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Saccular Aortic Aneurysms
Papers Presented at the Annual Meeting of the Canadian Society for Vascular Surgery
Saccular Aortic Aneurysms Brian V. Taylor, MD, and Peter G. Kalman, MD, Toronto, Canada
Most vascular surgeons believe that saccular aortic aneurysms have a more ominous natural history than the typical fusiform aneurysm, although this is not documented in the literature. Expeditious repair is indicated for symptomatic saccular aneurysms, and intervention is usually advocated even when they are asymptomatic because of the general belief that their unique shape predisposes them to rupture. The objective of this report is to review the presentation and surgical management of this uncommon pathology. The records of 10 patients who underwent surgical intervention for an aortic saccular aneurysm between 1985 and 1998 were reviewed. To summarize their presentation and management, we grouped patients according to anatomic location: group A (distal arch), group B (descending thoracic aorta), group C (visceral aorta), and group D (infrarenal aorta). From analysis of these data we conclude that although saccular aortic aneurysms are rare, when present, they are most commonly found in the thoracic and suprarenal aorta. Most cases treated with surgery are symptomatic. Most thoracic and suprarenal saccular aneurysms can be repaired with a patch graft, which spares thoracic intercostals. Repair of saccular aneurysms of the distal arch are only feasible when performed with the use of hypothermic circulatory arrest. Infrarenal saccular aneurysms generally require tube graft replacement because the coexistent atherosclerosis makes patch repair difficult. Endovascular techniques may be the procedure of choice in the future. (Ann Vasc Surg 1999;13:555-559.)
INTRODUCTION A true arterial aneurysm is defined as a permanent, localized (i.e., focal) dilation having at least a 50% increase in diameter compared to the expected normal diameter of the artery in question, with the aorta being the most common artery involved and the infrarenal segment the most common site.1 The shape is further described as either the typical fusiform configuration or the relatively uncommon From The Toronto Hospital Vascular Center, Department of Surgery, University of Toronto, Toronto, Ontario, Canada. Presented at the Annual Meeting of the Canadian Society for Vascular Surgery, Toronto, Ontario, Canada, September 25-26, 1998. Correspondence to: P.G. Kalman, MD, The Toronto HospitalGeneral Division, Eaton Building 5EC-307, 200 Elizabeth Street, Toronto, Ontario, Canada M5G 2C4.
saccular type. The etiology of fusiform aneurysms has generally been ascribed to wall degeneration secondary to atherosclerosis, whereas the saccular type has been attributed to either a focal aortic wall infection (active or remote)2,3 or the end result of an entity termed the penetrating aortic ulcer.4 Although the first report of successful repair of a fusiform abdominal aneurysm was more than four decades ago,5 disagreement continues about the true natural history with respect to risk of rupture and indications for elective surgery.6 Most vascular surgeons consider the saccular aortic aneurysm to be a separate entity with a more ominous natural history than the typical fusiform configuration, although there is no documentation for this in the literature. The objective of this report is to review the clinical presentation and surgical management of this uncommon pathology at various sites along the aorta. 555
556
Taylor and Kalman
Annals of Vascular Surgery
Fig. 2. Group B saccular aneurysm located in middescending thoracic aorta.
Fig. 1. Group A saccular aneurysm located on the inferior aspect of aortic arch opposite the left subclavian artery.
PATIENT POPULATION All patients who underwent repair of a saccular aortic aneurysm at The Toronto Hospital between 1985 and 1998 were identified in the divisional vascular surgery audit and reviewed. A patient was considered to have a saccular aneurysm when a focal or asymmetric aortic enlargement was identified, where a portion of the circumference of the aorta was considered normal. For classification of the clinical presentation and surgical management, patients were grouped into distinct categories according to site: group A (distal arch, Fig. 1), group B (descending thoracic aorta, Fig. 2), group C (visceral aorta, Fig. 3), and group D (infrarenal aorta, Fig. 4). The clinical presentation, surgical management, and postoperative outcome are summarized for each patient in Table I.
