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Ann Thorac Surg 1997;63:28-36
© 1997 The Society of Thoracic Surgeons
Baylor College of Medicine/The Methodist Hospital, Houston, Texas
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Abstract |
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 TopFootnotes Abstract IntroductionPatients and MethodsResultsCommentAppendix 1.Appendix 2.References |
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Methods. Six hundred sixty patients underwent thoracoabdominal aortic aneurysm repair from 1986 through 1995 using selective atriodistal bypass, liberal reattachment of critical intercostal arteries, moderate heparinization, and permissive mild hypothermia. Dissection was present in 163 patients (24.7%) and absent in 497 (75.3%).
Results. Early mortality occurred in 7.4% overall, and did not differ between patients with nondissection, acute dissection, or chronic dissection. The incidence of P/P was 5.4% overall, 5.5% without dissection, and 5.0% with dissection. The risk of P/P for acute versus chronic dissection was 19% versus 2.9%, respectively (p = 0.011). Rupture and Crawford extent II were predictive of the development of P/P. In patients at high risk for P/P (ie, Crawford extent I or II), atriodistal bypass reduced the intercostal artery ischemic time, and reattachment of critical intercostal arteries (T8 to L1) reduced the incidence of P/P.
Conclusions. Acute dissection increases the risk of P/P after thoracoabdominal aortic aneurysm repair; using contemporary methods, however, chronic dissection does not increase the risk of postoperative P/P. Critical intercostal artery reattachment and atriodistal bypass are beneficial in patients undergoing extensive repairs.
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Introduction |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAppendix 1.Appendix 2.References |
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Lower body neurologic sequelae resulting from spinal cord ischemia remains the most devastating complication after thoracoabdominal aortic aneurysm (TAAA) repair. In addition to the inherent physical disability, patients suffering paraparesis or paraplegia (P/P) have been shown to have decreased long-term survival as compared with patients without postoperative spinal dysfunction [1, 2]. Five-year survival in patients after TAAA repair is 62% for those patients without P/P versus 44% for patients with P/P (p < 0.0001) [2]. In previous reports on the surgical treatment of TAAAs, aortic dissection-present in at least 17% of TAAAs [3]—has been significantly associated with increased risk for the development of postoperative P/P [1,2,4–6]. The purpose of this retrospective study was to establish whether aortic dissection, using current techniques for TAAA repair, remains a significant variable associated with the development of postoperative paraplegia or paraparesis.
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Patients and Methods |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAppendix 1.Appendix 2.References |
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Our current operative techniques for resection and graft replacement of TAAAs have been recently described in detail (Fig 1
) [7, 8]. Regarding spinal cord protection, routine reattachment of patent segmental intercostal and lumbar arteries in the T8 to L1 region was performed whenever possible. Intercostal arteries in the region from T4 to T8 were usually ligated if they exhibited heavy retrograde bleeding when the aorta was opened. If the intercostal arteries between T8 and L1 were occluded by intimal atherosclerosis, however, the patent proximal intercostal arteries (T4 to T8) were reattached to preserve circulation. Cerebrospinal fluid drainage, intrathecal papaverine, intravenous naloxone, and somatosensory or motor evoked potential monitoring were not used in any of the patients in this series. In the most recent 388 patients, intravenous heparin (100 U/kg) was routinely administered before aortic clamping. Left atriodistal bypass (ADB) was selectively used in 116 patients (17.6%). Patients selected for ADB were those thought to be at high risk for distal ischemic complications, ie, patients with extent I or II TAAAs, aortic dissection, or Marfan's syndrome. When distal aortic perfusion was employed, distal aortic control was achieved by mid to lower descending aortic cross-clamping. The aortic segment between T5 and the celiac axis must be of an appropriate size and anatomic nature to allow safe distal cross-clamping for ADB; therefore, ADB was not used in patients with larger aneurysms (>9 cm), friable intraluminal thrombi, or severe mural calcification at this level. A Biomedicus (Minneapolis, MN) centrifugal pump, primed with normal saline solution and 1,000 units of heparin, was used in the ADB circuit. A no. 26 USCI aortic cannula (C.R. Bard, Inc, Tewksberry, MA) was used for left atrial cannulation. The left femoral artery was cannulated with an 18F to 