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Ann Thorac Surg 2002;73:1107-1116
© 2002 The Society of Thoracic Surgeons


J. Maxwell Chamberlain memorial paper

Morbidity and mortality after extent II thoracoabdominal aortic aneurysm repair

Joseph S. Coselli, MD*a, Scott A. LeMaire, MDa, Lori D. Conklin, MDa, Cüneyt Köksoy, MDa, Zachary C. Schmittling, 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, The Michael E. DeBakey Department of Surgery, Division of Cardiothoracic Surgery, Baylor College of Medicine, 6560 Fannin St, Suite 1100, Houston, TX 77030 USA
e-mail: jcoselli{at}bcm.tmc.edu

Presented at the Thirty-seventh Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 29–31, 2001.

Abstract

Background. Surgical repair of Crawford extent II thoracoabdominal aortic aneurysms (TAAAs) carries substantial risk for morbidity and mortality. The purpose of this study was to analyze the results of a large consecutive series of extent II TAAA repairs and identify factors that influence morbidity and survival.

Methods. Of 1,415 consecutive patients who underwent TAAA operations over a 13-year period, 442 (31.2%) had extent II repairs. Data from a prospectively maintained database were analyzed to determine which factors were associated with death and major complications.

Results. The operative mortality was 10.0% (44 patients). Postoperative complications included paraplegia/paraparesis in 33 patients (7.5%), pulmonary complications in 158 (35.7%), and renal failure in 69 (15.9%). Multivariable analysis revealed that renal insufficiency (odds ratio [OR] 2.6), increasing age (OR 1.1/year), and increasing red blood cell transfusion requirements (OR 1.1/U) were predictors for mortality; renal insufficiency (OR 2.8) and peptic ulcer disease (OR 9.3) were predictors of renal failure; and rupture (OR 6.3) was a predictor of paraplegia. Left heart bypass was an independent protective factor against paraplegia (OR 0.4).

Conclusions. This contemporary experience demonstrates acceptable levels of morbidity and mortality in this high-risk group. Left heart bypass was found to provide protection against paraplegia in these patients.

Throughout the history of thoracoabdominal aortic aneurysm (TAAA) repair—from the first successful repairs reported by Etheridge and Rob in 1955, through Crawford’s monumental experience with 1,509 patients, and into the current era—surgical teams have tried to reduce the mortality and morbidity associated with this demanding operation [14]. Although these efforts have led to improved outcomes, extent II TAAA repairs, which generally involve the entire thoracoabdominal segment (Fig 1), continue to carry substantial risk. Over the past decade, extent II TAAA repairs have consistently been associated with the highest levels of mortality (13% to 42%), paraplegia (up to 32%), and renal failure (16% to 26%) [515]. Our recent analysis of elective TAAA operations in 1,108 patients identified extent II repair as an independent predictor of operative mortality [16]. The purpose of the current study was to analyze the results of a large consecutive series of extent II TAAA repairs and identify factors that influence morbidity and survival in this high-risk group.



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Fig 1. (A) Preoperative drawing and computed tomography scan of a patient with an extent II thoracoabdominal aortic aneurysm. (B) Postoperative drawing after surgical repair.

 
Patients and methods

Patients
Between January 11, 1986, and December 31, 1999, 1,415 consecutive patients underwent graft repair of TAAAs by the senior author (J.S.C.). All aneurysms were categorized based on Crawford’s classification [17]. Extent II TAAA repairs, which began in the upper descending thoracic aorta and extended into the lower infrarenal abdominal aorta, were performed in 442 (31.2%) patients; this group was the focus of the following analysis. Throughout the 14-year experience, data were abstracted from patient records at the time of hospital discharge and entered into a prospectively maintained database.