RESULTS The median age of these six women and four men was 73 years (range 63 to 86 years). The athero-
Fig. 3. Group C saccular aneurysm located above renal arteries in visceral segment of aorta.
sclerotic risk factors and comorbid conditions of these patients were similar to those in cohorts of aneurysm patients of similar age. Nine (90%) had a history of smoking, and eight (80%) had hypertension. Two patients (20%) had undergone a previous repair of a fusiform infrarenal aortic aneurysm (one from group A and one from group C). Comorbid conditions included coexisting coronary disease in four patients (40%), three of whom were in group A; three patients (30%) had a history of cerebro-
Vol. 13, No. 6, 1999
Fig. 4. Group D saccular aneurysm of infrarenal aorta.
vascular disease; two patients (20%) had symptomatic peripheral vascular disease; and two patients (20%) had chronic lung disease. Of the ten patients, six (60%) presented with a symptom and four (40%) were asymptomatic (in whom the aneurysm was an incidental finding on imaging for an unrelated problem). In group A, two patients presented with acute hoarseness (both had contained ruptures), one patient presented with chest pain and intrapleural bleeding (contained rupture), and one patient presented with hemoptysis. In group B, one patient presented with chest pain (contained rupture) and one was asymptomatic. In group C, one patient presented with flank pain (contained rupture) and one was asymptomatic. The two group D patients were both asymptomatic. The median anteroposterior (AP) diameter of the saccular outpouching was 5.5 cm (range 2.0 to 9.0 cm), with an average AP diameter of 5.6 cm. All group A patients underwent repair using cardiopulmonary bypass and temporary hypothermic circulatory arrest. The remainder of the groups were repaired with the clamp-and-sew technique. Three group A patients underwent repair with a patch graft, and one required tube graft replacement with reimplantation of the left subclavian artery. In group A, the conditions of two patients (both patch grafts) were uncomplicated, one patient (patch graft) had seizures and transient left arm paresis postoperatively, and one patient (tube graft) could not be weaned from the pump after suffering a massive myocardial infarct. All group B and C patients underwent patch graft repair, and both of the group D patients required tube graft replacement. There were no postoperative complications in groups B, C, or D. Surgical Technique The procedures for the four patients in group A were all performed through a posterolateral thora-
Saccular aortic aneurysms 557
cotomy through the bed of the resected fifth rib. All procedures were performed with cardiopulmonary bypass that included using temporary hypothermic circulatory arrest (20°C) because proximal control with the clamp-and-sew technique in these cases was neither safe nor possible. Three aneurysms were repaired with a Dacron patch graft, and one required tube graft replacement and reattachment of the left subclavian artery because more than 50% of the aortic wall circumference was involved. With the first case (patient 1), cardiopulmonary bypass was achieved through femoral (venous)-femoral (arterial) cannulation. This patient suffered postoperative seizures and transient left arm paresis, presumably secondary to emboli caused by reversal of her circulation. The cannulation technique was changed to pulmonary artery (venous)-to-distal aortic (arterial) to minimize the risk of cerebral embolization, and was used in the last three group A patients. The other advantage of the latter technique is more rapid cooling and rewarming, as well as better venous return and better cardiac offloading. After cooling the patient to 20°C (nasopharyngeal), the pump is shut off and the repair is performed in a bloodless field. The goal for an upper limit of safe circulatory arrest time is 45 min, and the average duration for these four patients was 37.8 min (range 26 to 58 min). The average cardiopulmonary bypass pump time was 172.5 min (range 143 to 229 min). The remaining thoracic and abdominal aneurysms were repaired using the clamp-and-saw technique, without distal aortic perfusion. The two descending thoracic aneurysms (group B) were repaired through sixth interspace posterolateral thoracotomies, and both were repaired with patches [one Dacron, one polytetrafluoroethylene (PTFE)]. The two saccular aneurysms located in the visceral aortic segment (group C) were exposed through a thoracoabdominal incision with medial visceral rotation, and both were repaired with Dacron patches. The two patients with an infrarenal saccular aneurysm (group D) underwent repair through a retroperitoneal abdominal incision. Both patients required Dacron tube graft replacement of the aorta from below the renal arteries to the aortic bifurcation because of diffuse atherosclerosis of the remaining wall, which precluded simple patching. Morbidity and Mortality In the group A patients (distal arch), two cases were entirely uncomplicated. A third patient awoke with seizures and transient paresis of her left arm that resolved after 1 week. This neurologic complication
558
Taylor and Kalman
Annals of Vascular Surgery
TABLE I. Summary of 10 patients with saccular aneurysms Patient
Group 1 2 3 4 Group 5 6 Group 7 8 Group 9 10
Symptoms
Repair
Pump (min)
Hypothermic arrest (min)
Complications
Hoarseness Hoarseness Hemoptysis Chest pain
Patch Patch Patch Tube + L. subcl
162 156 143 229
26 58 39 28
Seizures, transient paresis Nil Nil MI (death)
