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Ann Thorac Surg 2003;75:113-120
© 2003 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, St. Louis, Missouri, USA
b Division of Vascular Surgery, Washington University School of Medicine, St. Louis, Missouri, USA
* Address reprint requests to Dr Sundt, Division of Cardiovascular Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA
e-mail: sundt.thoralf{at}mayo.edu
Presented at the Thirty-eighth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 28–30, 2002.
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Abstract |
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 Top Abstract IntroductionMaterial and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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METHODS: We reviewed our most recent 5-year experience with thoracic and thoracoabdominal reconstruction to examine the incidence of and potential contributors to delayed paraplegia or paraparesis.
RESULTS: Between June 1996 and June 2001, 60 patients (29 men, 31 women) underwent repair of isolated thoracic (n = 26) or thoracoabdominal aortic aneurysm (Crawford I, n = 7; Crawford II, n = 14; Crawford III, n = 12; Crawford IV, n = 1) by the cardiac and vascular surgical services collaboratively. Repair was performed endovascularly in 6, and open with either circulatory arrest in 12, partial left heart bypass in 37, or partial femorofemoral bypass in 5. Operative mortality was 9.3% (5 of 54 patients) for open repair and 0% for endovascular repair. Paraplegia or paraparesis occurred in 6 (10%) patients of which 83.3% (5 of 6) were delayed in onset. All patients with delayed paraplegia or paraparesis had degenerative aneurysms of Crawford extent II (n = 3) or III (n = 2), had intraoperative left heart bypass, and had perioperative spinal drainage. Delayed paraplegia or paraparesis occurred up to 27 days postoperatively, and was associated with a documented episode of hypotension in 60% (3 of 5) of patients.
CONCLUSIONS: Improvements in intraoperative management may have reduced immediate paraplegia or paraparesis among vulnerable patients only to leave them at risk of delayed-onset deficit. Postoperative care, including assiduous attention to avoidance of even transient hypotension, must be tailored to this patient population.
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Introduction |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Efforts to reduce the risk of paraplegia or paraparesis have appropriately focused up to this time largely on intraoperative management strategies. Alternative perfusion strategies to protect the spinal cord ranging from profound hypothermia and circulatory arrest [1,2] to partial left heart bypass [3, 4] have been advocated by various authors with success. Partial left heart bypass may be supplemented with cerebrospinal fluid drainage [5–8], permissive hypothermia [9], and attention to segmental aortic clamping [10]. Intercostal artery reimplantation has also been advocated by some [11, 12], although not all [13, 14], authors. These efforts have reduced the reported incidence of postoperative paraplegia or paraparesis to a range of approximately 3% to 15% in recent series [2, 3, 6, 8, 13, 15, 16].
We recently adopted a number of these recommendations in the context of a collaborative team approach to thoracoabdominal aneurysm repair involving specified members of the divisions of cardiac and vascular surgery. Although gratified by what appeared to be a low incidence of short-term paraplegia or paraparesis, we were dismayed to observe a significant incidence of paraplegia or paraparesis delayed in onset for up to 27 days postoperatively. We therefore undertook a retrospective review of our most recent 5-year experience with thoracic and thoracoabdominal aneurysm repair with the aim of characterizing our experience more systematically in the hope of identifying patients at risk, contributing factors, and possible strategies for prevention.
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Material and methods |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Perioperative data were collected prospectively according to The Society of Thoracic Surgeons database guidelines. Individual chart review was undertaken for patients with neurologic deficits. This study was approved by the Washington University Human Research Committee in August 2000.
Study group
The demographics of the study population are summarized in Table 1. Of the 60 aneurysms, six repairs were performed endovascularly. As the impact of endovascular therapy on perioperative paraplegia or paraparesis remains ill-defined and the impact of interruption of collateral circulation by open or closed techniques may fairly be expected to be similar, these cases were included in the study group. Indeed others have reported both short-term [17] and delayed [18] neurologic deficits after endovascular repairs.
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Operative technique
During the 5-year study interval our approach evolved with an increasing preference for the use of partial left heart bypass whenever it was technically feasible to place a proximal aortic clamp distal to the left subclavian artery. As shown in Table 2, femorofemoral partial bypass was used in a small number of cases. When partial left heart bypass was used, patients were anticoagulated with heparin to maintain an activated clotting time of 200 to 250 seconds. Coagulation studies were performed frequently throughout the procedure, and at least every 30 minutes during the bypass run. An aggressive posture toward factor replacement with fresh-frozen plasma and platelet administration was adopted during and after the bypass run.
