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Ann Thorac Surg 2005;80:2173-2179
© 2005 The Society of Thoracic Surgeons

Original article: Cardiovascular

Evolution of Risk for Neurologic Deficit After Descending and Thoracoabdominal Aortic Repair

Hazim J. Safi, MD * , Anthony L. Estrera, MD, Charles C. Miller, PhD, Tam T. Huynh, MD, Eyal E. Porat, MD, Ali Azizzadeh, MD, Riad Meada, MD, Jennifer S. Goodrick, RN

Department of Cardiothoracic and Vascular Surgery, The University of Texas at Houston Medical School, Memorial Hermann Hospital, Houston, Texas

Accepted for publication May 17, 2005.

* Address correspondence to Dr Safi, Department of Cardiothoracic and Vascular Surgery, The University of Texas Health Science Center, Memorial Hermann Hospital, 6410 Fannin, Suite 450, Houston, TX 77030 (Email: hazim.j.safi{at}uth.tmc.edu).

Presented at the Forty-first Annual Meeting of The Society of Thoracic Surgeons, Tampa, FL, Jan 24–26, 2005.


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 
BACKGROUND: Cross-clamp time has been reported to correlate with risk of neurologic deficit after thoracoabdominal aortic aneurysm repair. Introduction of cerebrospinal fluid drainage and distal aortic perfusion (adjunct) has greatly reduced the incidence of neurologic deficit. We reevaluated the effect of cross-clamp time before and after introduction of adjunct during a 13-year period.

METHODS: Between 1991 and 2004, we repaired 1,106 thoracic and thoracoabdominal aortic aneurysms. Four hundred one patients were female and 705 were male (median age, 67 years). Selective use of adjunct was begun in late 1992, with its routine use by 1993.

RESULTS: Aortic cross-clamp times have increased significantly (34 seconds/year; p < 0.0001) since 1991. Despite this increase in cross-clamp time, neurologic deficit rates have declined from the first to the fourth quartile (p < 0.02). This decrease in neurologic deficit is most pronounced with the extent II thoracoabdominal aortic aneurysms (21.1% to 3.3%). The use of the adjunct increased the cross-clamp time by a mean of 12 minutes (p < 0.0001), but was associated with a significant protective effect against neurologic deficit (odds ratio = 0.4; p < 0.0002). Although other previously established risk factors remained significantly associated with neurologic deficit, cross-clamp time is no longer significant.

CONCLUSIONS: Adjunct significantly reduced the risk of neurologic deficit, despite increasing cross-clamp time. The use of the adjunct appears to blunt the effect of the cross-clamp time and may provide the surgeon the ability to operate without being hurried. Because cross-clamp time has been effectively eliminated as a risk factor with the use of the adjunct, using this variable to construct risk models becomes irrelevant in our experience.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 
Neurologic deficit (paraplegia and paraparesis) remains a devastating complication associated with repairs of the descending thoracic and thoracoabdominal aorta. Various methods to protect the spinal cord have been developed since the 1960s with varying success, including passive shunts, distal aortic perfusion (left heart bypass), total cardiopulmonary bypass, profound hypothermic circulatory arrest, spinal cord cooling, and pharmacological agents [1–7]. Despite the development of these techniques, the "clamp and sew" approach remained the predominant method for these complex aneurysm repairs through the 1980s. At the end of that era, the overall incidence of neurologic deficit remained significant at 16%, with an incidence of 31% in the high-risk extent II thoracoabdominal aortic aneurysm (TAAA) repair [1]. It was established that duration of aortic cross-clamp occlusion, aneurysm extent, rupture, increasing age, presence of concurrent proximal aneurysm, and renal dysfunction were associated with early neurologic deficit. Moreover, a cross-clamp time of greater than 45 minutes in a patient undergoing repair of an extent II TAAA was associated with 50% incidence of neurologic deficit [1].

Since 1992 we have used the adjunct that has included cerebrospinal fluid drainage, distal aortic perfusion, and passive moderate hypothermia with good success. The adaptation of the adjunct was the result of a prospective study that demonstrated a benefit in patients with extent I and II TAAA repairs [8]. Subsequent analyses of our experience continue to demonstrate improved results regarding neurologic deficit with use of the adjunct [9, 10]. The purpose of this report is to analyze the effect of the adjunct on the incidence of neurologic deficit during repairs of the descending thoracic and thoracoabdominal aorta and examine its relationship to aortic cross-clamp time.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Discussion
 Acknowledgments
 References
 
Between 1991 and 2004, we repaired 1,106 thoracoabdominal and descending thoracic aortic aneurysms. Seven hundred five were men and 401 were women. The median age was 67 years (range, 8 to 92 years). The extent of the aneurysms was classified as previously described (Fig 1). For statistical analysis, the period of the study was divided into quartiles: quartile 1 (February 1991 to January 1995), quartile 2 (February 1995 to May 1998), quartile 3 (June 1998 to July 2001), and quartile 4 (August 2001 to September 2004).