Chest pain Asymptomatic
Patch Patch
NA NA
NA NA
Nil Nil
Flank pain Asymptomatic
Patch Patch
NA NA
NA NA
Nil Nil
Asymptomatic Asymptomatic
Tube Tube
NA NA
NA NA
Nil Nil
A
B
C
D
L. subcl, left subclavian artery; MI, myocardial infarction; NA, not applicable.
was presumed to be secondary to cerebral embolic debris during cardiopulmonary bypass. A fourth patient died after suffering a massive myocardial infarct and could not be weaned from the pump. The remaining patients (groups B, C, and D) recovered from surgery without complication.
DISCUSSION Vascular surgeons rarely encounter saccular aortic aneurysms. The 10 patients described in this report represent only 1% of all cases of aortic aneurysms (abdominal, thoracoabdominal, thoracic) that were treated surgically at this institution during this time period. There are two currently favored etiologies for the development of saccular aortic aneurysms. Most are considered secondary to focal aortic wall infection, either active or remote,2,3 or secondary to an entity known as a penetrating aortic ulcer.4 Mycotic aneurysms typically have a saccular configuration that can be explained by the pathogenesis. In the preantibiotic era, bacterial endocarditis with embolism of infected valvular vegetation was commonly identified. This is now relatively unusual because of prompt and effective antimicrobial treatment.7 Intact intima confers resistance to infection for the underlying arterial wall,8 and the most likely mechanism at present for infection is bacterial seeding at the site of a defect in the intima during transient bacteremia. The intimal lesion is usually an atherosclerotic plaque9; however, any circumstance that causes intimal injury could be responsible, such as a chronic arteriovenous fistula10
or an aortic coarctation.11 Although multiple organisms have been isolated (particularly staphylococci and streptococci), Salmonella species with their affinity toward invasion and growth on atherosclerotic plaque are also frequently implicated.12 A second postulated mechanism for the saccular aneurysm is that it originates from a penetrating aortic ulcer, most commonly found in the descending thoracic aorta, which is becoming increasingly recognized.4 Presumably, an atherosclerotic plaque ulcerates and penetrates through the internal elastic lamina into the media, causing a localized dissection and often a pseudoaneurysm. Extension of the wall hemorrhage is prevented and localized by the surrounding transmural inflammation. However, the adventitia may rupture freely or remain contained by the pleura and mediastinal tissues as a hematoma.13 The diagnosis of a penetrating ulcer is made by computed tomography (CT) scan, magnetic resonance imaging (MRI), or transesophageal echocardiography.14 In some cases there is no evidence of an ulcer by imaging studies, but an intramural hematoma producing a saccular aneurysm is observed. This entity is distinguished from the more common aortic dissection by the absence of an intimal flap in the ascending (type A) or proximal descending (type B) thoracic aorta. The common finding of acute expansion with a contained rupture explains the frequent presenting symptom of pain that is well localized to the appropriate segment of the aorta. In patients with an aneurysm in the vicinity of the left subclavian artery (group A), hoarseness can be a finding with the acute expan-
Vol. 13, No. 6, 1999
sion of a contained rupture. If the pseudoaneurysm stabilizes and becomes walled off with tissue organization, a chronic saccular aneurysm develops. We know very little about the natural history of saccular aortic aneurysms. In the report from the subcommittee of the Joint Council of the Society for Vascular Surgery and the International Society for Cardiovascular Surgery, it was recommended that saccular aneurysms may represent an indication for surgery regardless of size.15 This recommendation is widely held by most vascular surgeons despite the fact that nothing is known about the natural history, beyond anecdotal experience. Surgeons fear that the asymmetric, focal bulge represents an area of extreme thinning of the aortic wall with a greater tendency to rupture. In our series, a contained rupture was common (5 of 10 patients). Although there are no clinical natural history data available, extrapolation of the observations from an interesting report on