Incidental Discovery of a Chronically Thrombosed Abdominal Aortic Aneurysm: Case Report and Literature Review Chris Y. Wu, and John E. Rectenwald, Ann Arbor, Michigan
Chronic spontaneously thrombosed abdominal aortic aneurysms (AAAs) are rare. We present a patient with a completely thrombosed abdominal aortic aneurysm found incidentally on imaging for evaluation of unrelated abdominal pain. The patient was asymptomatic with regards to the aneurysm due to extensive collateralization of the intercostal and lumbar arteries to the bilateral hypogastric and internal mammary arteries to the common femoral arteries bilaterally. Follow-up imaging after 10 months showed no aneurysmal change. Further study is needed regarding indications for elective repair, medical therapy, and surveillance modality and schedule for patients with chronically occluded AAAs as these patients are at risk for aneurysm rupture and thrombus propagation.
Chronic thrombosis of abdominal aortic aneurysms (AAAs) is a rare entity that usually presents with progressive intermittent claudication.1,2 We present the case of a patient with an asymptomatic and stable chronically thrombosed AAA. Few therapeutic recommendations from the literature are available for these patients despite the fact that they are at risk for aneurysm complications.
CASE REPORT We present the case of a 74-year-old woman who initially presented to our emergency department (ED) with watery diarrhea and lower abdominal pain secondary to Clostridium difficile colitis. An abdominal computed tomography (CT) obtained in the ED showed a 5.3-cm thrombosed infrarenal AAA with extensive
Section of Vascular Surgery, Department of Surgery, University of Michigan, Ann Arbor, MI. Correspondence to: John E. Rectenwald, MD, MS, Section of Vascular Surgery, Department of Surgery, CVC 5463, 1500 East Medical Center Drive, SPC 5867, Ann Arbor, MI 48109-5867, USA; E-mail: [email protected] Ann Vasc Surg 2015; 29: 1018.e1–1018.e4 http://dx.doi.org/10.1016/j.avsg.2015.01.004 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: July 14, 2014; manuscript accepted: January 7, 2015; published online: March 11, 2015.
calcification and occluded common iliac arteries at the aortic bifurcation (Fig. 1). Arterial flow was noted in the distal external iliac arteries secondary to extensive collateralization to the bilateral hypogastric arteries and internal mammary arteries. Notable history includes hypertension, asymptomatic left carotid stenosis, and active smoking with a 100 pack-year history. Relevant medications included Plavix, Norvasc, and lisinopril. The patient denied any lower extremity claudication and had femoral and distal pedal signals on physical examination. She had no ulceration or tissue loss. An aortic angiogram, indicated to rule out and potentially treat mesenteric disease as a cause of the patient’s ischemic colitis, confirmed complete occlusion of the AAA with extensive collaterals via intercostal and lumbar arteries; there were no significant mesenteric arterial disease (Fig. 2A, B). We elected not to attempt aneurysm repair because of lack of lower extremity ischemic symptoms and the complete thrombosis of the aneurysm in light of the patient’s significant medical comorbidities. An abdominal CT 10 months later demonstrated no change in aneurysm diameter. The patient later expired after a hospitalization for congestive heart failure and aspiration pneumonia.
DISCUSSION Thrombosis is a rare complication of AAAs. The incidence of acutely thrombosed AAAs in patients who 1018.e1
1018.e2 Case reports
Fig. 1. CT showing 5.3-cm thrombosed infrarenal AAA.