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  		Fig 1. Classification of thoracoabdominal aortic aneurysms. Extent I, distal to the left subclavian artery to above the renal arteries. Extent II, distal to the left subclavian artery to below the renal arteries; this is the most extensive type of aneurysm and the only extent that is still associated with risk of paraplegia, with the use of adjunct distal aortic perfusion, cerebrospinal fluid, and moderate hypothermia. Extent III, from the sixth intercostal space to below the renal arteries. Extent IV, from the twelfth intercostal space to the iliac bifurcation (total abdominal aortic aneurysm). Extent V, below the sixth intercostal space to just above the renal arteries.

 
Outcome Variables
Preoperative characteristics analyzed in this study include age, gender, hypertension, cerebrovascular disease, chronic obstructive pulmonary disease, acute dissection, chronic dissection, and aneurysm extent. Intraoperative data included aortic cross-clamp time, intercostal artery reattachment, distal aortic perfusion time (pump time), and the adjunct used (Table 1). Adjunct use referred to the combined use of distal aortic perfusion and cerebrospinal fluid drainage with moderate passive hypothermia. Postoperative neurologic deficit was defined as paraplegia or paraparesis related to spinal cord ischemia or infarction. Immediate neurologic deficit refers to paraplegia or paraparesis observed when the patient was awakening from anesthesia. Associated aortic dissection was denoted as acute when the surgery was performed within 14 days and otherwise chronic. Current smoking was tobacco use within 2 weeks of surgery. Cerebrovascular disease was defined as any previous history of cerebrovascular accident or having undergone intervention for carotid artery disease. Preoperative renal dysfunction was defined as having a serum creatinine greater than 2.0 mg/dL, a previous history of renal failure of insufficiency, or being on active dialysis.


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  		Table 1. Risk Factors for Early Neurologic Deficit
 
Our operative technique for repairing thoracoabdominal and descending thoracic aortic aneurysms has been described previously [9, 10]. In brief, since September 1992 we began to use the adjunct distal aortic perfusion, cerebrospinal fluid drainage, and moderate hypothermia (33 to 34°C). Patients excluded from adjunct use were those with hemodynamic instability due to rupture of the aneurysm, active infection, and severe coagulopathy. Cerebrospinal fluid pressure is maintained below 10 mm Hg throughout the surgery and for 3 days postoperatively, using a lumbar drain placed percutaneously in the third or fourth lumbar space immediately prior to surgery. To achieve distal aortic perfusion, we cannulate the left atrium through the left inferior pulmonary vein or atrial appendage. We attach a BioMedicus pump (Minneapolis, MN) with an inline heat exchanger to this cannula. We then establish arterial inflow by cannulating the left common femoral artery or the distal aorta if the femoral artery is not accessible. To minimize the ischemic time to the spinal cord, viscera, and kidneys, we use sequential cross-clamping technique. Other adjunctive measures include the use of visceral and renal perfusion with cold blood or crystalloid solution to lower the renal temperature to less than 15°C. All patent intercostal arteries (eighth to twelfth) are reattached. Somatosensory evoked potentials are used to monitor spinal cord function during surgery.

Statistical Methods
Data collection for this project was approved by the Committee for the Protection of Human Subjects (Institutional Review Board) of the University of Texas Health Sciences Center at Houston. Data were entered into a specially designed Microsoft (Redmond, WA) access database and were stored on a secure server. Analyses were conducted using SAS software version 8.2. (SAS Institute Inc, Cary, NC). Univariate statistics (Table 1) were computed using contingency table methods. Continuous data were divided into quartiles for contingency table analysis, and were also evaluated in their continuous form by univariate logistic regression. Multivariate analysis was performed using multiple logistical regression. The effect of aortic cross-clamp time during the years of the study was analyzed using linear regression analysis. The null hypothesis for statistical tests was rejected at p < 0.05.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Discussion
 Acknowledgments
 References
 
The overall incidence of neurologic deficit was 3.3% (36 of 1,106). The percent adjunct use for each type of TAAA repair for the study period is depicted in Figure 2. Neurologic deficit per quartile is listed in Table 1. Incidence of neurologic deficit for the entire cohort by quartile is depicted in Figure 3.