three-dimensional computer models of aneurysms and their rupture risk may be useful.16 The authors concluded that asymmetry is as important as diameter in determining wall stress and rupture risk.16 The surgical conduct and technique vary according to the location. If obvious acute infection is encountered at the time of repair, debridement, aortic closure, and extraanatomic bypass will be feasible only with infrarenal involvement, although a conduit from the ascending to visceral aorta can be considered to exclude an infected descending thoracic aorta. It is more practical to consider using a substitute such as a bovine patch or banked cadaveric aorta. None of the saccular aneurysms in this report were acutely infected at the time of surgery, therefore the etiology was either remote infection or penetrating atherosclerotic ulcer. For thoracic aortic aneurysms, it is advantageous to perform a patch aortoplasty when <50% of the wall circumference is involved and normal tissue exists at the rim. This ensures sparing of thoracic intercostal arteries and minimizes the risk of spinal cord ischemia. This was possible in three of the four distal arch aneurysms, and all of the descending thoracic (two) and visceral aortic (two) aneurysms. Both infrarenal aortic aneurysms required tube graft placement because of diffuse atherosclerosis and calcification of the remaining wall, precluding simple patching. In summary, saccular aortic aneurysms are an unusual variant with an unknown natural history. Most surgeons feel that their unique configuration
Saccular aortic aneurysms 559
predisposes them to rupture, although there are no reliable data in the literature to support this. If <50% of the aortic circumference is involved, there is sufficient healthy wall to repair the aorta with a patch graft. The typically small, eccentrically placed neck of the aneurysm makes it particularly amenable to repair with a covered stent graft using endovascular techniques that will undoubtedly be more popular in the future. REFERENCES 1. Johnston KW, Rutherford RB, Tilson MD, Shah DM, Hollier L, Stanley JC. Suggested standards for reporting on arterial aneurysms. J Vasc Surg 1991;13:444-450. 2. Brown SL, Busuttil RW, Baker JD, Machleder HI, Moore WS, Barker WF. Bacteriologic and surgical determinants of survival in patients with mycotic aneurysms. J Vasc Surg 1984;1:541-547. 3. Reddy DJ, Lee RE, Oh HK. Suprarenal mycotic aortic aneurysm: surgical management and follow-up. J Vasc Surg 1986;3:917-920. 4. Coady MA, Rizzo JA, Haemmond GL, Pierce JG, Kopf GS, Elefteriades JA. Penetrating ulcer of the thoracic aorta: What is it? How do we recognize it? How do we manage it? J Vasc Surg 1998;27:1006-1016. 5. Dubost C, Allary M, Oeconomos N. Resection of an aneurysm of the abdominal aorta: re-establishment of the continuity by a preserved arterial graft, with results after five months. Arch Surg 1952;64:405-411. 6. Hollier LH, Taylor LM, Ochsner J. Report of a subcommittee of the Joint Council of the Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery. J Vasc Surg 1992;15:1046-1056. 7. Perdue GD, Smith RB III. Surgical treatment of mycotic aneurysms. South Med J 1967;60:848-851. 8. Mendelowitz DS, Ramstedt R, Yao JST, Bergan J. Abdominal aortic salmonellosis. Surgery 1979;85:514-519. 9. Davies OG, Thorburn JD, Powell P. Cryptic mycotic abdominal aortic aneurysms. Am J Surg 1978;136:96-101. 10. Perdue GD, Yancy AG. Mycotic aneurysmal change in the dilated artery proximal to arteriovenous fistula. South Med J 1972;65:1142-1144. 11. Schneider JA, Rheuban KS, Crosby IK. Rupture of postcoarctation mycotic aneurysms of the aorta. Ann Thorac Surg 1979;27:185-190. 12. Trairatvorkul P, Sriphojanart S, Sathapatayavongs B. Abdominal aortic aneurysms infected with salmonella: problems of treatment. J Vasc Surg 1990;12:16-19. 13. Roberts WC. Aortic dissection: anatomy, consequences and causes. Am Heart J 1981;101:195-214. 14. Yucel EK, Steinberg FL, Egglin TRK, Geller SC, Waltman AC, Athansoulis CA. Penetrating aortic ulcers: diagnosis with MR imaging. Radiology 1990;177:779-781. 15. Hollier LH, Taylor LM, Ochsner J. Recommended indications for operative treatment of abdominal aortic aneurysms. J Vasc Surg 1992;16:274-278. 16. Vorp DA, Raghavan BS, Webster MW. Mechanical wall stress in abdominal aortic aneurysm: influence of diameter and asymmetry. J Vasc Surg 1998;27:632-639.