Preoperative variables
Thirty-one preoperative and operative variables were selected for univariate analysis of their association with complications. The preoperative characteristics of the 442 patients are detailed in Table 1. Dissection was classified as acute if operation was required within 14 days of the onset of pain. Patients were considered symptomatic when any symptom (acute or chronic, severe or mild) related to the aneurysm was present, including pain, hoarseness, and dysphagia. Acute presentations were defined as acute pain, rupture, contained rupture, and complicated acute dissection [18]. Renal insufficiency was defined as serum creatinine exceeding 3.0 mg/dL or need for hemodialysis. Chronic obstructive lung disease was defined as the need for pharmacologic therapy for the treatment of chronic pulmonary compromise or an forced expiratory volume in 1 second (FEV1) less than 75% of predicted value. Cerebrovascular disease was defined as a history of transient ischemic attack or stroke, documented carotid stenosis more than 50%, or a history of carotid endarterectomy or other cerebrovascular operation. Coronary artery disease was defined as documented coronary stenosis more than 50% or a history of angina, myocardial infarction, or coronary artery angioplasty or bypass. Hypertension was defined as a history of high blood pressure (exceeding 140/90 mm Hg) or the need for antihypertensive medication.


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Table 1. Preoperative and Intraoperative Characteristics of 442 Patients Undergoing Repair of Extent II Thoracoabdominal Aortic Aneurysm

 
Surgical technique and operative variables
Our current approach to extent II TAAA repair has been recently described in detail (Table 2) [1921]. Although the surgical technique has evolved substantially during the 14-year period, several aspects have remained consistent. In all cases, the aorta was exposed using a left thoracoabdominal incision with circumferential division of the diaphragm. Moderate systemic heparinization (1 mg/kg), mild permissive hypothermia (32°C to 34°C, nasopharyngeal), and aggressive reattachment of critical segmental arteries (T8-L1) were used routinely throughout the study period. 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. To reverse cooling at operative completion, the field was irrigated with warm saline. No other means of rewarming the patient were used during the operation. Warm air blankets were used postoperatively. Neither sensory- evoked nor motor-evoked potential monitoring was used.


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Table 2. Current Strategy for Spinal Cord, Visceral, and Renal Protection During Repair of Extent II Thoracoabdominal Aortic Aneurysm

 
We used left heart bypass (LHB) with a centrifugal pump in 286 patients (64.7%). The closed LHB circuit did not include a cardiotomy reservoir, an oxygenator, or a warming device. The drainage cannula was inserted into the left atrium (usually through the left inferior pulmonary vein) and the return cannula was inserted into the left common femoral artery or, more commonly, the aneurysmal mid-descending thoracic aorta; we favor the latter insertion site because it eliminates the complications associated with femoral artery cannulation. In most cases, LHB was used only during the proximal anastomosis. After completion of the proximal anastomosis, LHB was discontinued and the aortic cannula and distal aortic clamp were removed. After opening the remainder of the aneurysm to its distal extent, balloon cannulas connected to the LHB circuit were inserted into the origins of the celiac axis, superior mesenteric artery, and both renal arteries; selective renal and visceral perfusion was then performed by redirecting pump flow into the balloon cannulas. After reattaching the intercostal, visceral, and renal vessels, the balloon cannulas were removed.

Operative variables are presented in Table 1. An emergent repair was defined as operation performed as soon as possible because of immediate threat to life or organ [22]. Cerebral spinal fluid drainage, a recently added adjunct, was used in 44 patients (10%) [23]. In 8 patients, profound hypothermic circulatory arrest was required because proximal aortic clamping could not be achieved due to aneurysm size or rupture. Left heart bypass times included only the period of distal aortic perfusion; they did not include the period of selective visceral and renal perfusion from the LHB circuit after removal of the aortic cannula. Therefore, the LHB times reflect the time required to complete the proximal anastomosis. Visceral, renal, and intercostal ischemic times were each defined as the time between initial aortic clamping (or circulatory arrest) and restoration of physiologic flow to the respective region; the ischemic times included any period of nonphysiologic perfusion, that is, LHB and selective visceral and renal perfusion through balloon catheters.