were managed with open surgery was 0.7e2.8%.3e5 The first thrombosed AAA was reported by Schumacker3 in 1959, and the first successful revascularization procedure was reported in 1960 by Janetta and Roberts6 after they treated an acutely thrombosed AAA with an aortobifemoral bypass. Thrombosis of AAAs usually presents acutely and is a surgical emergency presenting with profound acute lower limb ischemia and pain, skin mottling up to level of the umbilicus, and lower extremity neuromuscular deficits.5e8 Abdominal pain is an atypical finding in acute thrombosis, and its presence suggests rupture.5,9 Mortality rates in cases of acute thrombosis approach 50%.6e8 In contrast, chronic occlusion of an AAA usually presents with progressive intermittent lower extremity claudication.1,2,10 The woman in our case, however, presented with an incidental finding of a thrombosed AAA on abdominal CT. In the setting of a 50-year history of 2 packs-per-day smoking, the chronic nature of her underlying coexisting iliac occlusive disease allowed adequate collaterals to develop, preventing the development of lower extremity ischemic symptoms when her AAA completely thrombosed. Aortoiliac occlusive disease (AIOD) has been associated with acute occlusion of AAAs,11,12 and the heavy calcification seen in our case suggests that AIOD may be involved in this patient’s chronic thrombosed AAA. It has been proposed that AIOD leads to stasis and then thrombosis with subsequent retrograde propagation that can lead to complete thrombosis of the AAA7; the time course of this progression and the presence of associated risk factors may determine acuity or chronicity of presentation. Many other risk factors and mechanisms for acute AAA thrombosis have been described in the literature including surgical
Annals of Vascular Surgery
manipulation, trauma, fever, thromboembolic disease, dehydration, hypercoagulability, hypotension, atrial fibrillation, neoplasm, intraplaque hemorrhage, dislodgment of mural thrombus, and AAA rupture.5e7 These risk factors are absent in the medical history of our presented patient. The decision to surgically intervene in acute AAA thrombosis is mandatory to prevent death from massive myonecrosis and subsequent multisystem organ failure. Furthermore, the decision to intervene in patients who have symptoms of aortoiliac occlusive disease or complications from proximal extension of the AAA thrombus such as renal impairment or mesenteric ischemia is also a straightforward one. Endovascular repair options are limited with only one reported case of an acute AAA thrombosis treated with an endovascular stent graft.13 Options for open surgical repair include aneurysm resection with in-line aortic graft replacement (either straight graft or bifurcated to the iliac or femoral arteries) or extra-anatomic bypass for patients with severe cardiac, respiratory, or renal comorbidities.1,5,9 Aorta-based inflow procedures have been shown to be superior to axillobifemoral bypass (2-year patency rates of 92% vs. 44%, respectively).14 There are no indications from the literature for elective repair of asymptomatic chronically thrombosed AAAs. For patients managed nonoperatively, there are currently no guidelines regarding medical therapy for patients with chronically occluded AAAs. Although our patient’s thrombosed AAA remained stable on follow-up imaging, patients with chronically thrombosed AAAs are at significant risk for complications secondary to proximal propagation of the thrombus leading to occlusion of the renal and mesenteric arteries.5,15 Corson et al.4 reported that in 14 of 27 chronically occluded AAAs, the thrombus involved the renal arteries, suggesting that the natural history of AAAs may involve proximal extension. Additionally, Starrett et al.16 reported a 46% mortality for patients with infrarenal aortic occlusion that extended to the renal or mesenteric arteries who were managed nonoperatively. Possible medical interventions to prevent proximal propagation may include antiplatelet and anticoagulation with aspirin, Plavix (which our patient was on), heparin, or warfarin though there is currently no evidence for any specific medical intervention. There is also no research regarding lifestyle interventions such as diet, exercise, and smoking cessation. It should be noted that there is significant controversy in the literature regarding risk of proximal thrombus propagation of the infrarenal aorta.5,17,18
Vol. 29, No. 5, July 2015
Case reports 1018.e3
Fig. 2. (A, B) Aortic angiogram demonstrating collaterals around thrombosed aneurysm segment via intercostals and lumbar arteries.