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Additional intraoperative adjunctive measures included maintenance of distal perfusion pressures of more than 70 mm Hg and passive hypothermia to a target temperature of 32° to 34°C [9]. Patent intercostals between T6 and L2 were routinely reimplanted whenever technically possible [11, 12]. Segmental aortic cross-clamping was a consistent technique used throughout this period [10]. We also instituted visceral artery perfusion through a sidearm from the bypass pump with the intention of minimizing visceral ischemia and, importantly, augmenting any collateral circulation from this source to support the spinal perfusion [20].
Postoperative care
Postoperative care also evolved with experience, particularly as our awareness of the incidence of delayed-onset deficit heightened. As it became increasingly apparent that the intensive care unit management of patients was quite different from that to which the cardiac surgical nursing and resident house staff were accustomed, a set of specific directives were routinely posted in the patient’s intensive care unit room. This facilitated effective communication of these directives through staff changes from shift to shift. It was our impression that this reduced confusion and presumably avoided errors.
Routine postoperative guidelines included an aggressive transfusion practice with maintenance of a hematocrit greater than 30% rather than tolerating normovolemic hemodilution as was routine in our unit after most cardiac surgical procedures, volume replacement with colloid with the aim of minimizing tissue edema acutely, and extubation within 24 hours whenever possible to minimize hemodynamic fluctuations related to varying levels of sedation. The greatest emphasis was on the maintenance of an adequate perfusion pressure by tolerating and indeed encouraging the acceptance of blood pressures greater than those routinely maintained among our postcardiac surgical patients. A mean blood pressure of 90 mm Hg and systolic blood pressure of 120 mm Hg were set as minimum values. This resulted in the routine preparation of pressors before any procedure associated with hypotension such as reintubation or institution of dialysis. The use of nitroprusside was also avoided to the extent practicable [21]. Patients were not routinely given heparin postoperatively.
Delayed paraplegia or paraparesis
Delayed-onset paraplegia or paraparesis was defined as a new neurologic deficit developing after the patient awakened from the operation with a normal examination. When paraplegia or paraparesis was identified, immediate interventions included aggressive blood pressure support, transfusion if the hematocrit was below the target value, and, in cases still within several days of operation, reinsertion of a spinal drain. For those patients more than 1 week postoperatively, it was not our routine to reinsert a drain. Intravenous steroids were administered acutely in all cases. An emergent magnetic resonance imaging study was obtained and neurology consultation sought.
An independent neurologist confirmed all cases of paraplegia or paraparesis and documented the extent of motor deficit. Deficits were graded as 0 = no muscular contraction, 1 = a barely detectable flicker or trace of contraction, 2 = active movement with gravity eliminated, 3 = active movement against gravity, 4 = active movement against gravity and resistance, and 5 = normal. A significant improvement in paraplegia or paraparesis defined as an improvement of at least two motor gdes.
Statistics
Continuous data are represented as the mean ± one standard deviation, and clinically important ratios are shown with 70% confidence limits based on a normal distribution. The Student’s t test was used to compare continuous variables and Fisher’s exact test was used to compare categorical data. Risk factors identified by univariate analysis were included within a multivariable analysis for the determination of relative risks of paraplegia or paraparesis. A p value less than 0.05 was used as an indicator of statistical significance.
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Results |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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The adjuvant techniques and postoperative course for all patients with delayed-onset paraplegia or paraparesis are shown in Table 3. Passive cooling to a target bladder temperature of 32°C was permitted. All of these patients had left heart bypass and cerebrospinal fluid drainage intraoperatively. Intercostal reimplantation was possible in 60% (3 of 5) of patients. Despite these measures, delayed-onset paraplegia or paraparesis occurred as late as 27 days postoperatively. The development of delayed paraplegia or paraparesis was associated with a documented hypotensive episode immediately preceding the neurologic deficit in 3 of 5 patients.
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All other cases of paraplegia or paraparesis (n = 5) were delayed in onset and occurred after elective repair of a degenerative aneurysm of Crawford extent II (n = 3) or III (n = 2). One patient experienced the onset of paraparesis 3 days postoperatively after an episode of hypotension with systolic blood pressure of 80 mm Hg secondary to antihypertensive medication. His perioperative course was complicated by renal insufficiency with fluctuating volume status and hemodynamic instability related to intermittent atrial fibrillation. He had bilateral deficit with 2 of 5 motor score, which persisted despite reinstitution of spinal drainage and maintenance of a mean arterial blood pressure greater than 90 mm Hg.
A second patient underwent elective repair of a Crawford extent III degenerative aneurysm using left heart bypass, a spinal drain, visceral artery perfusion, and intercostal vessel reimplantation. After awakening neurologically intact on postoperative day 1, she experienced paralysis of the left lower extremity (0 of 5). There were no documented episodes of anemia, hypotension, or hypoxia. A magnetic resonance imaging study demonstrated no epidural hematoma. A question was raised about the function of her spinal drain; therefore, another drain was inserted in addition to the administration of steroids and maintenance of blood pressure in the target range. At the time of discharge her strength had improved to 3 of 5.