Outcome variables and statistical analysis
Operative mortality was defined as death occurring within 30 days or during the initial hospitalization [24]. All patients with postoperative neurologic deficits involving the lower extremities were included in the paraplegia category, regardless of whether the deficit was weakness (paraparesis) or paralysis, immediate or delayed, or transient or permanent. This group included patients with unilateral lower extremity deficits, unless an associated deficit involving the ipsilateral upper extremity (indicating a stroke) was present. Strokes were defined as any new clinically evident brain injury present after operation, including deficits that were focal or global, transient or permanent. Renal failure was defined as an increase in serum creatinine concentration to more than 3.0 mg/dL or the need to initiate hemodialysis. Pulmonary complications were defined as ventilator support exceeding 48 hours, reintubation, adult respiratory distress syndrome, atelectasis requiring bronchoscopy, chylothorax, prolonged air leak, pleural effusion requiring drainage, pneumonia, or pneumothorax requiring evacuation. Cardiac complications included myocardial infarction, dysrhythmias, persistent low cardiac output requiring inotropic support or intraaortic balloon placement, cardiac tamponade requiring drainage, and congestive heart failure. A composite end point, termed adverse outcome, was defined as the occurrence of any of the following: death within 30 days, death before discharge from the hospital, paraplegia, paraparesis, stroke, or acute renal failure requiring dialysis [25].

The statistical analyses were performed using the SAS system for Windows (release 6.12; SAS Institute, Inc, Cary, NC). The preoperative and intraoperative variables listed in Table 1 were analyzed for their association with operative mortality, paraplegia, renal failure, hemodialysis, and adverse outcome. Categorical variables were analyzed using the {chi}2 or Fisher’s exact test. Continuous data are reported as mean ± standard deviation and were analyzed using Student’s t test. Risk factors that emerged with significance levels below 0.25 on univariate analysis were entered into the multivariable analysis using stepwise logistic regression. Actuarial survival was estimated using the Kaplan-Meier method; survival curves were compared using the log-rank test. Associations with outcomes were considered statistically significant when p values were less than 0.05.

Results

Overall operative results
There were 44 operative deaths (10.0%). Postoperative complications included paraplegia in 33 patients (7.5%); renal failure in 69 patients (15.9%), with 37 patients (8.5%) requiring hemodialysis; pulmonary complications in 158 patients (35.7%); bleeding requiring reoperation in 17 patients (3.8%); cardiac complications in 69 patients (15.6%); stroke in 11 patients (2.5%); and wound dehiscence in 31 patients (7.0%).

Mortality
There were no intraoperative deaths. All 44 operative deaths occurred during the initial hospitalization. Twenty-eight patients (6.3%) died within 30 days of operation. Univariate analysis revealed the following factors to be associated with operative death: increasing age (p < 0.001), renal arterial occlusive disease (p = 0.003), preoperative renal insufficiency (p = 0.001), and preoperative hemodialysis (p = 0.036). Patients who had intercostal arteries reattached had a lower operative mortality (33 of 349 patients, 9.5%) than those without intercostal artery reattachment (11 of 49, 22.4%; p = 0.036). Previous aortic aneurysm repairs were also associated with a reduction in operative mortality (p = 0.015 for prior aneurysm repair and p = 0.027 for prior thoracic aneurysm repair). Patients with chronic dissection had a lower mortality than those with acute dissection or medial degenerative disease (Table 3); this difference did not reach statistical significance. On multivariable analysis, preoperative renal insufficiency, increasing red blood cell transfusion requirements, and increasing age were the only three variables predictive of operative mortality (Table 4). The causes of operative mortality are listed in Table 5.


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Table 3. Impact of Aneurysm Cause on Outcome After Repair of Extent II Thoracoabdominal Aortic Aneurysm

 

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Table 4. Results of Multivariable Analyses for Operative Mortality, Paraplegia, Renal Failure, and Adverse Outcome

 

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Table 5. Causes of Operative Mortality After Repair of Extent II Thoracoabdominal Aortic Aneurysm

 
Figure 2 presents the Kaplan-Meier curves for cumulative survival rates for patients who underwent extent II TAAA repairs versus those who underwent extent I, III, or IV repairs. The actuarial 5-year survival rate for extent II TAAA repair is 66.0%, which is significantly lower than the survival after the other extents (75.4%, p = 0.045).