Saccular Aortic Aneurysms Brian V. Taylor, MD, and Peter G. Kalman, MD, Toronto, Canada
Most vascular surgeons believe that saccular aortic aneurysms have a more ominous natural history than the typical fusiform aneurysm, although this is not documented in the literature. Expeditious repair is indicated for symptomatic saccular aneurysms, and intervention is usually advocated even when they are asymptomatic because of the general belief that their unique shape predisposes them to rupture. The objective of this report is to review the presentation and surgical management of this uncommon pathology. The records of 10 patients who underwent surgical intervention for an aortic saccular aneurysm between 1985 and 1998 were reviewed. To summarize their presentation and management, we grouped patients according to anatomic location: group A (distal arch), group B (descending thoracic aorta), group C (visceral aorta), and group D (infrarenal aorta). From analysis of these data we conclude that although saccular aortic aneurysms are rare, when present, they are most commonly found in the thoracic and suprarenal aorta. Most cases treated with surgery are symptomatic. Most thoracic and suprarenal saccular aneurysms can be repaired with a patch graft, which spares thoracic intercostals. Repair of saccular aneurysms of the distal arch are only feasible when performed with the use of hypothermic circulatory arrest. Infrarenal saccular aneurysms generally require tube graft replacement because the coexistent atherosclerosis makes patch repair difficult. Endovascular techniques may be the procedure of choice in the future. (Ann Vasc Surg 1999;13:555-559.)
INTRODUCTION A true arterial aneurysm is defined as a permanent, localized (i.e., focal) dilation having at least a 50% increase in diameter compared to the expected normal diameter of the artery in question, with the aorta being the most common artery involved and the infrarenal segment the most common site.1 The shape is further described as either the typical fusiform configuration or the relatively uncommon From The Toronto Hospital Vascular Center, Department of Surgery, University of Toronto, Toronto, Ontario, Canada. Presented at the Annual Meeting of the Canadian Society for Vascular Surgery, Toronto, Ontario, Canada, September 25-26, 1998. Correspondence to: P.G. Kalman, MD, The Toronto HospitalGeneral Division, Eaton Building 5EC-307, 200 Elizabeth Street, Toronto, Ontario, Canada M5G 2C4.
saccular type. The etiology of fusiform aneurysms has generally been ascribed to wall degeneration secondary to atherosclerosis, whereas the saccular type has been attributed to either a focal aortic wall infection (active or remote)2,3 or the end result of an entity termed the penetrating aortic ulcer.4 Although the first report of successful repair of a fusiform abdominal aneurysm was more than four decades ago,5 disagreement continues about the true natural history with respect to risk of rupture and indications for elective surgery.6 Most vascular surgeons consider the saccular aortic aneurysm to be a separate entity with a more ominous natural history than the typical fusiform configuration, although there is no documentation for this in the literature. The objective of this report is to review the clinical presentation and surgical management of this uncommon pathology at various sites along the aorta. 555
556
Taylor and Kalman
Annals of Vascular Surgery
Fig. 2. Group B saccular aneurysm located in middescending thoracic aorta.
Fig. 1. Group A saccular aneurysm located on the inferior aspect of aortic arch opposite the left subclavian artery.
PATIENT POPULATION All patients who underwent repair of a saccular aortic aneurysm at The Toronto Hospital between 1985 and 1998 were identified in the divisional vascular surgery audit and reviewed. A patient was considered to have a saccular aneurysm when a focal or asymmetric aortic enlargement was identified, where a portion of the circumference of the aorta was considered normal. For classification of the clinical presentation and surgical management, patients were grouped into distinct categories according to site: group A (distal arch, Fig. 1), group B (descending thoracic aorta, Fig. 2), group C (visceral aorta, Fig. 3), and group D (infrarenal aorta, Fig. 4). The clinical presentation, surgical management, and postoperative outcome are summarized for each patient in Table I.