A third patient with delayed paraplegia underwent elective repair of a Crawford extent II degenerative aneurysm with left heart bypass, spinal cord drainage, visceral perfusion, and intercostal reimplantation. The latter was accomplished with an 8-mm sidearm graft. The spinal drain was removed on postoperative day 2, and the patient was discharged to the stepdown unit. After walking to a bedside chair to eat lunch, she became paralyzed. There was no hypotensive episode documented. Despite reinsertion of a spinal drain and administration of steroids she had no improvement. Imaging to evaluate the patency of the sidearm graft to the intercostals was deferred given logistic considerations. The patient had no improvement in lower extremity strength by the time of discharge.
A fourth patient experienced delayed-onset paraplegia after elective repair of a Crawford extent II degenerative aneurysm with left heart bypass, spinal drainage, and intercostal reimplantation. She exhibited progressive renal insufficiency postoperatively requiring the institution of continuous venovenous hemodialysis and respiratory insufficiency requiring tracheostomy. On postoperative day 27 after transfer from bed to chair she experienced transient hypotension to a systolic blood pressure of approximately 80 mm Hg, after which time she had bilateral lower extremity paralysis that remained unimproved at the time of discharge.
The fifth patient in this series to demonstrate delayed neurologic deficit underwent elective repair of a Crawford extent II degenerative aneurysm using left heart bypass, spinal drainage, visceral artery perfusion, and intercostal vessel reimplantation. She experienced small bowel obstruction requiring adhesiolysis on postoperative day 16. She awoke from operation with 0 of 5 motor score on the right lower extremity and 2 of 5 on the left. Review of her anesthesia record revealed several prolonged episodes of hypotension to systolic blood pressures of 80 mm Hg. Aggressive blood pressure support was instituted in the cardiac surgical unit after paraparesis had been identified, but a spinal drain was not reinserted. At the time of discharge her lower extremity strength had improved to 4 of 5 bilaterally.
Statistical analysis of risk factors
Although the small number of patients in this series limits the statistical power of any analysis, we investigated 13 preoperative variables as possible predictors of delayed paraplegia or paraparesis in an attempt to better define patients at particular risk of this devastating complication. As shown in Table 4,
univariate analysis identified the diagnosis of coronary artery disease (p = 0.03) and extent of aortic resection (p = 0.12) as potential risk factors. In multivariable analysis, neither of these variables reached statistical significance (coronary artery disease, p = 0.12; aneurysm extent, p = 0.25). Age (p = 0.90), sex (p = 0.6), hypertension (p = 0.95), history of tobacco abuse (p = 0.4), chronic obstructive pulmonary disease (p = 0.95), preoperative renal insufficiency (p = 0.95), diabetes mellitus (0.95), diagnosis of aortic dissection (p = 0.54 and p = 0.58 for short-term and long-term, respectively), history of previous aortic operation (p = 0.95), or emergent status (p = 0.95) were not significantly different between patients with and without neurologic deficit.
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Comment |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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This review was stimulated by our clinical impression that as our intraoperative management strategies improved, there was a shift in the pattern of paraplegia or paraparesis in our practice with more occurring in a delayed fashion than we had previously observed. Indeed, delayed-onset deficit became the predominant form observed in our series. We hypothesize that as intraoperative protection improved with the adoption of adjunctive measures suggested by others, an increasing number of patients at risk for paraplegia or paraparesis skirted this complication intraoperatively but remained vulnerable during the postoperative period.
This experience resulted in the adoption of a set of specific guidelines for the nursing staff and resident house staff involved in the care of these patients, empha-sizing the differences in their perioperative care as compared with routine cardiac surgical patients. With the very small number of patients in this study, the impact of these guidelines cannot be proven, although they were embraced by the staff involved in the care of these patients. We made no attempt to formally define the time course of the shift in the pattern of paraplegia or paraparesis, as a major change in the makeup of the surgical team involved in these cases at the Barnes Hospital campus of Washington University occurred in the years just before the study period. A variety of intraoperative approaches were used during that interval, and it was only during the study period that a consistent team of cardiac and vascular surgeons as well as anesthesiologists approached these cases in a formalized, collaborative, and systematic manner. Furthermore, the observation of a predominance of delayed-onset neurologic deficits over short-term–onset deficits is, we believe, the value of our study and stands independently of such comparisons.
We were unable to define risk factors for delayed-onset deficit with rigor because of the limited power of the study. Indeed, although the extent of resection is widely accepted as a risk factor for paraplegia or paraparesis [4, 13, 26], we were unable to demonstrate this statistically with our data set. There was a suggestion from our data that the presence of coronary artery disease was a marker for risk, likely as a reflection of the presence of atherosclerotic disease involving small vessels responsible for collateral circulation. Griepp and colleagues [13] have previously identified a history of smoking as a risk factor for perioperative deficit, possibly by the same mechanism.
