cases; retroperitoneal
Fig. 2. Cavogram, anteroposterior view, showing concentric compression of infrarenal vena cave due to aortic aneurysm developing to the right.
22
ILIOCA VAL VENOUS C O M P R E S S I O N
ANNALS OF VASCULAR SURGERY
Fig. 3. Cavogram, lateral view, showing anterior compression of infrarenai vena cava by aortic aneurysm developing on right (same patient as in Figure 2).
Fig. 5. Sonogram, longitudinal plane, showing associated femoral artery aneurysm responsible for compression of femoral vein.
Fig. 4. Aortogram showing aneurysm of infrarenal aorta developing on right (same patient as in Figure 2).
Fig. 6. Iliocavogram showing thrombosis of inferior vena cava with collateral circulation developed on right.
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23
ILIOCA VAL V E N O U S C O M P R E S S I O N
44 months. At the time of this writing seven patients are alive and have no arterial symptoms; edema has regressed completely in five instances and partially in two. One patient has residual edema due to extended iliocaval thrombosis.
DISCUSSION
Fig. 7. Computed tomography showing inflammatory aneurysm wroth perianeurysmal fibrosis affecting inferior vena cava and left ureterohydronephrosis.
hematoma in two cases; and major retroperitoneal fibrosis (Fig. 7) in one case. There were two instances of associated ureteral complications: compression of the ureter by a common iliac artery aneurysm and ureteral stenosis secondary to retroperitoneal fibrosis. Treatment Six patients were treated by heparin followed by oral anticoagulant therapy, and two patients underwent partial interruption of the inferior vena cava because of repeated pulmonary embolization, one by a Mobin Uddin device, the other by Greenfield filter. Nine patients had operations. In seven patients, the aneurysms were incised and a graft was inserted. Five patients had an aortoiliac bifurcation graft while an aortoaortic tube graft and an aortofemoral bifurcation graft were inserted in one case each. Two patients were treated by exclusion of their aneurysm associated with an axillary bifemoral bypass.
RESULTS One patient, operated on for retroperitoneal rupture, died in the immediate postoperative period of myocardial infarction. Two patients died 18 months after operation, one of congestive heart failure with pulmonary edema, the other of rupture of an aneurysm of the abdominal aorta. One patient had occlusion of the left limb of his aortoiliac bifurcation graft and was treated by a femorofemoral crossover bypass. Follow-up ranged from three to
Although rarely mentioned, venous complications of aneurysms of the abdominal aorta are not uncommon. In our experience, they represent slightly less than 9% of all aortic aneurysms. This incidence is approximately that of urologic complications, which are more widely recognized [3]. In 1951 Herschowitz, cited by Snider [4], reported the case of inferior vena caval compression by aortic aneurysm in a 70-year-old man with lower limb edema who died when his aneurysm ruptured into the duodenum. In 1962 Natali and Stuhl published two cases of caval compression due to aneurysm [5]. One of these patients presented with hemorrhagic varices of the lower limbs and the perineum. Mechanical compressions, either related to the size or the location of the aneurysm, were predominant in our series. They were seen in the case of aneurysms of greater than 6 cm or those developing to the right (Figs. 2-4). This particular form of aneurysm predisposes to aortocaval or aortoduodenal fistulas and to initial caval compression syndromes [6-9]. In most cases aneurysmal compression involves the left common iliac vein and the origin and the left border of the vena cava (Fig. I). In aneurysms developing to the right, anteroposterior cavograms show regular narrowing while the lateral cavograms show anterior compression of the infrarenal vena cava. Noninvasive investigations, including sonography (Fig. 8) and CT scan, are usually remarkably demonstrative of these aspects [10,1 I]. Multiple level compressions can be found when the aortic aneurysm is associated with iliac artery aneurysm. Often the compression due to the iliac aneurysm is greater than that of the aortic aneurysm. Associated ureteral compression can be responsible for initial renal insufficiency with oligoanuria of mechanical origin [12]. Mechanical compression by retroperitoneal hematoma is not uncommon. Snider [4] and Gertner [13] reported cases of chronic rupture which progressed for two to four weeks. Retroperitoneal fibrosis, often an extension of perianeurysmal inflammation [14], can also be responsible for venous compression. The aneurysm is not always palpable or demonstrable by CT scan [15]. Retroperitoneal fibrosis often involves both the venous and urinary tract systems, which explains the frequency of associated urologic manifestations [3,7,12]. Infection has also been suggested as a possible cause of
24
ILIOCA VAL VENOUS COMPRESSION
Fig. 8. Sonogram, longitudinal view, showing large infrarenal aneurysm associated with parietal thrombosis and extrinsic compression of vena cava and thrombosis of left common lilac vein.
