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Ann Thorac Surg 2002;74:S1881-S1884
© 2002 The Society of Thoracic Surgeons


Session 4: Descending/Thoracoabdominal Aorta

Thoracoabdominal aortic aneurysm repair: review and update of current strategies

Joseph S. Coselli, MDa*, Lori D. Conklin, MDa, Scott A. LeMaire, MDa

a The Michael E. DeBakey Department of Surgery, Division of Cardiothoracic Surgery, Baylor College of Medicine, and The Methodist DeBakey Heart Center, Houston, Texas, USA

* Address reprint requests to Dr Coselli, 6560 Fannin St, Suite 1100, Houston, TX, 77030, USA
e-mail: jcoselli{at}bcm.tmc.edu

Presented at the Aortic Surgery Symposium VIII, May 2–3, 2002, New York, NY.

Abstract

BACKGROUND: Surgical repair of thoracoabdominal aortic aneurysms remains a technically challenging operation that requires a multimodality approach to preventing ischemic complications. The purpose of this report is to update our experience and highlight our current clinical strategies.

METHODS: Between January 1, 1986 and December 31, 2001, 1,773 patients underwent thoracoabdominal aortic aneurysm repair. The majority of these patients (1,153, 65%) required Crawford extent I or II repairs. Segmental intercostal or lumbar arteries were reattached in 1,082 patients (61%); left heart bypass was used in 686 patients (38.7%), and 173 patients (9.8%) had cerebrospinal fluid drainage.

RESULTS: The 30-day survival rate was 94.3% (1,672 patients). Postoperative complications included renal failure requiring hemodialysis in 105 patients (5.9%) and paraplegia or paraparesis in 79 patients (4.5%). Actuarial 5-year survival was 73.5% ± 1.6%.

CONCLUSIONS: This clinical experience demonstrates that current technical strategies enable patients to undergo thoracoabdominal aortic aneurysm repair with excellent early survival and acceptable morbidity.

Although results after the surgical repair of thoracoabdominal aortic aneurysms (TAAAs) continue to improve, patients remain susceptible to postoperative renal and neurologic complications, often culminating in death. Prevention of these complications requires a multimodality approach. The purpose of this report is to update our experience and highlight our current clinical strategies.

Patients and methods

Patients
Between January 11, 1986 and December 31, 2001, 1,773 consecutive patients with TAAAs underwent graft replacement by the senior author (J.S.C.). The repairs were categorized based upon Crawford’s original classification. For each patient, perioperative data were entered into a prospectively maintained database.

There were 1,034 men (58.3%) and 739 women (41.7%). Patient ages ranged from 18 to 88 years (mean, 65.5 ± 11.9 years; median, 68 years). Extensive TAAAs (ie, Crawford extents I and II) were present in 1,153 patients (65%). There were 126 patients (7.1%) with Marfan syndrome. Acute aortic dissection was present in 66 patients (3.7%), chronic dissection in 407 patients (23%), and degenerative aneurysms without dissection in 1,300 patients (73.3%). The aneurysms were symptomatic in 1,143 patients (64.5%). Emergent or urgent operations were required in 188 patients (10.6%) with acute presentation, including 109 (6.1%) with ruptured aneurysms.