We decided not to intervene on our patient given her age, medical comorbidities, and due to lack of conclusive guidelines for elective repair of chronically thrombosed AAAs and the absence of lifestyle-limiting symptoms secondary to the presence of extensive arterial collateralization signifying the stable, chronic nature of her thrombosis. The natural history of chronically thrombosed AAAs has not been well delineated. As a result, there are no indications for repair nor are there surveillance schedule recommendations. Chronically occluded AAAs are not uniformly stable as thrombosed aneurysms may still rupture, as documented in case reports in the literature of ruptured chronically thrombosed AAAs. Most of these cases are the result of surgically-induced acute thrombosis of AAAs followed by extra-anatomic bypass in patients not suitable for standard open AAA repair before the availability of endovascular aneurysm repair for treatment of this subset of patients.7,9,10,19,20 Schwartz et al.21 found that in 13 patients with AAA treated with extra-anatomic bypass and induced thrombosis, the delayed rupture rate at 6 months was 15%. Cases of rupture of nonsurgically spontaneously thrombosed aneurysms have also been reported.1 The effects of thrombus on tangential wall stress are unclear. Schurink et al.22 in 2000 used a 19-ga needle to measure intrathrombotic pressure just inside the aneurysm wall and found that intrathrombotic pressures correlated well with systemic
pressure, thus showing that thrombus did not reduce the mean or pulse pressure on the aneurysm wall.22 Takagi et al.23 performed similar experiments in patients with complete AAA thrombosis and reached similar conclusions. In contrast, there are many studies, many of them using computational analysis and biomechanical modeling that suggest thrombus decreases wall stress and thus protects against rupture risk.24,25 And finally, biochemical studies have shown that thrombus thickness may be positively associated with underlying vessel wall instability through localized hypoxia, inflammation, and elevation in proteolytic enzyme activity.26 Although the effect of thrombus on AAA wall stress and integrity is controversial, given the reported case reports of late rupture of completely thrombosed AAAs discussed previously and the fact that luminal thrombus has been associated with AAA growth, surveillance should be maintained.27 The best surveillance modality and interval are not established. Dalal et al.10 recently proposed that the concept of endotension (defined as pressurization of the aneurysm sac after endovascular repair) also applied to thrombosed AAAs.28 This endotension, caused by endoleaks that transmit pressure through the graft/thrombus, could potentially lead to expansion and rupture of thrombosed AAAs.28 Dalal et al.10 concluded that because of the risk of rupture, completely occluded AAAs should be monitored with regular ultrasounds to
1018.e4 Case reports
identify aneurysm expansion and if discovered should prompt a more sensitive modality for identifying patent channels perfusing the aneurysm sac such as levovist-enhanced duplex or contrast CT.28 Surveillance intervals were not commented on. Chronically thrombosed AAAs is an extremely rare presentation of AAAs. Although the natural history of chronically thrombosed AAAs has not been well studied, these patients appear to be at some risk for complications related to AAA rupture and proximal thrombus extension. Further studies are needed to delineate indications for elective repair, medical interventions that prevent complications, and surveillance modalities and schedules.
REFERENCES 1. Sincos IR, da Silva ES, Ragazzo L, et al. Chronic thrombosed abdominal aortic aneurysms: a report on three consecutive cases and literature review. Clinics (Sao Paolo) 2009;64: 1227e30. 2. Tsutsumi K, Inoue Y, Hashizume K, et al. Chronic occlusion of an abdominal aortic aneurysm. Ann Vasc Dis 2010;3:240e3. 3. Schumacker HB Jr. Surgical treatment of aortic aneurysms. Postgrad Med 1959;25:535e48. 4. Corson JD, Brewster DC, Darling RC. The surgical management of infrarenal aortic occlusion. Surg Gynecol Obstet 1982;155:369e72. 5. Suliman AS, Raffetto JD, Seidman CS, et al. Acute thrombosis of abdominal aortic aneurysms: report of two cases and review of the literature. Vasc Endovascular Surg 2003;37:71e5. 6. Jannetta PJ, Roberts B. Sudden complete thrombosis of an aneurysm of the abdominal aorta. N Engl J Med 1961;264: 434e6. 7. Leke MA, Rowe VL, Hood DB, et al. Rupture of a previously thrombosed thoracoabdominal aneurysm. Ann Vasc Surg 2003;17:143e7. 8. Hirose H, Takagi M, Hashiyada H, et al. Acute occlusion of an abdominal aortic aneurysm: case report and review of the literature. Angiology 2000;51:515e23. 9. Leather RP, Shah D, Goldman M, et al. Nonresective treatment of abdominal aortic aneurysm. Use of acute thrombosis and axillofemoral bypass. Arch Surg 1979;114:1402e8. 10. Dalal S, Donlon M, Beard JD. Thrombosed abdominal aortic aneurysms. Do they need surveillance to prevent late rupture? Eur J Vasc Endovasc Surg 2001;22:570e2. 11. Saha SP, Nunn DB. Sudden thrombotic occlusion of abdominal aortic aneurysm: a report of 2 patients. Am Surg 1974;40:246e7.