venous thrombosis, for example in the case of an aneurysm due to Salmonella infection [16]. Venous compression is very often clinically silent because paraspinal venous collaterals develop. Typical symptoms include peripheral edema, generally bilateral, the importance of which can range from simple premalleolar edema to massive edema involving the root of the thigh and the perineum. Associated urinary signs, including hematuria, renal colic, uni- or bilateral ureterohydronephrosis, or anuria [12] are not infrequent and may be misleading. When the aneurysm is palpable, the cause of venous compression is readily suggested. Otherwise, sonography or CT scans are diagnostic [I0]. The prognostic significance of venous complications of aneurysms of the abdominal aorta must be underscored. The study of our 10 cases and of 15 other cases in the literature shows that venous compression often heralds rupture. Of these 25 cases, 16 aneurysms had a diameter of between 6 and 9 cm [17]. Ten aneurysms, two of small size and associated with retroperitoneal fibrosis [13-15], had ruptured. Rupture was retroperitoneal in four cases, into the duodenum in two cases, and into the inferior vena cava in four cases. Other acute complications included acute thrombosis of the aneurysm in two cases [18] and thrombosis of the inferior vena cava associated with femoral embolism in one case [19]. Onset of venous compression is an additional argument for rapid surgical treatment of aneurysm.
ANNALS OF VASCULARSURGERY
Retroperitoneal fibrosis can complicate surgery. In reality, however, retroperitoneal fibrosis rarely overruns the second lumbar vertebra [20] and the iliac bifurcation or external iliac artery. Gaining control of the neck of the aneurysm and the iliac arteries is generally easy. When the aneurysm is extensive, arterial control may be obtained by inserting an intravascular catheter with an inflatable balloon by the iliac or axillary route. In certain cases it may be necessary to implant the prosthetic graft on the supraceliac or lower thoracic aorta. When this is needed, a tunnel is created ventral to the pancreas, thus avoiding the retroperitoneal fibrosis. The aneurysm is then excluded by ligation of the iliac arteries and completed by embolization of the aneurysm whenever necessary. The presence of collateral circulation can be a factor of postoperative hemorrhage. Leitz and associates [8] have recommended against dissection of the iliac vessels and for anastomosis of the prosthetic graft directly to the femoral arteries. In truth, as underscored by Cayot [19], tunneling is equally dangerous. In our experience, venous collateral circulation was not a major problem as long as dissection was started at the distal pole of the aneurysm and continued along its left side proximally. Prevention of thromboembolic accidents in the case of venous compression warrants discussion. Rosenthal [21] and Brichon [22] recommend interrupting the vena cava by a clip concomitantly with treating the aneurysm. In our opinion, this is excessive. We believe the indications for interruption of the inferior vena cava include an aneurysm revealed by pulmonary embolism, thrombosis of the inferior vena cava, contraindications to anticoagulant therapy, and borderline cardiorespiratory status. Rather than the Adams-DeWeese device, we prefer to insert an endocaval filter percutaneously, prior to anesthesia induction and surgery. In all other cases, direct operation on the aneurysm reduces the venous stasis due to mechanical compression, making partial interruption o f the vena cava unnecessary if pre-, intra-, and postoperative prophylaxis of the thromboembolic disease is employed.
REFERENCES 1. DE BAKEY ME, COOLEY DA, MORRIS GC Jr, COLLINS H. Arteriovenous fistula involving the abdominal aorta: report of 4 cases with successful repair. Ann Surg 1958;147:646-657. 2. CHEVALIER JM, ROY P, BONDEUX JP, BRUNEAU L. Rupture spontan6e d'un an6vrysme de l'aorte abdominale dans la veine cave inf6rieure. J Chir 1976;111:69-74. 3. CHAMPAULT G, KIEFFER E, MARAVAL M, NATALI J. Les aspects urologiques des an~vrysmes de l'aorte abdominale. Ann Urol 1976;10:83-90. 4. SNIDER RL, PORTER JM, EIDEMILLER LR. Inferior vena caval obstruction caused by expansion of an abdominal
VOLUME 4 No 1 - 1990
5.
6.
7,
8.
9, 10.
11.
12.
13.
ILIOCA VAL VENOUS COMPRESSION
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