Surgical technique
The surgical technique has evolved substantially during the 15-year period. The principal aspects of our current method for graft repair of TAAAs have recently been described in detail (Table 1) [1]. We routinely used moderate systemic heparinization (1.0 mg/kg); the heparin was reversed with protamine sulfate after completing all anastomoses. Mild permissive hypothermia (32°C to 34°C, nasopharyngeal) also was used routinely to minimize ischemic complications. To reverse cooling at operative completion, the field was irrigated with warm saline. Segmental intercostal and lumber arteries were reattached to the graft in 1,082 patients (61%). Localized aortic endarterectomy was used whenever mural calcification interfered with obtaining a hemostatic anastomosis; this method often allowed reattachment of important intercostal arteries located in a severely diseased portion of aortic wall. Cerebral spinal fluid (CSF) drainage (a recent addition to our armamentarium) was used in 173 patients (9.8%) [2]. We used Left Heart Bypass (LHB) with a centrifugal pump in 686 patients (38.7%) [3]. The closed LHB circuit did not include a cardiotomy reservoir, an oxygenator, or a warming device. In most cases, LHB was used only during the proximal anastomosis. Whenever possible, the LHB circuit was used to provide selective perfusion (through balloon catheters) to the celiac, superior mesenteric, and renal arteries. If LHB was not used (as in most extent III or IV repairs), the renal arteries were perfused with cold (4°C) crystalloid [4]. Neither somatosensory nor motor-evoked potential monitoring was used.


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Table 1. Current Strategy for Spinal Cord, Visceral, and Renal Protection During Thoracoabdominal Aortic Aneurysm Repair

 
Results

Six patients (0.3%) died in the operating room. There were 131 operative deaths (7.4%); this included 127 patients who died in-hospital (7.2%) and 101 patients who died within 30 days (5.7%), 4 of whom died after discharge. Adverse outcomes (operative death, stroke, paraplegia, paraparesis, or need for hemodialysis) occurred in 242 patients (13.6%) [6]. The incidence of paraplegia/paraparesis was 4.5% (79 of 1,749; excludes 6 patients who died during operation and 18 patients with preoperative paraplegia). Renal failure developed in 6.0% of patients (105 of 1,740; excludes 6 patients who died during operation and 27 patients on hemodialysis preoperatively). Stratified early results based on aneurysm extent are listed in Table 2.


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Table 2. Results of 1,773 Patients Undergoing Thoracoabdominal Aortic Aneurysm Repair

 
The overall actuarial 5-year survival rate was 73.5% ± 1.6% (Fig 1A). In contrast, in Crawford and DeNatale’s [5] report of 94 patients with untreated TAAAs, fewer than 20% survived 5 years after diagnosis (Fig 1B). Patients who underwent extent I repairs had significantly better midterm survival than patients who had either extent II or IV repairs (Fig 1C). Twenty-six patients required reoperation on the descending thoracic (n = 8) or thoracoabdominal (n = 18) aorta. Actuarial freedom from death and reoperation was 69.7% ± 1.8% at 5 years (Fig 1D).



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Fig 1. Kaplan-Meier curves illustrating outcomes after thoracoabdominal aortic aneurysm repair in 1,773 consecutive patients. Values are reported with standard deviations. (A) Overall survival. (B) Overall survival compared with survival in 94 patients with untreated thoracoabdominal aortic aneurysms [5]. (C) Survival curves based on extent of repair. Patients who had extent I repairs had significantly better midterm survival (p = 0.007 vs extent II and p = 0.04 vs extent IV, log-rank test). (D) Freedom from death and reoperation on the descending thoracic or thoracoabdominal aorta.

 
Comment

The operative technique involved in TAAA repair has evolved substantially over the last 15 years, resulting in decreased mortality, paraplegia, and renal failure rates. Furthermore, risk analyses have improved management decisions and patient selection [68]. In striving to minimize morbidity and mortality, our recent efforts have focused on spinal cord and renal protection.