22F cannula whenever feasible; when left femoral cannulation was not appropriate, alternative sites for distal perfusion included the right common femoral artery, the abdominal aorta, and the distal descending thoracic aorta. After partial anticoagulation, ADB was initiated at 500 mL/min. Patient core temperatures were allowed to fall 3° to 4°C to achieve mild hypothermia. A heat exchanger was not used to maintain normothermia or rewarm the patient. After aortic clamping, flows of 1,500 to 2,500 mL/min were used to achieve a distal mean pressure near 70 mm Hg. Sodium nitroprusside was frequently used in conjunction with ADB to achieve and maintain normal proximal arterial pressures, albeit at lower doses than those required without ADB. When a limited distal resection was anticipated, ADB was stopped after completion of the proximal anastomosis, the proximal aortic clamp was moved from the distal arch to the proximal graft, the distal aortic clamp was removed, and the remainder of the aneurysm was opened and replaced. With more extensive aneurysms, the distal aortic clamp was moved down in a sequential fashion to the level of the celiac axis to allow continued retrograde perfusion of the visceral and renal vessels during intercostal artery reattachment. Balloon occlusion of the distal aortic lumen during ADB was not used.
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All patients received careful preoperative neurologic examinations with documentation of lower extremity motor function. Postoperatively, lower extremity strength was evaluated by physical examination immediately upon awakening from anesthesia, and daily thereafter until discharge home. Formal evaluation by a neurologist was obtained in all patients in whom any neurologic deficit was identified. Paraparesis and paraplegia were respectively defined as lower limb weakness or flaccid paralysis, and included both immediate and delayed deficits. Unilateral deficits, unless associated with an ipsilateral upper limb deficit (ie, stroke), were also included in the P/P group.
Thirty variables—15 preoperative, 8 intraoperative, and 7 postoperative—were evaluated for their association with early mortality and lower extremity neurologic deficits (see Appendices I and II). Univariate analysis was performed using the 
2 test with the Yates correction, Fisher exact test (two-tailed), and Student's t test. Stepwise logistic regression was used for multivariate analysis. The statistical analysis was performed using the SAS statistical software (SAS Institute, Inc, Cary, NC) and Quatro Pro spreadsheet (Borland International, Inc, Scotts Valley, CA) programs for Windows 3.1.
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Results |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAppendix 1.Appendix 2.References |
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). The risk of P/P for acute versus chronic dissection was 19% versus 2.9% (p = 0.011), respectively (Table 2). On multivariate analysis, rupture (p = 0.0001) and extent II (p = 0.0001) were the only preoperative or intraoperative factors predictive of spinal cord dysfunction. The use of ADB did not result in a significant difference in overall P/P rates (Table 3). Although the ADB group required transfusion with more packed red blood cells and fresh frozen plasma than the non-ADB group, there was no increase in the need for reoperation for bleeding; additionally, there was no difference between the two groups with respect to postoperative pulmonary complications. The mean total aortic clamp time was greater for patients with chronic dissection (51.9 minutes) than for patients without dissection (39.9 minutes). Intercostal arteries were reattached in 389 of 660 patients (58.9%) overall, and in 337 of 419 (80.4%) with extent I or II TAAAs. The mean aortic clamp time in patients with extent I or II repairs in whom ADB was used was 60.9 minutes, versus 38.5 minutes in patients in whom ADB was not used (p = 0.0001). The mean intercostal ischemic time in patients with extent I or II repairs was 27.3 minutes in patients with ADB and 33.3 minutes in patients without ADB (p = 0.0001). Postoperative neurologic deficits in patients with extent I or II repairs occurred in 5.3% (18/337) of patients with intercostal artery reattachment, versus 13.4% (11/82) patients without intercostal artery reattachment (p < 0.025).
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Comment |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAppendix 1.Appendix 2.References |
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Estimated number of deficits = ((C1+ C2)/total number of patients) x 0.15 x E1,where E1= 0.1C1+ 0.2C2+ 0.05C3+ 0.02C4+ 0.01TA + (0.3 x (number acute + number dissections)), C1,2,3,4 are the number of patients in the respective Crawford TAAA extent groups, TA refers to the number of patients with descending thoracic aortic aneurysms, and "number acute" are those patients with an acute presentation, i.e., rupture, acute dissection, or acute pain.