Annals of Vascular Surgery
12. Bell JW. Acute thrombosis of the subrenal abdominal aorta. Arch Surg 1967;95:681e4. 13. Kumar V. Endovascular treatment of an acutely thrombosed AAA. J Endovasc Ther 2005;12:70e3. 14. Ligush J Jr, Criado E, Burnham SJ, et al. Management and outcome of chronic atherosclerotic infrarenal aortic occlusion. J Vasc Surg 1996;24:394e405. 15. Le Minh T, Motte S, Hoang AD, et al. Occluding aortic endoluminal stent graft combined with extra-anatomical axillofemoral bypass as alternative management of abdominal aortic aneurysms for patients at high risk with complex anatomic features: a preliminary report. J Vasc Surg 1998;28:651e6. 16. Starrett RW, Stoney RJ. Juxtarenal aortic occlusion. Surgery 1974;76:890e7. 17. McCullough JL Jr, Mackey WC, O’Donnell TF Jr, et al. Infrarenal aortic occlusion: a reassessment of surgical indications. Am J Surg 1983;146:178e82. 18. Reilly LM, Sauer L, Weinstein ES, et al. Infrarenal aortic occlusion: does it threaten renal perfusion or function? J Vasc Surg 1990;11:216e24. 19. Ricotta JJ, Kirshner RL. Case report: late rupture of a thrombosed abdominal aortic aneurysm. Surgery 1984;95:753e5. 20. Schanzer H, Papa MC, Miller CM. Rupture of surgically thrombosed abdominal aortic aneurysm. J Vasc Surg 1985;2:278e80. 21. Schwartz RA, Nichols WK, Silver D. Is thrombosis of the infrarenal abdominal aortic aneurysm an acceptable alternative? J Vasc Surg 1986;3:448e55. 22. Schurink GW, van Baalen JM, Visser MJ, et al. Thrombus within an aortic aneurysm does not reduce pressure on the aneurysmal wall. J Vasc Surg 2000;31:501e6. 23. Takagi H, Yoshikawa S, Mizuno Y, et al. Intrathrombotic pressure of a thrombosed abdominal aortic aneurysm. Ann Vasc Surg 2005;19:108e12. 24. Bluestein D, Dumont K, De Beule M, et al. Intraluminal thrombus and risk of rupture in patient specific abdominal aortic aneurysmdFSI modeling. Comput Methods Biomech Biomed Engin 2009;12:73e81. 25. Li ZY, U-King-Im J, Tang TY, et al. Impact of calcification and intraluminal thrombus on the computed wall stresses of abdominal aortic aneurysm. J Vasc Surg 2008;47: 928e35. 26. Koole D, Zandovoort HJ, Schoneveld A, et al. Intraluminal abdominal aortic aneurysm thrombus is associated with disruption of wall integrity. J Vasc Surg 2013;57:77e83. 27. Parr A, McCann M, Bradshaw B, et al. Thrombus volume is associated with cardiovascular events and aneurysm growth in patients who have abdominal aortic aneurysms. J Vasc Surg 2011;53:28e35. 28. Gilling-Smith G, Brennan J, Harris P, et al. Endotension after endovascular aneurysm repair: definition, classification, and strategies for surveillance and intervention. J Endovasc Surg 1999;6:305e7.