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Fig 2. Kaplan-Meier curves comparing actuarial survival rates between patients who underwent extent II thoracoabdominal aortic aneurysm repair and those who underwent extent I, III, or IV repair (p = 0.045).

 
Paraplegia
The incidence of paraplegia was 7.5% (33 of 439, excludes 3 patients with preoperative paraplegia). Univariate analysis revealed that acute presentation (p = 0.002), rupture (p < 0.001), emergent repair (p = 0.002), and renal arterial occlusive disease (p = 0.049) were associated with paraplegia. Dissection did not increase the incidence of paraplegia (Table 3). The impact of LHB on spinal cord protection was further evaluated by comparing the 286 patients in whom this adjunct was used with the 156 patients who did not have LHB. The group in whom LHB was used had a lower paraplegia rate (13 of 286 [4.5%] with LHB versus 20 of 153 [13.1%] without LHB, p = 0.002) despite having significantly longer aortic clamp times (65.5 ± 15.8 min with LHB versus 50.6 ± 14.2 min without LHB; p < 0.0001). Previous thoracic aortic aneurysm repair was also associated with a reduced incidence of spinal cord deficits. The independent predictors of paraplegia based on multivariable analysis were rupture and operation without LHB (Table 4). Patients with rupture were 6.3 times more likely to develop paraplegia than those without rupture. Patients who had undergone previous thoracic aortic aneurysm repair were at lower risk for paraplegia.

Renal failure
Renal failure occurred in 69 patients (15.9%, excludes 8 patients receiving hemodialysis preoperatively). Factors associated with renal failure on univariate analysis included the following: increasing age (p = 0.057), rupture (p = 0.026), renal arterial occlusive disease (p = 0.041), renal insufficiency (p = 0.051), and peptic ulcer disease (p = 0.014). Both renal insufficiency and peptic ulcer disease were predictive of renal failure in the multivariable analysis (Table 4).

Thirty-seven (54%) of the patients with renal failure required hemodialysis. Univariate analysis revealed that increasing age (p = 0.054), renal insufficiency (p = 0.015), and renal artery occlusive disease (p = 0.059) were associated with the need for postoperative dialysis. Patients with TAAAs due to medial degenerative disease had a significantly higher incidence of renal failure requiring dialysis than those with acute or chronic dissection (Table 3). Previous aortic aneurysm repair and thoracic aortic aneurysm repair were both associated with a lower incidence of hemodialysis (p = 0.055 and 0.014, respectively); thoracic aortic aneurysm repair was also identified as a protective factor by multivariable analysis. Multivariable analysis revealed that renal insufficiency, increasing red blood cell transfusion requirements, and increasing aortic clamp times were predictive of the need for dialysis (Table 4); patients with chronic dissection were at lower risk for dialysis than those with medial degenerative disease.

Adverse outcome
Ninety-six patients (21.7%) had an adverse outcome, as defined previously [25]. On univariate analysis, the factors associated with this composite end point included increasing age (p = 0.005), symptomatic aneurysms (p = 0.044), acute presentation (p = 0.007), rupture (p < 0.001), emergency operation (p = 0.012), renal arterial occlusive disease (p = 0.001), and renal insufficiency (p = 0.001). The independent predictors from multivariable analysis were rupture, renal insufficiency, renal arterial occlusive disease, and increasing aortic clamp times (Table 4). Patients who had a previous thoracic aortic aneurysm repair were less likely to have an adverse outcome (OR 0.48).

Aortic dissection versus medial degenerative disease
Patients with aortic dissection (acute and chronic) were compared with those with medial degenerative disease (Table 3). During TAAA repair, patients with dissection had longer ischemic times and were more likely to have LHB and intercostal artery reattachment. In contrast, patients with medial degenerative disease were older and had a significantly higher prevalence of renal insufficiency, chronic lung disease, and atherosclerotic occlusive disease involving the coronary, carotid, cerebral, and renal arteries. Operative mortality, renal failure requiring dialysis, and cardiac complications were more common in patients with medial degenerative disease. The incidence of paraplegia was similar in the two groups, despite more emergent repairs and longer ischemic times in the dissection group.