When applied to data from several recent TAAA series, this formula was shown to have extremely strong predictive power (correlation coefficient = 0.997), supporting the importance of dissection on neurologic outcome [5]. Interestingly, based on this formula, the calculated expected number of patients with spinal cord dysfunction in our current series would be 146 (22.1%), attesting to the relatively high risk status of these patients, ie, many with extent I or II, acute presentation, or both.
Other reports have not demonstrated an association between dissection and postoperative P/P. Cox and co-workers [9] found no difference in a review of 129 patients with TAAA repairs performed between 1966 and 1991. In this Cleveland Clinic experience, there were 16 patients (12.4%) with dissection; among these, there was a 44% mortality (p = 0.433 versus no dissection) and a 35% incidence of paralysis (p = 0.192 versus no dissection). Their overall incidence of postoperative P/P was 21% (25 of 116 survivors). In a more recent experience, Kouchoukos and colleagues [10], using hypothermic bypass and circulatory arrest for intraoperative organ protection, were unable to identify a difference in the incidence of paraplegia or paraparesis among the 27 survivors of TAAA repair, 13 of whom had aortic dissection. An aggressive approach to the reattachment of intercostal arteries was used in their series. Schepens and associates [11], in a report on 50 patients with TAAAs treated from 1987 to 1993, also showed no relationship between the presence of dissection and the development of postoperative lower limb neurologic deficits. They used lumbar and intercostal artery reattachment in 93% of patients (43/50) and routinely used left heart bypass (100%). A number of the larger clinical series of TAAA repair have not stated the incidence of paraplegia/paraparesis in patients with dissection versus those with no dissection [12, 13].
An increased risk for P/P after TAAA repair in acute versus chronic dissection has been well described [2, 14]. Surgical repair of the acutely dissecting thoracoabdominal aorta represents the minority of patients in this series, and was performed only when ischemic complications developed, rupture was suspected, acute dissection was superimposed on a preexisting TAAA, or the patient remained symptomatic despite aggressive medical antihypertensive therapy. The results of the surgical treatment of patients with TAAA and acute dissection, as presented here, indicate that operations on such patients clearly carry an increased risk for the development of P/P (19%). Conditions related to acute dissection (see Table 2
), such as emergency operation, rupture, and extensive TAAA may contribute to this complication.
The benefit of reattaching patent intercostal arteries in the critical region between T11 and L1 has been demonstrated in a prospective series [15]. The current series supports the importance of intercostal artery reattachment. In this work, an aggressive posture was taken to reattach all patent available intercostal or lumbar arteries between T8 and L1; overall, 58% of patients (385/660) had intercostal arteries reattached. The great anterior radiculomedullary artery (artery of Adamkiewicz), the all-important arterial connection between the intercostal circulation and the anterior spinal artery, arises from T8 to L1 in approximately 90% of individuals and from a left-sided intercostal artery in more than 80% of cases [16, 17]. Among those patients at greatest risk for P/P (extent I and II) in this series, 80.4% (377/419) had segmental arteries reattached. In this group (extent I and II), the incidence of P/P was 5.3% (18/337) in those with intercostal artery reattachment, compared with 13.4% (11/82) in those without (p < 0.025).