Paraplegia and paraparesis remain a major cause of morbidity and mortality after extensive TAAA repair. Cross-clamping the proximal descending aorta evokes several interdependent mechanisms that ultimately can contribute to the development of spinal cord ischemia, such as distal hypoperfusion and increased CSF pressure. Therefore, we use a multimodality approach to optimize spinal cord protection during the repair (Table 1). We recently completed a randomized clinical trial that focused solely on the impact CSF drainage had in preventing neurologic deficits after TAAA repair [2]. Neurologic injuries occurred in 2 of 76 patients (3%) in the CSF drainage group and in 9 of 69 patients (13%) in the control group (p = 0.03). This marked difference was attributable to the elimination of immediate paraplegia in the treatment group and corresponded to an 80% reduction in the relative risk of deficits. Regarding LHB, we conducted a retrospective review of 710 patients who underwent extent I or II TAAA repairs, and found that LHB reduced the risk of spinal cord deficits [3]. We are currently investigating the feasibility of using near infrared spectroscopy (NIRS) to detect spinal cord ischemia during aortic repair. NIRS is entirely noninvasive and uses transcutaneous sensors to quantify the focal oxyhemoglobin fraction in underlying tissues. In an animal model, we found that regional spinal cord ischemia was detectable using transcutaneous NIRS in pigs weighing up to 70 kg [9]. Based on these results, we have initiated a study to evaluate this monitor in patients undergoing TAAA repair.

Renal failure after TAAA continues to be a significant and potentially lethal complication [10]. We recently conducted a randomized clinical trial comparing renal perfusion with cold crystalloid versus normothermic blood during extent II repairs [4]. Renal dysfunction (defined as an elevation in serum creatinine beyond 50% above baseline) occurred in 63% of patients (10/16) in the normothermic blood group versus only 21% (3/14) in the cold crystalloid group (p = 0.003). Reduced kidney temperature was associated with renal protection, and the use of cold crystalloid was an independent predictor of preserved renal function. In light of their differing mechanisms of protection, we propose that combining hypothermia and blood perfusion may provide additional benefit; a randomized clinical trial comparing cold blood and cold crystalloid perfusion is underway. In this new study, we are also investigating the use of more sensitive molecular markers to detect postoperative renal injury. We are using urinary retinol binding protein, {alpha}1 microglobulin, microalbumin, and N-acetyl-ß-D-glucosamidase to compare the incidence of renal injury between the study groups. Defining the role of mediators involved in ischemia-reperfusion injury, such as xanthine oxidase, may serve as the foundation for future randomized clinical trials involving inhibitors of free radical formation as a means of preventing postoperative complications associated with their formation.

Although we have performed endovascular repair of descending thoracic aortic aneurysms, we have not used stent grafts for TAAA repair. The experience with endovascular TAAA repair remains anecdotal and has had mixed results. Three groups have reported successful TAAA repair using an approach that combines stent graft placement and open visceral bypass grafting [1113]. In a related hybrid approach, Lawrence-Brown and colleagues [14] repaired extent I TAAAs in 2 patients by placing a stent graft beyond the celiac axis and then performing a laparotomy to ligate the celiac trunk, confirm adequate hepatic and splenic perfusion, and directly anchor the distal landing site. Kinney and colleagues [15] successfully repaired a TAAA using a fenestrated endograft. Inoue and colleagues [16] successfully performed an extent III repair with an endograft that included a single side branch placed into the celiac axis. Chuter and colleagues [17] used a stent graft with four separate visceral branch grafts to perform an extent III repair; this case was complicated by delayed paraplegia and kinking of the celiac and superior mesenteric stumps, which required revision with additional stents. Ohata and colleagues [18] reported a fatal rupture due to distal type I endoleak after repair of an extent I TAAA using a straight stent graft. Until prospective studies demonstrate consistent and favorable results, endovascular TAAA repair must be considered purely investigational.

In conclusion, this clinical experience demonstrates that current technical strategies enable patients to undergo TAAA repair with excellent early survival and acceptable morbidity. Combining the latest advances in TAAA repair with new areas of investigation (including the use of molecular markers to enhance detection of postoperative complications and the development of noninvasive monitors to assess tissue perfusion) will allow continued reduction in the morbidity and mortality associated with this procedure.