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  		Fig 2. Percent adjunct use by aneurysm extent per quartile. (DTAA = descending thoracic aortic aneurysm.)

 


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  		Fig 3. Incidence (percent) of neurologic deficit (ND) for the entire cohort per quartile. (DTAA = descending thoracic aortic aneurysm.)

 
Univariate risk factors associated with neurologic deficit were age (odds ratio [OR] = 1.03; p = 0.02), TAAA extent II (OR = 8.09; p < 0.0001), history of cerebrovascular disease (OR = 2.49; p = 0.03), and history of renal dysfunction (OR = 2.55; p = 0.007). The use of the adjunct and female gender were protective against neurologic deficit (OR = 0.42; p = 0.008 and OR = 0.40; p = 0.04, respectively). Aortic cross-clamp time was not associated with neurologic deficit (p = 0.11). Independent risk factors for neurologic deficit as determined by multiple logistic regression were extent II TAAA and renal dysfunction (Table 2).


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  		Table 2. Multiple Logistic Regression Model Determinants of Immediate Neurologic Deficit
 
Using multiple logistic regression analysis, Figures 4 and 5 Go depict the relationships of the aortic cross-clamp time with the incidence of neurologic deficit without and with adjunct use, respectively. In Figure 5, the effect of aortic cross-clamp time with regard to neurologic deficit when the adjunct was used has become insignificant.



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  		Fig 4. Multiple logistic regression analysis according to risk of neurologic deficit (ND) and aortic cross-clamp time without adjunct use. Solid line represents extent II thoracoabdominal aortic aneurysm (TAAA), and the dashed line represents all other extents.

 


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  		Fig 5. Multiple logistic regression analysis according to risk of neurologic deficit (ND) and aortic cross-clamp time with adjunct use. Solid line represents extent II thoracoabdominal aortic aneurysm (TAAA), and the dashed line represents all other extents.

 
Mean aortic cross-clamp time was 46 minutes, and mean distal aortic perfusion time was 44 minutes. Aortic cross-clamp times have increased significantly (34 seconds/year; p < 0.0001) since 1991 during the study period (Fig 6). Despite this increase in aortic cross-clamp time, neurologic deficit rates have declined for the period of surgery (p = 0.02) (Fig 3). This decrease in neurologic deficit is most pronounced with the extent II thoracoabdominal aortic aneurysms (21.1% to 3.3%). The use of the adjunct has increased the aortic cross-clamp time by a mean of 12 minutes (p = 0.0001), but it is associated with a significant protective effect against neurologic deficit (OR = 0.4; p = 0.0002). Although other previously established risk factors have remained significantly associated with neurologic deficit, aortic cross-clamp time is no longer significant.



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  		Fig 6. Linear regression analysis of aortic cross-clamp time with regard to study year.

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Discussion
 Acknowledgments
 References
 
During the clamp and sew era, aortic cross-clamp time was the principle predictor of immediate postoperative neurologic deficit during repairs of the thoracic and thoracoabdominal aorta. In Crawford's experience with 1,509 patients, aortic cross-clamp time greater than 60 minutes was associated with an incidence of paraplegia of 27% for the entire group, and when extent II TAAA were specifically analyzed, the rate of paraplegia was as high as 50% [1]. The incidence of paraplegia in patients whose aortic cross-clamp time was less than 30 minutes was still significant at 8% [1]. Similar to these results, we reported an overall paraplegia rate of 20% for patients undergoing repairs of both extent I and II TAAAs with a paraplegia rate of 48% when the aortic cross-clamp time surpassed 45 minutes [8]. Despite overall relative improvements in outcome when compared with earlier series, these results were unsettling and ultimately led to the adoption of the combined adjuncts of distal aortic and cerebrospinal fluid drainage.