Emergent repairs
Compared with patients undergoing nonemergent repair, those requiring emergency surgery were older (68.9 ± 9.5 years versus 63.7 ± 12.7 years, p = 0.002), had a higher prevalence of chronic lung disease (22 of 42 [52.4%] versus 135 of 400 [33.8%], p = 0.026), and were less likely to have had a previous aortic aneurysm repair (7 of 42 [16.7%] versus 185 of 400 [46.3%], p = 0.001). Intercostal artery reattachment was more common in the nonemergent cases (351 of 400 [87.8%] versus 31 of 42 [73.8%], p = 0.023). Emergent repairs were associated with a higher incidence of paraplegia (9 of 41 [22.0%] versus 24 of 398 [6.0%], p = 0.002) and adverse outcome (16 of 42 [38.1%] versus 80 of 400 [20.0%], p = 0.012).

Comment

Patients undergoing extent II TAAA repairs are often marginal operative candidates because of their advanced age and coexistent comorbidities, including cardiac, pulmonary, and renal disease. Over the last 20 years, early mortality after extent II repairs has ranged from 13% to 42% (Table 6) [510, 14]. Without surgical repair, however, the outlook is grim, with less than 35% of patients surviving for more than 2 years after diagnosis [26].


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Table 6. Mortality in Contemporary Series of Extent II Thoracoabdominal Aortic Aneurysm Repair

 
Paraplegia and paraparesis remain a major cause of morbidity after extent II TAAA repair and often contribute to early mortality. The multifactorial nature of spinal cord ischemia has led to difficulty in preventing this complication. Despite the use of several different adjuncts, paraplegia continues to occur in up to 32% of reported cases (Table 7) [57, 9, 10, 1315]. Recent advances—especially cerebrospinal fluid (CSF) drainage and LHB—have led to improved spinal cord protection and a reduction in the incidence of paraplegia.


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Table 7. Paraplegia and Paraparesis in Contemporary Series of Extent II Thoracoabdominal Aortic Aneurysm Repairs

 
Over the last decade, several groups have reported results that suggest CSF drainage is beneficial in extensive TAAA operation [18, 2731]. In these series, patients receiving CSF drainage were less likely to experience postoperative neurologic deficits. However, these studies were inconclusive in determining if CSF drainage was responsible for the improved outcome, because patients undergoing CSF drainage were simultaneously treated with other adjuncts, such as permissive hypothermia, naloxone, thiopental, distal aortic perfusion, and intrathecal papaverine. Our recent randomized clinical trial focused solely on the impact of CSF drainage in preventing neurologic deficits after extensive TAAA repair [23]. The control and treatment groups were well matched with respect to risk factors and a consistent surgical strategy was used in both groups. The incidence of paraplegia was 12% (9 of 74 patients) in the control group and 3% (2 of 82) in the CSF drainage group (p = 0.03). This finding corresponded to an 80% reduction in the relative risk of deficits. Based on these data, we currently use perioperative CSF drainage for all patients undergoing elective extent I or II TAAA repairs. We also use CSF drainage in the setting of ruptured TAAAs, provided the patient is hemodynamically stable enough to allow the time for catheter placement.

Recent retrospective clinical studies have also supported the use of LHB as a neuroprotective adjunct [9, 32]. However, these reports combined the use of LHB with CSF drainage, again making it difficult to attribute benefits to either variable alone. Our recent retrospective analysis examined patients undergoing extent I and II TAAA repairs with versus without LHB; during the period studied, intraoperative CSF drainage was not used in either group. Although patients in the LHB group had longer mean aortic clamp times, their mean intercostal ischemic times were shorter. Left heart bypass reduced the incidence of paraplegia from 13.1% (18 of 137) to 4.8% (9 of 189, p = 0.007) in 326 patients with extent II TAAA repairs (both elective and emergent cases) [33]. In a subsequent analysis of LHB use in 339 elective extent II repairs, this adjunct did not significantly reduce the incidence of paraplegia or paraparesis: the incidence of spinal cord deficit was 5.3% (11 of 209) with LHB and 7.7% (10 of 130) without LHB (p = 0.48) [25]. The similar paraplegia rates, however, occurred despite the substantially longer aortic clamp time in the LHB group (67.8 ± 15.8 min versus 50.9 ± 14.1 min without LHB, p < 0.0001), again supporting the protective benefit of this strategy. Both univariate and multivariable analyses of the current series confirmed the benefits of LHB during extent II TAAA repairs (Table 4). While all of our recent retrospective analyses suggest that LHB allows the aorta to be clamped safely for a longer time by reducing intercostal ischemic time, the benefits have yet to be confirmed by a randomized clinical trial.