RESULTS The median age of these six women and four men was 73 years (range 63 to 86 years). The athero-
Fig. 3. Group C saccular aneurysm located above renal arteries in visceral segment of aorta.
sclerotic risk factors and comorbid conditions of these patients were similar to those in cohorts of aneurysm patients of similar age. Nine (90%) had a history of smoking, and eight (80%) had hypertension. Two patients (20%) had undergone a previous repair of a fusiform infrarenal aortic aneurysm (one from group A and one from group C). Comorbid conditions included coexisting coronary disease in four patients (40%), three of whom were in group A; three patients (30%) had a history of cerebro-
Vol. 13, No. 6, 1999
Fig. 4. Group D saccular aneurysm of infrarenal aorta.
vascular disease; two patients (20%) had symptomatic peripheral vascular disease; and two patients (20%) had chronic lung disease. Of the ten patients, six (60%) presented with a symptom and four (40%) were asymptomatic (in whom the aneurysm was an incidental finding on imaging for an unrelated problem). In group A, two patients presented with acute hoarseness (both had contained ruptures), one patient presented with chest pain and intrapleural bleeding (contained rupture), and one patient presented with hemoptysis. In group B, one patient presented with chest pain (contained rupture) and one was asymptomatic. In group C, one patient presented with flank pain (contained rupture) and one was asymptomatic. The two group D patients were both asymptomatic. The median anteroposterior (AP) diameter of the saccular outpouching was 5.5 cm (range 2.0 to 9.0 cm), with an average AP diameter of 5.6 cm. All group A patients underwent repair using cardiopulmonary bypass and temporary hypothermic circulatory arrest. The remainder of the groups were repaired with the clamp-and-sew technique. Three group A patients underwent repair with a patch graft, and one required tube graft replacement with reimplantation of the left subclavian artery. In group A, the conditions of two patients (both patch grafts) were uncomplicated, one patient (patch graft) had seizures and transient left arm paresis postoperatively, and one patient (tube graft) could not be weaned from the pump after suffering a massive myocardial infarct. All group B and C patients underwent patch graft repair, and both of the group D patients required tube graft replacement. There were no postoperative complications in groups B, C, or D. Surgical Technique The procedures for the four patients in group A were all performed through a posterolateral thora-
Saccular aortic aneurysms 557
cotomy through the bed of the resected fifth rib. All procedures were performed with cardiopulmonary bypass that included using temporary hypothermic circulatory arrest (20°C) because proximal control with the clamp-and-sew technique in these cases was neither safe nor possible. Three aneurysms were repaired with a Dacron patch graft, and one required tube graft replacement and reattachment of the left subclavian artery because more than 50% of the aortic wall circumference was involved. With the first case (patient 1), cardiopulmonary bypass was achieved through femoral (venous)-femoral (arterial) cannulation. This patient suffered postoperative seizures and transient left arm paresis, presumably secondary to emboli caused by reversal of her circulation. The cannulation technique was changed to pulmonary artery (venous)-to-distal aortic (arterial) to minimize the risk of cerebral embolization, and was used in the last three group A patients. The other advantage of the latter technique is more rapid cooling and rewarming, as well as better venous return and better cardiac offloading. After cooling the patient to 20°C (nasopharyngeal), the pump is shut off and the repair is performed in a bloodless field. The goal for an upper limit of safe circulatory arrest time is 45 min, and the average duration for these four patients was 37.8 min (range 26 to 58 min). The average cardiopulmonary bypass pump time was 172.5 min (range 143 to 229 min). The remaining thoracic and abdominal aneurysms were repaired using the clamp-and-saw technique, without distal aortic perfusion. The two descending thoracic aneurysms (group B) were repaired through sixth interspace posterolateral thoracotomies, and both were repaired with patches [one Dacron, one polytetrafluoroethylene (PTFE)]. The two saccular aneurysms located in the visceral aortic segment (group C) were exposed through a thoracoabdominal incision with medial visceral rotation, and both were repaired with Dacron patches. The two patients with an infrarenal saccular aneurysm (group D) underwent repair through a retroperitoneal abdominal incision. Both patients required Dacron tube graft replacement of the aorta from below the renal arteries to the aortic bifurcation because of diffuse atherosclerosis of the remaining wall, which precluded simple patching. Morbidity and Mortality In the group A patients (distal arch), two cases were entirely uncomplicated. A third patient awoke with seizures and transient paresis of her left arm that resolved after 1 week. This neurologic complication
558
Taylor and Kalman
Annals of Vascular Surgery
TABLE I. Summary of 10 patients with saccular aneurysms Patient
Group 1 2 3 4 Group 5 6 Group 7 8 Group 9 10
Symptoms
Repair
Pump (min)
Hypothermic arrest (min)
Complications
Hoarseness Hoarseness Hemoptysis Chest pain
Patch Patch Patch Tube + L. subcl
162 156 143 229
26 58 39 28
Seizures, transient paresis Nil Nil MI (death)