Encouraged by the work of Hollier and colleagues [11] with cerebrospinal fluid drainage and Connolly and colleagues' [12] report using distal aortic perfusion for thoracic aortic aneurysm repairs, we hypothesized that by increasing distal aortic perfusion pressure using left heart bypass in combination with decreasing cerebrospinal fluid pressure with drainage, we could improve spinal cord perfusion and ultimately neurologic outcome during thoracoabdominal aortic repair. Thus, beginning September 18, 1992, we initiated a prospective study using distal aortic perfusion and cerebrospinal fluid drainage in patients during repairs of extent I and II TAAAs, and we found that the overall incidence of neurologic deficit was reduced from 31% to 9% (p = 0.0034) [8]. Inspired by this study, the use of the adjunct was adopted for TAAA extent I and II. In this report, the incidence of adjunct use was 45% and 71% for extent I and II, respectively for quartile 1, and has subsequently increased to 91% and 96%, respectively by quartile 4 (Fig 2).

Although extent III TAAA had been associated with neurologic deficit rates as high as 7% to 9% during the clamp and sew era [1, 8], adjunct was not used initially from these repairs (Fig 3). Confidence with the adjunct and observations of its benefits with regard to neurologic outcome led to its use with extent III TAAA so that by quartile 4 the adjunct was used in 90% of the cases. In our previous report, extent III, like extent II was demonstrated to be a risk factor associated with neurologic deficit [13]. In 1995, we modified Crawford's classification of TAAAs adding an extent V (Fig 1). With this modification, our analysis revealed that extent V TAAA was associated with lower risk for neurologic deficit, whereas extent III TAAA became significantly associated with neurologic deficit [13]. Thus, the reclassification leading to a reduction in the total number of cases in the extent III TAAA group was likely responsible for this extent becoming associated with neurologic deficit. However, this report demonstrates that extent III TAAA is not associated with neurologic deficit; the only TAAA significantly associated with neurologic deficit remains extent II.

The incidence of neurologic deficit with TAAA extent IV remained low and was the primary reason that the adjunct was used sparingly in the early periods for this extent, 0% and 40% adjunct use were observed in quartiles 1 and 2, respectively. With dramatic improvements in the incidence of paraplegia, our focus began to broaden with the adoption of a multiorgan protective strategy [9]. Subsequently, studies related to visceral, renal, and pulmonary protection were performed [14–17]. From these works, the approach to TAAA evolved and clinical benefits of the adjunct were observed for all TAAA extents. Thus, in our current experience, we use the adjunct in greater than 90% of all thoracoabdominal and descending thoracic aortic repairs.

Figure 4 depicts the relationship of aortic cross-clamp time and neurologic deficit for the most risky extent II TAAA with no adjunct. With the adjunct (Fig 5), the risk of neurologic deficit has been significantly blunted and has now become almost negligible. Although the graphic depicts a flat line relationship, a limit does theoretically exist, but it was not defined because the number of patients with aortic cross-clamp times that was greater than 120 minutes was relatively small. Others have graphically depicted the relationship of the aortic cross clamp-time with incidence of neurologic deficit. What we have now observed is that such predictive models using aortic cross-clamp time as a risk factor have become insignificant with the use of the adjunct; therefore, constructing predictive models using aortic cross-clamp time as a variable has become irrelevant.

Although the use of adjunct may have prolonged cross-clamp time, it has clearly improved spinal cord protection and allowed the surgeon to be more deliberate and less hurried. Consequently, the incidence of neurologic deficit significantly decreased during the study period with adjunct use. Most remarkable is the decrease in the incidence of neurologic deficit with extent II TAAAs during the study period. The incidence of neurologic deficit in this well established high-risk group steadily decreased to an incidence of 3.3% in the last quartile (Fig 3). Moreover, the risk of neurologic deficit in extent II TAAA repair is now independent of aortic cross-clamp time (Fig 5).

Previously established risk factors associated with neurologic deficit have included aneurysm extent, rupture, increasing age, presence of concurrent proximal aneurysm, and renal dysfunction [1, 9]. Excluding aortic cross-clamp time, these factors remain significant. Consistent with our previous report, cerebrovascular disease was associated with neurologic deficit (p = 0.03) [13]. Female gender was protective of neurologic deficit (OR = 0.41; p = 0.04) on univariate analysis; the reason for this is unclear.

This study must be viewed with certain limitations. This report is a retrospective analysis and must accept its inherent limitations. In addition, prolongation of the aortic cross-clamp time may be associated with other adverse outcomes such as respiratory failure, renal failure, coagulopathy, and gastrointestinal complications during complex aortic repairs; this was not addressed in this report. It must also be emphasized that the purpose of this study was to analyze the effect of aortic cross-clamp time with regard to immediate neurologic deficit in our experience. Although we continue to advocate the adjunct as a multimodal approach to these complex repairs, which includes distal aortic perfusion, cerebral spinal fluid drainage, and moderate passive hypothermia, we emphasize that our experience is likely more entailed than just this. What is not mentioned and is also difficult to apply to statistical models, is the contributions of the anesthesia, perfusion, neuromonitoring, and nursing teams, and then ultimately the surgeons' skill to our overall outcomes. Our report focused on the adjunct as a multimodal approach that was not individually separated and then analyzed. Although each individual technique may not show a significant benefit by itself, it does not mean that each individual technique may not have a benefit when used in a certain individualized patient situation.