Despite improvements in surgical techniques and postoperative care, renal failure has remained a significant and often lethal complication after TAAA repair. In an attempt to alleviate postoperative renal failure and its associated mortality, several techniques and intraoperative strategies have been used, including intraoperative administration of diuretics, minimization of ischemic times, renal hypothermia, and renal artery perfusion with oxygenated blood. However, despite the use of adjuvant techniques, the incidence of kidney failure after extent II TAAA repair still ranges from 16% to 26% (Table 8) [812].


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Table 8. Postoperative Renal Failure in Contemporary Series of Extent II Thoracoabdominal Aortic Aneurysm Repair

 
In the current series, peptic ulcer disease was an independent predictor of postoperative renal failure. This association may be due to the nephrotoxic effects of histamine-2 blockers [34, 35]. Furthermore, patients with preexisting peptic ulcer disease are more susceptible to postoperative gastrointestinal bleeding, which may lead to renal complications.

We recently conducted a randomized clinical trial comparing cold crystalloid versus normothermic blood renal perfusion during extent II TAAA repairs [36]. Renal dysfunction—defined as an elevation in serum creatinine beyond 50% above baseline—occurred in 63% (10 of 16 patients) in the normothermic blood group versus only 21% (3 of 14) in the cold crystalloid group (p = 0.03). Reduced kidney temperature was associated with renal protection and the use of cold crystalloid was an independent predictor of preserved renal function. Therefore, we currently use cold crystalloid renal artery perfusion in all patients undergoing extent II TAAA repairs.

Pulmonary complications remain the most common source of morbidity associated with TAAA repair. This entity remains difficult to study secondary to the lack of a standardized set of defining parameters. The cause of respiratory failure is multifactorial and includes the extensive incision required, paralysis of the left hemidiaphragm, high transfusion requirements, the high frequency of preoperative lung disease, and surgical trauma to the left lung. Limited baseline pulmonary reserve has been associated with this complication; therefore, optimizing pulmonary function before operation (eg, smoking cessation and bronchodilator therapy for at least 2 weeks) may improve outcome [37]. However, preoperative pulmonary optimization is often not feasible because many of these patients require urgent or emergent operation. In patients with severe pulmonary disease, it is important to preserve the phrenic nerve. Circumferential division of the diaphragm avoids nerve injury while providing excellent exposure of the aorta. Engle and associates [38] have advocated a diaphragm-sparing technique that preserves an island of muscular tissue.

As populations continue to age, it is becoming increasingly common to perform major cardiovascular operations on older patients. This study confirms that TAAA repair in the elderly is associated with increased mortality and morbidity. The high prevalence of comorbid factors coupled with the fragility of older individuals contributes heavily to the development of complications. Our recent evaluation of TAAA repair in octogenarians suggested that, even though these patients were more likely to develop pulmonary, cardiac, and renal complications, outcomes remain acceptable and age alone should not exclude a patient from undergoing TAAA repair [39]. The dismal natural history of nonrepaired TAAAs further supports an aggressive surgical approach in elderly patients with reasonable physiologic reserve. In 1986, Crawford and DeNatale [26] reported a 5-year actuarial survival rate of only 19.2% for patients with untreated degenerative thoracic aortic aneurysms. In contrast, in our 442 patients treated surgically, the 5-year estimated survival rate was 66% ± 5.5%.