Chronic spontaneously thrombosed abdominal aortic aneurysms (AAAs) are rare. We present a patient with a completely thrombosed abdominal aortic aneurysm found incidentally on imaging for evaluation of unrelated abdominal pain. The patient was asymptomatic with regards to the aneurysm due to extensive collateralization of the intercostal and lumbar arteries to the bilateral hypogastric and internal mammary arteries to the common femoral arteries bilaterally. Follow-up imaging after 10 months showed no aneurysmal change. Further study is needed regarding indications for elective repair, medical therapy, and surveillance modality and schedule for patients with chronically occluded AAAs as these patients are at risk for aneurysm rupture and thrombus propagation.
Chronic thrombosis of abdominal aortic aneurysms (AAAs) is a rare entity that usually presents with progressive intermittent claudication.1,2 We present the case of a patient with an asymptomatic and stable chronically thrombosed AAA. Few therapeutic recommendations from the literature are available for these patients despite the fact that they are at risk for aneurysm complications.
CASE REPORT We present the case of a 74-year-old woman who initially presented to our emergency department (ED) with watery diarrhea and lower abdominal pain secondary to Clostridium difficile colitis. An abdominal computed tomography (CT) obtained in the ED showed a 5.3-cm thrombosed infrarenal AAA with extensive
Section of Vascular Surgery, Department of Surgery, University of Michigan, Ann Arbor, MI. Correspondence to: John E. Rectenwald, MD, MS, Section of Vascular Surgery, Department of Surgery, CVC 5463, 1500 East Medical Center Drive, SPC 5867, Ann Arbor, MI 48109-5867, USA; E-mail: [email protected] Ann Vasc Surg 2015; 29: 1018.e1–1018.e4 http://dx.doi.org/10.1016/j.avsg.2015.01.004 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: July 14, 2014; manuscript accepted: January 7, 2015; published online: March 11, 2015.
calcification and occluded common iliac arteries at the aortic bifurcation (Fig. 1). Arterial flow was noted in the distal external iliac arteries secondary to extensive collateralization to the bilateral hypogastric arteries and internal mammary arteries. Notable history includes hypertension, asymptomatic left carotid stenosis, and active smoking with a 100 pack-year history. Relevant medications included Plavix, Norvasc, and lisinopril. The patient denied any lower extremity claudication and had femoral and distal pedal signals on physical examination. She had no ulceration or tissue loss. An aortic angiogram, indicated to rule out and potentially treat mesenteric disease as a cause of the patient’s ischemic colitis, confirmed complete occlusion of the AAA with extensive collaterals via intercostal and lumbar arteries; there were no significant mesenteric arterial disease (Fig. 2A, B). We elected not to attempt aneurysm repair because of lack of lower extremity ischemic symptoms and the complete thrombosis of the aneurysm in light of the patient’s significant medical comorbidities. An abdominal CT 10 months later demonstrated no change in aneurysm diameter. The patient later expired after a hospitalization for congestive heart failure and aspiration pneumonia.
DISCUSSION Thrombosis is a rare complication of AAAs. The incidence of acutely thrombosed AAAs in patients who 1018.e1
1018.e2 Case reports
Fig. 1. CT showing 5.3-cm thrombosed infrarenal AAA.