Furthermore, we do not suggest that clamp time is unimportant in the absence of perfusion adjuncts. We intend rather to communicate our finding that a decade of study and refinement of these adjuncts has led to separation of clamp time from ischemic time when multimodality adjuncts are used as we use them. We admit that risk models should be generalizable. Here, however, they are only generalizable to populations in which a multimodality adjunct is used. Our data are so heavily influenced by our long-term use of adjuncts that a simple regression model term to account for them would not be sufficient to make a model generated from our data applicable to a clamp-and-sew population. Adjunct modifies the effects of other risk factors (eg, clamp time and extent) to such a great degree that we cannot produce estimates that are generalizable outside of a population in which such adjuncts are used.

In conclusion, adjunct use during repairs of the thoracoabdominal aorta significantly reduced the risk of neurologic deficit, despite increasing aortic cross-clamp time. The use of the adjunct seems to blunt the effect of the aortic cross-clamp time and may provide the surgeon the ability to operate without being rushed. In our experience, because aortic cross-clamp time has been effectively eliminated as a risk factor with the use of the adjunct, using this variable to construct risk models becomes irrelevant.


   Discussion
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
Acknowledgments
 References
 
DR JOSEPH BAVARIA (Philadelphia, PA): The first question is about extent IV thoracoabdominal aneurysms. When you use the term adjunct, do you mean CSF drainage and distal aortic perfusion or just CSF drainage alone?

DR ESTRERA: When we define adjunct we mean both CSF drainage and distal aortic perfusion. With regard to extent IV, we have found that cold visceral perfusion in our animal studies actually improved outcome with regard to hepatic and gastrointestinal function. For this reason, we applied the use of distal aortic perfusion with active visceral perfusion to extent IV aneurysms with the ultimate goal of improving outcome.

DR SULAIMAN HASAN (Charleston, WV): I want to congratulate you on this elegant presentation. A couple of questions. Have you been able to identify the effect of intercostal reimplantation on your paraplegia rate, and have you considered cooling the patient during the cross-clamp time?

DR ESTRERA: With regard to cooling, we try not to actively cool the patient, but we do use passive moderate hypothermia with the goal core temperature between 32 and 34°C. Hence, we do use a heat exchanger to warm the patient once the aortic reconstruction is completed. With regard to intercostal artery reattachment, it was performed on 39% of our patients in this series. We reattach intercostal arteries T8 to T12 when patent, except in cases of acute dissection. Although Dr Safi was able to show that intercostal artery reattachment was significant in a paper published in 1998, as an overall adjunct, it was not significant in this series.

DR BAVARIA: Did this study eliminate all hypothermic cases or cases involving circulatory arrest with an "open proximal" anastomosis at the distal arch? Were there any cases utilizing deep hypothermia as circulation management for extent I and II TAAAs in this series?

DR ESTRERA: All left chest hypothermic circulatory arrest cases were excluded from this study.

DR R. MORTON BOLMAN III (Minneapolis, MN): Your results are outstanding. Was there any difference in neurologic deficit with respect to the etiology of the aneurysm (ie, does dissection versus nondissection, as the underlying cause of the aneurysm, have any bearing on the likelihood of neurologic injury)?

DR ESTRERA: In our analysis, acute and chronic dissection were not significant risk factors for neurologic deficit in this analysis when the adjunct was used. During the clamp and go era, acute dissection, and even in some series chronic dissection, were significant risk factors, but in this series they were not.

DR BAVARIA: Was it the opposite, because some series have actually shown that with circulatory adjuncts presently used that actually you get a higher incidence of paraplegia with atherosclerotic aneurysms with the use of adjuncts than you do with acute or chronic dissections?

DR ESTRERA: We did not see that.

DR ALEXANDER G. STEIN (Los Angeles, CA): Thank you very much for sharing your data with us. It is very exciting to see that we have confirmed some modalities of reducing this terrible complication. I noticed that you did perfuse mesenteric vessels. Did you do any perfusion of the intercostals or any intercostals during this time period?