Atriodistal bypass was selectively used in patients thought to be at highest risk, namely those with extent I or II TAAAs, dissection, or Marfan's syndrome. The latter situation is especially amenable to ADB due to the relatively high incidence of extent I and II TAAAs, the increased incidence of dissection, and the more time-consuming proximal anastomosis required to carefully secure a hemostatic suture line along the friable aortic wall [18]. Although chronic dissection per se does not appear to be an independent risk factor for development of P/P, the associated longer aortic clamp time (see Table 2) warrants use of ADB. By reducing intercostal artery ischemic time (see Table 3), ADB improves the safety of TAAA repair in high-risk patients, ie, those who require longer clamp times (Fig 2). Thus, a decreased incidence of P/P can be achieved despite longer aortic clamp times (Fig 3). Significant reductions in P/P by using ADB during repair of extent I and II TAAAs have been demonstrated previously [20, 21]. In the series reported here, ADB was employed in 17.6% (116/660) of the entire experience, and in the group at greatest risk for P/P (extent I and II), ADB was used in 26.5% (111/419). Of the 337 patients with extent I or II who underwent intercostal artery reattachment, 102 (30%) had ADB and 235 (70%) did not. The mean intercostal ischemic time was 27.3 minutes in the former and 33.3 minutes in the latter. By unloading the proximal circulation, ADB may yield additional benefits such as decreased cardiac and cerebrovascular complications [22]. Our data do not support concerns regarding an increase in postoperative pulmonary complications after ADB (see Table 3). Transfusion requirements may be higher with ADB, but we found no increase in risk of postoperative bleeding requiring reoperation.
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In addition to liberal reattachment of critical intercostal arteries and selective ADB, our current strategy for preventing P/P during TAAA repair involves moderate heparinization, expeditious surgical repair, passive mild hypothermia, and avoidance of perioperative hypotension. Moderate heparinization is used in all patients to reduce the risk of thrombosis of critical intercostal, collateral, and spinal cord vessels. Although surgical technique must be expeditious, meticulous suturing is required to ensure hemostatic anastomoses, thereby avoiding the need for repeat cross-clamping. Passive mild hypothermia may extend the period of safe ischemic time. Careful attention to perioperative hemodynamics with avoidance of hypotension is critical. Delayed P/P, which has accounted for 44% of P/P cases in the literature [23], is often associated with postoperative hypotension from bleeding, sepsis, hemodialysis, or cardiac complications.
Patients with chronic aortic dissection tend to be younger than those with aneurysms secondary to medial degenerative disease (see Table 2), and generally have less mural atherosclerotic debris [3, 15, 23]. This has several ramifications that we believe contribute to a lower risk of P/P for patients with TAAAs due to chronic dissection. First, with minimal debris present in the true aortic lumen, from which the intercostal arteries generally arise, the risk of embolization into these vessels is less likely. Additionally, the aortic wall in chronic dissection frequently allows suturing unencumbered by the calcified, necrotic tissue common in medial degenerative aneurysms, making the reattachment of intercostal arteries a technically easier task. A previous report [15] has demonstrated that older patients are more likely to have intercostal arteries between T11 and L1 oversewn due to technical difficulties such as surrounding calcification, and that the inability to reattach patent intercostal arteries in this region significantly increases the risk of P/P. Finally, in nondissecting TAAAs, aortic mural atherosclerotic disease often results in chronic stenosis or occlusion of many intercostal arteries. Not only does this result in fewer intercostal arteries available for reattachment (see Table 2), it also makes spinal cord arterial circulation dependent on more tenuous collateral circulation [15]. Therefore, although spinal cord ischemic time ends when the clamp is placed distal to an island of patent reattached intercostal arteries, during repair of aneurysms in patients in whom spinal cord perfusion is dependent on distal collateral blood flow, spinal cord ischemic time continues until flow is reestablished in these vessels. Staged distal aortic clamping may be beneficial by allowing continued ADB perfusion of the spinal cord via distal collaterals during intercostal artery reattachment. The association between preoperative renal artery occlusive disease and postoperative P/P (p = 0.043) lends support to the role of mural atherosclerotic disease as a risk factor for lower extremity neurologic deficits.
In conclusion, we have demonstrated that there is no longer a relationship between chronic dissection and the development of postoperative P/P in patients after TAAA repair. It appears evident that an evolution in techniques, including an aggressive approach to intercostal artery reattachment and the selective use of left ADB in high-risk patients, has contributed to this overall equalization of risk for P/P between patients with chronic dissection and nondissection.
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Appendix 1. |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAppendix 1.Appendix 2.References |
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Appendix 2. |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAppendix 1.Appendix 2.References |
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Footnotes |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAppendix 1.Appendix 2.References |
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Address reprint requests to Dr Coselli, 6560 Fannin, #1144, Houston, TX 77030.
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References |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAppendix 1.Appendix 2.References |
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