were managed with open surgery was 0.7e2.8%.3e5 The first thrombosed AAA was reported by Schumacker3 in 1959, and the first successful revascularization procedure was reported in 1960 by Janetta and Roberts6 after they treated an acutely thrombosed AAA with an aortobifemoral bypass. Thrombosis of AAAs usually presents acutely and is a surgical emergency presenting with profound acute lower limb ischemia and pain, skin mottling up to level of the umbilicus, and lower extremity neuromuscular deficits.5e8 Abdominal pain is an atypical finding in acute thrombosis, and its presence suggests rupture.5,9 Mortality rates in cases of acute thrombosis approach 50%.6e8 In contrast, chronic occlusion of an AAA usually presents with progressive intermittent lower extremity claudication.1,2,10 The woman in our case, however, presented with an incidental finding of a thrombosed AAA on abdominal CT. In the setting of a 50-year history of 2 packs-per-day smoking, the chronic nature of her underlying coexisting iliac occlusive disease allowed adequate collaterals to develop, preventing the development of lower extremity ischemic symptoms when her AAA completely thrombosed. Aortoiliac occlusive disease (AIOD) has been associated with acute occlusion of AAAs,11,12 and the heavy calcification seen in our case suggests that AIOD may be involved in this patient’s chronic thrombosed AAA. It has been proposed that AIOD leads to stasis and then thrombosis with subsequent retrograde propagation that can lead to complete thrombosis of the AAA7; the time course of this progression and the presence of associated risk factors may determine acuity or chronicity of presentation. Many other risk factors and mechanisms for acute AAA thrombosis have been described in the literature including surgical
Annals of Vascular Surgery
manipulation, trauma, fever, thromboembolic disease, dehydration, hypercoagulability, hypotension, atrial fibrillation, neoplasm, intraplaque hemorrhage, dislodgment of mural thrombus, and AAA rupture.5e7 These risk factors are absent in the medical history of our presented patient. The decision to surgically intervene in acute AAA thrombosis is mandatory to prevent death from massive myonecrosis and subsequent multisystem organ failure. Furthermore, the decision to intervene in patients who have symptoms of aortoiliac occlusive disease or complications from proximal extension of the AAA thrombus such as renal impairment or mesenteric ischemia is also a straightforward one. Endovascular repair options are limited with only one reported case of an acute AAA thrombosis treated with an endovascular stent graft.13 Options for open surgical repair include aneurysm resection with in-line aortic graft replacement (either straight graft or bifurcated to the iliac or femoral arteries) or extra-anatomic bypass for patients with severe cardiac, respiratory, or renal comorbidities.1,5,9 Aorta-based inflow procedures have been shown to be superior to axillobifemoral bypass (2-year patency rates of 92% vs. 44%, respectively).14 There are no indications from the literature for elective repair of asymptomatic chronically thrombosed AAAs. For patients managed nonoperatively, there are currently no guidelines regarding medical therapy for patients with chronically occluded AAAs. Although our patient’s thrombosed AAA remained stable on follow-up imaging, patients with chronically thrombosed AAAs are at significant risk for complications secondary to proximal propagation of the thrombus leading to occlusion of the renal and mesenteric arteries.5,15 Corson et al.4 reported that in 14 of 27 chronically occluded AAAs, the thrombus involved the renal arteries, suggesting that the natural history of AAAs may involve proximal extension. Additionally, Starrett et al.16 reported a 46% mortality for patients with infrarenal aortic occlusion that extended to the renal or mesenteric arteries who were managed nonoperatively. Possible medical interventions to prevent proximal propagation may include antiplatelet and anticoagulation with aspirin, Plavix (which our patient was on), heparin, or warfarin though there is currently no evidence for any specific medical intervention. There is also no research regarding lifestyle interventions such as diet, exercise, and smoking cessation. It should be noted that there is significant controversy in the literature regarding risk of proximal thrombus propagation of the infrarenal aorta.5,17,18
Vol. 29, No. 5, July 2015
Case reports 1018.e3
Fig. 2. (A, B) Aortic angiogram demonstrating collaterals around thrombosed aneurysm segment via intercostals and lumbar arteries.