Not surprisingly, our patients who required emergent repairs were more likely to have adverse outcomes. Patients presenting with rupture are typically sicker and are unable to undergo a thorough preoperative evaluation of their cardiac, pulmonary, and cerebrovascular systems. The operations can also be more technically challenging secondary to friable aortic tissue, obscured planes of dissection, and perioperative coagulopathies.

When comparing patients with medial degenerative disease to those with dissection, patients with medial degenerative disease have a higher incidence of adverse outcomes, including renal failure requiring hemodialysis and operative mortality (Table 3). Medial degenerative disease is more commonly found in older patients with extensive arteriosclerosis of the thoracic and abdominal aorta, renal arteries, and coronary arteries. These patients may have such severe atherosclerotic disease in the thoracoabdominal aorta that—even after an aortic wall endarterectomy—no suitable intercostal arteries are available for reattachment (Fig 1). Similarly, coronary artery disease and renal artery stenosis contribute to postoperative sequelae, including myocardial infarction, dysrhythmias, and renal failure.

Patients with thoracic aneurysms have a propensity to develop aortic aneurysms in other locations. Crawford and Cohen [40] reported that multiple aneurysms developed in 60% of patients previously treated for aneurysms involving the ascending, transverse arch, or descending thoracic aorta. In the present study, recurrent thoracic aneurysms were present in 27% of patients; those patients were less likely to require postoperative hemodialysis or experience an adverse outcome. We have previously demonstrated that patients who had prior thoracic aortic aneurysm repairs had favorable outcomes when compared to those without prior repair [41]. The primary explanations for the improved outcome in patients with prior thoracic aortic repairs include their younger age and lower prevalence of comorbid disease. Also, patients who have had a previous repair undergo more careful medical follow-up after the initial operation, often resulting in a better preoperative condition and earlier intervention.

Although extent II TAAA repairs have consistently been associated with high levels of mortality, paraplegia, and renal failure, the actuarial survival rates in patients treated surgically remains superior to those managed medically. This contemporary experience demonstrates acceptable levels of morbidity and mortality and supports the use of LHB as an adjunct to reduce postoperative paraplegia. Building on the accomplishments from the past 40 years, we must continue to look to the future for the development of new and novel treatment strategies that will further decrease the complications associated with this high-risk operation.

Acknowledgments

The authors gratefully acknowledge Autumn Jamison for providing database management, statistical analysis, and invaluable assistance with abstract and manuscript preparation. Ada Kyriasoglou provided additional assistance with patient follow-up.

Discussion

DR R. SCOTT MITCHELL (Stanford, CA): Doctor Matloff, Dr Murray, members and guests. This is a superb article and an excellent presentation from Dr Coselli, appropriately selected as the J. Maxwell Chamberlain paper. Doctor Coselli and his colleagues have continued in the tradition of Dr Crawford to operate on a huge number of patients and then educate us as to which items in their complex management of these patients are helpful. They have systematically established the positive contributions toward survival and protective effects on paraplegia afforded by left heart bypass, intercostal artery perfusion, and cerebrospinal fluid drainage. We are profoundly in their debt for these scientific contributions as we strive to produce the best clinical outcomes for these complex patients.

The article answers many questions, but raises still more. First, one cannot fail to be impressed by the relationship between renal artery occlusive disease and any adverse outcome. I can understand its negative impact on survival and renal failure, but I am curious if you have any insight to explain its relationship to paraplegia. Second, you note the protective effect of cold crystalloid solution on postoperative renal function, and I wonder if you have considered actually using cold blood renal perfusate. And lastly, again, focusing on the importance of renal function, have you had any experience with the selective dopamine agonists such as fenoldopam to try and improve your clinical results?

I congratulate Dr Coselli and his colleagues on a terrific presentation and a critical analysis of an immensely complex data set, and I thank the Society for the privilege of this discussion.