DR ESTRERA: Thank you, Dr Stein. No. We basically temporarily occlude (balloon catheters) the patent intercostals if there is significant bleeding from these that we are going to reattach. We do not actively perfuse the intercostal arteries.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
References
 
We thank Kirk Soodhalter for his editorial assistance.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 

  1. Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ. Experience with 1509 patients undergoing thoracoabdominal aortic operations J Vasc Surg 1993;17:357-368discussion 368–70.[Medline]
  2. Miyamoto K, Veno A, Wada T, Kimoto S. A new and simple method of preventing spinal cord damage following temporary occlusion of the thoracic aorta by withdrawing cerebrospinal fluid J Cardiovasc Surg 1960;16:188-197.
  3. Acher CW, Wynn MM, Archibald J. Naloxone and spinal fluid drainage as adjuncts in the surgical treatment of thoracoabdominal and thoracic aneurysms Surgery 1990;108:755-761discussion 761-2.[Medline]
  4. Safi HJ. Role of the BioMedicus pump and distal aortic perfusion in thoracoabdominal aortic aneurysm repair Artif Organs 1996;20:694-699.[Medline]
  5. Safi HJ, Hess KR, Randel M, et al. Cerebrospinal fluid drainage and distal aortic perfusionreducing neurologic complications in repair of thoracoabdominal aortic aneurysm types I and II. J Vasc Surg 1996;23:223-228discussion 229.[Medline]
  6. Rokkas CK, Kouchoukos NT. Profound hypothermia for spinal cord protection in operations on the descending thoracic and thoracoabdominal aorta Semin Thorac Cardiovasc Surg 1998;10:57-60.[Medline]
  7. Svensson LG. An approach to spinal cord protection during descending or thoracoabdominal aortic repairs Ann Thorac Surg 1999;67:1935-1936discussion 1953-8.[Abstract/Free Full Text]
  8. Safi HJ, Bartoli S, Hess KR, et al. Neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysmsthe role of cerebral spinal fluid drainage and distal aortic perfusion. J Vasc Surg 1994;20:434-444discussion 442-3.[Medline]
  9. Safi HJ, Miller 3rd CC, Huynh TTT, Estrera AL. Distal aortic perfusion and cerebrospinal fluid drainage for thoracoabdominal and descending thoracic aortic repairten years of organ protection. Ann Surg 2003;238:372-381.[Medline]
  10. Estrera AL, Rubenstein FS, Miller 3rd CC, et al. Descending thoracic aortic aneurysmsurgical approach and treatment using the adjuncts cerebrospinal fluid drainage and distal aortic perfusion. Ann Thorac Surg 2001;72:481-486.[Abstract/Free Full Text]
  11. Hollier LH, Money SR, Naslund TC, et al. Risk of spinal cord dysfunction in patients undergoing thoracoabdominal aortic replacement Am J Surg 1992;164:210-213discussion 213-4.[Medline]
  12. Connolly JE, Wakabayashi A, German JC, Stemmer EA, Serres EJ. Clinical experience with pulsatile left heart bypass without anticoagulation for thoracic aneurysms J Thorac Cardiovasc Surg 1971;62:568-576.[Medline]
  13. Estrera AL, Miller 3rd CC, Huynh TT, Porat E, Safi HJ. Neurologic outcome after thoracic and thoracoabdominal aortic aneurysm repair Ann Thorac Surg 2001;72:1225-1230discussion 1230-1.[Abstract/Free Full Text]
  14. Safi HJ, Harlin SA, Miller CC, et al. Predictive factors for acute renal failure in thoracic and thoracoabdominal aortic aneurysm surgery [published erratum appears in J Vasc Surg 1997;25(1):93] J Vasc Surg 1996;24:338-344discussion 344-5.[Medline]
  15. Safi H, Miller CI, Carr C, et al. The importance of intercostal artery reattachment during thoracoabdominal aortic aneurysm repair J Vasc Surg 1998;27:58-68.[Medline]
  16. Engle J, Safi HJ, Miller 3rd CC, et al. The impact of diaphragm management on prolonged ventilator support after thoracoabdominal aortic repair J Vasc Surg 1999;29:150-156.[Medline]
  17. Hassoun HT, Safi HJ, Miller 3rd CC, Huynh TTT, Al E. Cold visceral perfusion improves early survival in patients with acute renal failure after thoracoabdominal aortic aneurysm repair J Vasc Surg 2004;39:506-512.[Medline]



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