Chest pain Asymptomatic
Patch Patch
NA NA
NA NA
Nil Nil
Flank pain Asymptomatic
Patch Patch
NA NA
NA NA
Nil Nil
Asymptomatic Asymptomatic
Tube Tube
NA NA
NA NA
Nil Nil
A
B
C
D
L. subcl, left subclavian artery; MI, myocardial infarction; NA, not applicable.
was presumed to be secondary to cerebral embolic debris during cardiopulmonary bypass. A fourth patient died after suffering a massive myocardial infarct and could not be weaned from the pump. The remaining patients (groups B, C, and D) recovered from surgery without complication.
DISCUSSION Vascular surgeons rarely encounter saccular aortic aneurysms. The 10 patients described in this report represent only 1% of all cases of aortic aneurysms (abdominal, thoracoabdominal, thoracic) that were treated surgically at this institution during this time period. There are two currently favored etiologies for the development of saccular aortic aneurysms. Most are considered secondary to focal aortic wall infection, either active or remote,2,3 or secondary to an entity known as a penetrating aortic ulcer.4 Mycotic aneurysms typically have a saccular configuration that can be explained by the pathogenesis. In the preantibiotic era, bacterial endocarditis with embolism of infected valvular vegetation was commonly identified. This is now relatively unusual because of prompt and effective antimicrobial treatment.7 Intact intima confers resistance to infection for the underlying arterial wall,8 and the most likely mechanism at present for infection is bacterial seeding at the site of a defect in the intima during transient bacteremia. The intimal lesion is usually an atherosclerotic plaque9; however, any circumstance that causes intimal injury could be responsible, such as a chronic arteriovenous fistula10
or an aortic coarctation.11 Although multiple organisms have been isolated (particularly staphylococci and streptococci), Salmonella species with their affinity toward invasion and growth on atherosclerotic plaque are also frequently implicated.12 A second postulated mechanism for the saccular aneurysm is that it originates from a penetrating aortic ulcer, most commonly found in the descending thoracic aorta, which is becoming increasingly recognized.4 Presumably, an atherosclerotic plaque ulcerates and penetrates through the internal elastic lamina into the media, causing a localized dissection and often a pseudoaneurysm. Extension of the wall hemorrhage is prevented and localized by the surrounding transmural inflammation. However, the adventitia may rupture freely or remain contained by the pleura and mediastinal tissues as a hematoma.13 The diagnosis of a penetrating ulcer is made by computed tomography (CT) scan, magnetic resonance imaging (MRI), or transesophageal echocardiography.14 In some cases there is no evidence of an ulcer by imaging studies, but an intramural hematoma producing a saccular aneurysm is observed. This entity is distinguished from the more common aortic dissection by the absence of an intimal flap in the ascending (type A) or proximal descending (type B) thoracic aorta. The common finding of acute expansion with a contained rupture explains the frequent presenting symptom of pain that is well localized to the appropriate segment of the aorta. In patients with an aneurysm in the vicinity of the left subclavian artery (group A), hoarseness can be a finding with the acute expan-
Vol. 13, No. 6, 1999
sion of a contained rupture. If the pseudoaneurysm stabilizes and becomes walled off with tissue organization, a chronic saccular aneurysm develops. We know very little about the natural history of saccular aortic aneurysms. In the report from the subcommittee of the Joint Council of the Society for Vascular Surgery and the International Society for Cardiovascular Surgery, it was recommended that saccular aneurysms may represent an indication for surgery regardless of size.15 This recommendation is widely held by most vascular surgeons despite the fact that nothing is known about the natural history, beyond anecdotal experience. Surgeons fear that the asymmetric, focal bulge represents an area of extreme thinning of the aortic wall with a greater tendency to rupture. In our series, a contained rupture was common (5 of 10 patients). Although there are no clinical natural history data available, extrapolation of the observations from an interesting report on