We decided not to intervene on our patient given her age, medical comorbidities, and due to lack of conclusive guidelines for elective repair of chronically thrombosed AAAs and the absence of lifestyle-limiting symptoms secondary to the presence of extensive arterial collateralization signifying the stable, chronic nature of her thrombosis. The natural history of chronically thrombosed AAAs has not been well delineated. As a result, there are no indications for repair nor are there surveillance schedule recommendations. Chronically occluded AAAs are not uniformly stable as thrombosed aneurysms may still rupture, as documented in case reports in the literature of ruptured chronically thrombosed AAAs. Most of these cases are the result of surgically-induced acute thrombosis of AAAs followed by extra-anatomic bypass in patients not suitable for standard open AAA repair before the availability of endovascular aneurysm repair for treatment of this subset of patients.7,9,10,19,20 Schwartz et al.21 found that in 13 patients with AAA treated with extra-anatomic bypass and induced thrombosis, the delayed rupture rate at 6 months was 15%. Cases of rupture of nonsurgically spontaneously thrombosed aneurysms have also been reported.1 The effects of thrombus on tangential wall stress are unclear. Schurink et al.22 in 2000 used a 19-ga needle to measure intrathrombotic pressure just inside the aneurysm wall and found that intrathrombotic pressures correlated well with systemic
pressure, thus showing that thrombus did not reduce the mean or pulse pressure on the aneurysm wall.22 Takagi et al.23 performed similar experiments in patients with complete AAA thrombosis and reached similar conclusions. In contrast, there are many studies, many of them using computational analysis and biomechanical modeling that suggest thrombus decreases wall stress and thus protects against rupture risk.24,25 And finally, biochemical studies have shown that thrombus thickness may be positively associated with underlying vessel wall instability through localized hypoxia, inflammation, and elevation in proteolytic enzyme activity.26 Although the effect of thrombus on AAA wall stress and integrity is controversial, given the reported case reports of late rupture of completely thrombosed AAAs discussed previously and the fact that luminal thrombus has been associated with AAA growth, surveillance should be maintained.27 The best surveillance modality and interval are not established. Dalal et al.10 recently proposed that the concept of endotension (defined as pressurization of the aneurysm sac after endovascular repair) also applied to thrombosed AAAs.28 This endotension, caused by endoleaks that transmit pressure through the graft/thrombus, could potentially lead to expansion and rupture of thrombosed AAAs.28 Dalal et al.10 concluded that because of the risk of rupture, completely occluded AAAs should be monitored with regular ultrasounds to
1018.e4 Case reports
identify aneurysm expansion and if discovered should prompt a more sensitive modality for identifying patent channels perfusing the aneurysm sac such as levovist-enhanced duplex or contrast CT.28 Surveillance intervals were not commented on. Chronically thrombosed AAAs is an extremely rare presentation of AAAs. Although the natural history of chronically thrombosed AAAs has not been well studied, these patients appear to be at some risk for complications related to AAA rupture and proximal thrombus extension. Further studies are needed to delineate indications for elective repair, medical interventions that prevent complications, and surveillance modalities and schedules.
REFERENCES 1. Sincos IR, da Silva ES, Ragazzo L, et al. Chronic thrombosed abdominal aortic aneurysms: a report on three consecutive cases and literature review. Clinics (Sao Paolo) 2009;64: 1227e30. 2. Tsutsumi K, Inoue Y, Hashizume K, et al. Chronic occlusion of an abdominal aortic aneurysm. Ann Vasc Dis 2010;3:240e3. 3. Schumacker HB Jr. Surgical treatment of aortic aneurysms. Postgrad Med 1959;25:535e48. 4. Corson JD, Brewster DC, Darling RC. The surgical management of infrarenal aortic occlusion. Surg Gynecol Obstet 1982;155:369e72. 5. Suliman AS, Raffetto JD, Seidman CS, et al. Acute thrombosis of abdominal aortic aneurysms: report of two cases and review of the literature. Vasc Endovascular Surg 2003;37:71e5. 6. Jannetta PJ, Roberts B. Sudden complete thrombosis of an aneurysm of the abdominal aorta. N Engl J Med 1961;264: 434e6. 7. Leke MA, Rowe VL, Hood DB, et al. Rupture of a previously thrombosed thoracoabdominal aneurysm. Ann Vasc Surg 2003;17:143e7. 8. Hirose H, Takagi M, Hashiyada H, et al. Acute occlusion of an abdominal aortic aneurysm: case report and review of the literature. Angiology 2000;51:515e23. 9. Leather RP, Shah D, Goldman M, et al. Nonresective treatment of abdominal aortic aneurysm. Use of acute thrombosis and axillofemoral bypass. Arch Surg 1979;114:1402e8. 10. Dalal S, Donlon M, Beard JD. Thrombosed abdominal aortic aneurysms. Do they need surveillance to prevent late rupture? Eur J Vasc Endovasc Surg 2001;22:570e2. 11. Saha SP, Nunn DB. Sudden thrombotic occlusion of abdominal aortic aneurysm: a report of 2 patients. Am Surg 1974;40:246e7.