References

  1. Coselli J.S., LeMaire S.A. Surgical techniques: thoracoabdominal aorta. Cardiol Clin 1999;17:751-765.[Medline]
  2. Coselli J.S., LeMaire S.A., Köksoy C., Schmittling Z.C., Curling P.E. Cerebrospinal fluid drainage reduces paraplegia following thoracoabdominal aortic aneurysm repair: results of a randomized clinical trial. J Vasc Surg 2002;35:635-639.
  3. Coselli J.S., LeMaire S.A. Left heart bypass reduces paraplegia rates after thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 1999;67:1931-1934.[Abstract/Free Full Text]
  4. Köksoy C., LeMaire S.A., Curling P.E., et al. Renal perfusion during thoracoabdominal aortic operations: cold crystalloid is superior to normothermic blood. Ann Thorac Surg 2002;73:730-738.[Abstract/Free Full Text]
  5. Crawford E.S., DeNatale R.W. Thoracoabdominal aortic aneurysm: observations regarding the natural course of disease. J Vasc Surg 1986;3:578-582.[Medline]
  6. LeMaire S.A., Miller C.C., III, Conklin L.D., Schmittling Z.C., Köksoy C., Coselli J.S. A new predictive model for adverse outcomes after elective thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 2001;71:1233-1238.[Abstract/Free Full Text]
  7. Juvonen T., Ergin M.A., Galla J.D., et al. Prospective study of the natural history of thoracic aortic aneurysms. Ann Thorac Surg 1997;63:1533-1545.[Abstract/Free Full Text]
  8. Coselli J.S., LeMaire S.A., Miller C.C., III, et al. Mortality and paraplegia after thoracoabdominal aortic aneurysm repair: a risk factor analysis. Ann Thorac Surg 2000;69:409-414.[Abstract/Free Full Text]
  9. LeMaire SA, Conklin LD, Ündar A, et al. Transcutaneous near infrared spectroscopy detects intraoperative regional spinal cord ischemia. Cardiovasc Eng 2001;7:90
  10. Coselli J.S., LeMaire S.A., Conklin L.D., et al. Morbidity and mortality after extent II thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 2002;73:1107-1116.[Abstract/Free Full Text]
  11. Quiñones-Baldrich W.J., Panetta T.F., Vescera C.L., Kashyap V.S. Repair of type IV thoracoabdominal aortic aneurysm with a combined endovascular and surgical approach. J Vasc Surg 1999;30:555-560.[Medline]
  12. Wantabe Y., Ishimaru S., Kawaguchi S., et al. Successful endografting with simultaneous visceral artery bypass grafting for severely calcified thoracoabdominal aortic aneurysm. J Vasc Surg 2002;35:397-399.[Medline]
  13. Orend K.H., Kotsis T., Scharrer-Pamler R., et al. Endovascular repair of aortic rupture due to trauma and aneurysm. Eur J Vasc Endovasc Surg 2002;23:61-67.[Medline]
  14. Lawrence-Brown M., Sieunarine K., van Schie G., et al. Hybrid open-endoluminal technique for repair of thoracoabdominal aneurysm involving the celiac axis. J Endovasc Ther 2000;7:513-519.[Medline]
  15. Kinney E.V., Kaebnick H.W., Mitchell R.A., Jung M.T. Repair of mycotic paravisceral aneurysm with a fenestrated stent-graft. J Endovasc Surg 2000;7:192-197.
  16. Inoue K., Iwase T., Sato M., et al. Transluminal endovascular branched graft placement for a pseudoaneurysm: reconstruction of the descending thoracic aorta including the celiac axis. J Thorac Cardiovasc Surg 1997;114:859-861.[Free Full Text]
  17. Chuter T.A.M., Gordon R.L., Reilly L.M., Goodman J.D., Messina L.M. An endovascular system for thoracoabdominal aortic aneurysm repair. J Endovasc Ther 2001;8:25-33.[Medline]
  18. Ohata T., Fukuda S., Kigawa I., et al. Limitation of implantation of endovascular stent-graft: case report of a patient with thoracoabdominal aneurysm. J Thorac Cardiovasc Surg 1998;116:876-877.[Free Full Text]



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