DR NICHOLAS T. KOUCHOUKOS (St. Louis, MO): Doctor Coselli, these are truly outstanding results and you and your colleagues are to be commended for your achievements. You have used a variety of adjuncts during the study interval to protect the spinal cord and the kidneys. Several emerged as important and significant predictors of improved outcome. I note, however, that drainage of cerebrospinal fluid for spinal cord protection was not an independent predictor in your overall analysis. What are the adjuncts that you currently use and that you believe are most important for reducing the frequency of both spinal cord ischemic injury and renal failure? Do you use hypothermic cardiopulmonary bypass and circulatory arrest for any of your patients, and are they included in this analysis? We have found that with the use of this technique, our incidence of renal failure, paralysis, and multisystem organ failure is low, and we do not use any of the adjuncts that you have described, including cerebrospinal fluid drainage or direct perfusion of the visceral and renal arteries.

DR AHMAD RAJAII KHORASANI (Newark, NJ): It is an honor to congratulate Dr Coselli for his impressive work. In 1986, when this meeting was held in Baltimore, another impressive paper was presented from your institution, which I discussed. In that discussion, I introduced the concept of perfusion and reimplantation of the intercostal arteries as a superior alternative to the available techniques for prevention of paraplegia during descending aortic operation. The concept is based on the fact that the spinal cord is really not a distal organ, and the expectation that distal aortic perfusion will always supply the spinal cord (either directly via a distally located Adamkiewicz artery or indirectly through the collaterals) is simply unrealistic. Furthermore, the work of Drs Cooley and Crawford had taught us that reimplantation of the excluded intercostals by itself did not change the incidence of paraplegia. So the logical next step was to perfuse the excluded intercostals and reimplant these perfused vessels without interruption of their blood flow, a technique that I have been using since 1986. So my questions are, first, have you ever tried intercostal/lumbar perfusion?

Second, when you decide to reimplant intercostal arteries, on what basis do you choose a given set of intercostal arteries over the others? The anatomic studies have shown that the position of crucial intercostal/lumbar arteries varies, and we really do not know which intercostal/lumbar artery is critical in terms of contribution to the anterior spinal artery.

Again, thank you for this opportunity.

DR COSELLI: Thank you very much. First of all, I would like to thank Dr Mitchell for his kind comments. He raises a question that we struggle with, and that is, why renal artery disease preoperatively is a marker for the incidence postoperatively of paraplegia and paraparesis; and I am not certain of the answer. I can only speculate that renal artery occlusive disease in and of itself is a marker for diffuse atherosclerosis of the thoracoabdominal aorta and the number of intercostal arteries is reduced when that particular entity is present. It is a variable that we measure, and the number of intercostal arteries was not specifically analyzed in this particular work. Consequently, I think that renal artery occlusive disease stands out as a marker rather than as a specific variable in and of itself directly related.

We have used a cold saline perfusion of the kidneys and found it to be protective in these particular aneurysms, and Dr Mitchell brings up the question of whether or not to use cold blood. You can run only so many prospective randomized trials at one time, and that study is on our docket.

We have not had any experience with dopamine agonists yet. That class of drug, however, may be beneficial and warrants research both in the laboratory and in the operating room.

Doctor Kouchoukos’s comments are very much appreciated. Our current efforts to reduce the incidence of paraplegia and renal failure have taken a different tact from his work, however, using hypothermic circulatory arrest. As I presented in the article, our current approach in these extent II aneurysms is to use left heart bypass during most of the first portion of the operation, to perfuse the visceral vessels with blood from the left atrium during the latter part of the operation, and to use cold lactated Ringer’s solution perfusion of the kidneys for their protection. We use cerebrospinal fluid drainage routinely in these patients. Although I have used circulatory arrest to some degree in patients with descending thoracic aortic aneurysms extending into the transverse aortic arch, with the extent II thoracoabdominal aortic aneurysms, circulatory arrest comprises fewer than a handful of cases of our own work.

With regard to the perfusion of intercostal arteries during reconstruction, other than left heart bypass, intercostal perfusion is not a technique that we have used. We admit that the anatomy of the arterial circulation to the spinal cord with regard to the intercostal arteries is extremely variable among individuals with an overlay of pathology on top of that; but we focus on those intercostal arteries that we feel are widely patent between T7 and T8 down to T12 and L1.

And, again, thank you very much.

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