Annals of Vascular Surgery
12. Bell JW. Acute thrombosis of the subrenal abdominal aorta. Arch Surg 1967;95:681e4. 13. Kumar V. Endovascular treatment of an acutely thrombosed AAA. J Endovasc Ther 2005;12:70e3. 14. Ligush J Jr, Criado E, Burnham SJ, et al. Management and outcome of chronic atherosclerotic infrarenal aortic occlusion. J Vasc Surg 1996;24:394e405. 15. Le Minh T, Motte S, Hoang AD, et al. Occluding aortic endoluminal stent graft combined with extra-anatomical axillofemoral bypass as alternative management of abdominal aortic aneurysms for patients at high risk with complex anatomic features: a preliminary report. J Vasc Surg 1998;28:651e6. 16. Starrett RW, Stoney RJ. Juxtarenal aortic occlusion. Surgery 1974;76:890e7. 17. McCullough JL Jr, Mackey WC, O’Donnell TF Jr, et al. Infrarenal aortic occlusion: a reassessment of surgical indications. Am J Surg 1983;146:178e82. 18. Reilly LM, Sauer L, Weinstein ES, et al. Infrarenal aortic occlusion: does it threaten renal perfusion or function? J Vasc Surg 1990;11:216e24. 19. Ricotta JJ, Kirshner RL. Case report: late rupture of a thrombosed abdominal aortic aneurysm. Surgery 1984;95:753e5. 20. Schanzer H, Papa MC, Miller CM. Rupture of surgically thrombosed abdominal aortic aneurysm. J Vasc Surg 1985;2:278e80. 21. Schwartz RA, Nichols WK, Silver D. Is thrombosis of the infrarenal abdominal aortic aneurysm an acceptable alternative? J Vasc Surg 1986;3:448e55. 22. Schurink GW, van Baalen JM, Visser MJ, et al. Thrombus within an aortic aneurysm does not reduce pressure on the aneurysmal wall. J Vasc Surg 2000;31:501e6. 23. Takagi H, Yoshikawa S, Mizuno Y, et al. Intrathrombotic pressure of a thrombosed abdominal aortic aneurysm. Ann Vasc Surg 2005;19:108e12. 24. Bluestein D, Dumont K, De Beule M, et al. Intraluminal thrombus and risk of rupture in patient specific abdominal aortic aneurysmdFSI modeling. Comput Methods Biomech Biomed Engin 2009;12:73e81. 25. Li ZY, U-King-Im J, Tang TY, et al. Impact of calcification and intraluminal thrombus on the computed wall stresses of abdominal aortic aneurysm. J Vasc Surg 2008;47: 928e35. 26. Koole D, Zandovoort HJ, Schoneveld A, et al. Intraluminal abdominal aortic aneurysm thrombus is associated with disruption of wall integrity. J Vasc Surg 2013;57:77e83. 27. Parr A, McCann M, Bradshaw B, et al. Thrombus volume is associated with cardiovascular events and aneurysm growth in patients who have abdominal aortic aneurysms. J Vasc Surg 2011;53:28e35. 28. Gilling-Smith G, Brennan J, Harris P, et al. Endotension after endovascular aneurysm repair: definition, classification, and strategies for surveillance and intervention. J Endovasc Surg 1999;6:305e7.