three-dimensional computer models of aneurysms and their rupture risk may be useful.16 The authors concluded that asymmetry is as important as diameter in determining wall stress and rupture risk.16 The surgical conduct and technique vary according to the location. If obvious acute infection is encountered at the time of repair, debridement, aortic closure, and extraanatomic bypass will be feasible only with infrarenal involvement, although a conduit from the ascending to visceral aorta can be considered to exclude an infected descending thoracic aorta. It is more practical to consider using a substitute such as a bovine patch or banked cadaveric aorta. None of the saccular aneurysms in this report were acutely infected at the time of surgery, therefore the etiology was either remote infection or penetrating atherosclerotic ulcer. For thoracic aortic aneurysms, it is advantageous to perform a patch aortoplasty when <50% of the wall circumference is involved and normal tissue exists at the rim. This ensures sparing of thoracic intercostal arteries and minimizes the risk of spinal cord ischemia. This was possible in three of the four distal arch aneurysms, and all of the descending thoracic (two) and visceral aortic (two) aneurysms. Both infrarenal aortic aneurysms required tube graft placement because of diffuse atherosclerosis and calcification of the remaining wall, precluding simple patching. In summary, saccular aortic aneurysms are an unusual variant with an unknown natural history. Most surgeons feel that their unique configuration
Saccular aortic aneurysms 559
predisposes them to rupture, although there are no reliable data in the literature to support this. If <50% of the aortic circumference is involved, there is sufficient healthy wall to repair the aorta with a patch graft. The typically small, eccentrically placed neck of the aneurysm makes it particularly amenable to repair with a covered stent graft using endovascular techniques that will undoubtedly be more popular in the future. REFERENCES 1. Johnston KW, Rutherford RB, Tilson MD, Shah DM, Hollier L, Stanley JC. Suggested standards for reporting on arterial aneurysms. J Vasc Surg 1991;13:444-450. 2. Brown SL, Busuttil RW, Baker JD, Machleder HI, Moore WS, Barker WF. Bacteriologic and surgical determinants of survival in patients with mycotic aneurysms. J Vasc Surg 1984;1:541-547. 3. Reddy DJ, Lee RE, Oh HK. Suprarenal mycotic aortic aneurysm: surgical management and follow-up. J Vasc Surg 1986;3:917-920. 4. Coady MA, Rizzo JA, Haemmond GL, Pierce JG, Kopf GS, Elefteriades JA. Penetrating ulcer of the thoracic aorta: What is it? How do we recognize it? How do we manage it? J Vasc Surg 1998;27:1006-1016. 5. Dubost C, Allary M, Oeconomos N. Resection of an aneurysm of the abdominal aorta: re-establishment of the continuity by a preserved arterial graft, with results after five months. Arch Surg 1952;64:405-411. 6. Hollier LH, Taylor LM, Ochsner J. Report of a subcommittee of the Joint Council of the Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery. J Vasc Surg 1992;15:1046-1056. 7. Perdue GD, Smith RB III. Surgical treatment of mycotic aneurysms. South Med J 1967;60:848-851. 8. Mendelowitz DS, Ramstedt R, Yao JST, Bergan J. Abdominal aortic salmonellosis. Surgery 1979;85:514-519. 9. Davies OG, Thorburn JD, Powell P. Cryptic mycotic abdominal aortic aneurysms. Am J Surg 1978;136:96-101. 10. Perdue GD, Yancy AG. Mycotic aneurysmal change in the dilated artery proximal to arteriovenous fistula. South Med J 1972;65:1142-1144. 11. Schneider JA, Rheuban KS, Crosby IK. Rupture of postcoarctation mycotic aneurysms of the aorta. Ann Thorac Surg 1979;27:185-190. 12. Trairatvorkul P, Sriphojanart S, Sathapatayavongs B. Abdominal aortic aneurysms infected with salmonella: problems of treatment. J Vasc Surg 1990;12:16-19. 13. Roberts WC. Aortic dissection: anatomy, consequences and causes. Am Heart J 1981;101:195-214. 14. Yucel EK, Steinberg FL, Egglin TRK, Geller SC, Waltman AC, Athansoulis CA. Penetrating aortic ulcers: diagnosis with MR imaging. Radiology 1990;177:779-781. 15. Hollier LH, Taylor LM, Ochsner J. Recommended indications for operative treatment of abdominal aortic aneurysms. J Vasc Surg 1992;16:274-278. 16. Vorp DA, Raghavan BS, Webster MW. Mechanical wall stress in abdominal aortic aneurysm: influence of diameter and asymmetry. J Vasc Surg 1998;27:632-639.