An episode of hypotension was temporally related to the onset of paraplegia or paraparesis in 3 of 5 patients with a delayed-onset deficit. This observation is consonant with that of others [25, 27–29]. Furthermore, it is an event that, with adequate education and preparation, may be avoidable in many cases. We established guidelines for the intensive care staff of a systolic blood pressure always in excess of 120 mm Hg, tolerating systolic pressures up to 150 or 160 mm Hg. We also asked the intensive care unit staff to aim for a mean blood pressure in excess of 90 mm Hg. These guidelines were based on clinical judgment only. We made a concerted attempt to divest the staff of notions that the blood pressure must be maintained low to "protect suture lines" or to minimize "oozing from suture lines." In the absence of data, and with the experience of neurologic deficit as much as 4 weeks postoperatively, we attempted to enforce these guidelines for the entire duration of each patient’s intensive care unit stay.
Several cases of delayed-onset deficit occurred within 48 hours of operation without recognized hypotension. Although no improvement was observed with insertion of a new spinal drain, we now insist that spinal cord drainage be maintained for 72 hours in all cases. This is based on the observations of others suggesting that postoperative drainage is protective [6–8] and may even reverse delayed-onset deficit [25, 27–29]. In one of our cases, intercostal vessels were reimplanted using an 8-mm sidearm graft. It is possible that the deficit occurred with thrombosis of the sidearm graft, although this was not documented. We now make an attempt, however, to reimplant intercostals directly to the main graft as a Carrel patch as a consequence of this experience. We considered the use of postoperative heparin for the maintenance of intercostal patency, but have not adopted this strategy.
Our study does not address the optimal management of delayed-onset neurologic deficit. It was our practice to reinsert spinal drains if the deficit occurred within several days of the operation, but not for more-delayed deficits. This was based on the notion that perioperative edema would no longer be a component late after operation and that, therefore, there would be little to gain. It is possible that edema might occur with the late insult and that neurologic deficit could be minimized with reinsertion of a drain late; however, we have no data bearing on this theoretic possibility. Immediate blood pressure support, administration of steroids, and optimization of oxygen carrying capacity with maintenance of a hematocrit more than 30% are simple interventions and easily instituted with rapidity. These were the cornerstones of our management strategy. Clearly the best approach is avoiding the precipitating factors. The group at Mount Sinai has advocated postoperative continuous monitoring of somatosensory evoked potentials as a means of early warning that a patient is vulnerable [13]. We have not used this strategy in the operating room as advocated by these [13, 16] and other authors [23, 30] or postoperatively. Our observation of a significant incidence of delayed deficits, however, supports the notion that there may be value to continuing such monitoring in the intensive care unit.
The mechanism of delayed-onset paraplegia or paraparesis remains unknown. Kouchoukos and Rokkas [1] have suggested that, in some cases, intraoperative ischemic insult may trigger apoptosis, a recognized event in experimental models of spinal cord ischemia [31]. Our observations do not address this hypothesis directly. Although it may have been active at least in part in the cases occurring in the first few days, it is an unlikely mechanism for the cases occurring several weeks postoperatively. The latter cases in particular support, in our view, the importance of collateral circulation and intercostal artery reimplantation as suggested by others [10–12, 30] given their association with hypotensive episodes. We cannot comment on the role of elevated cerebrospinal fluid pressure as a contributor [4, 7, 15]; however, it is likely that such deficits may be multifactorial.
Our experience also does not directly address the optimal technique for performing the procedure. Although profound hypothermia and circulatory arrest were used early in our experience, as the experience became focused among a smaller number of interested cardiac and vascular surgeons, a decision was made to attempt to optimize our results using partial left heart bypass technique. With concentration on optimizing the results with a single technique, operative results improved. Our final approach included (1) left heart partial bypass, (2) permissive cooling to 32°C, (3) spinal cord drainage, (4) segmental clamping, (5) visceral artery perfusion, (6) reimplantation of intercostals below T6, and (7) avoiding the use of nitroprusside intraoperatively and postoperatively.
There are a number of weaknesses of this study, principle among them the relatively small numbers that render it inherently more of a descriptive report than a statistically powerful analysis. Despite this, our observation that patients remain at risk for delayed-onset paraplegia or paraparesis for days, and possibly weeks, postoperatively is important and worthy of more widespread recognition. Furthermore, we suspect that the increase in this phenomenon may be observed by others as current approaches to intraoperative spinal cord protection are more widely adopted. In addition, although it could be argued that our observations apply only to patients undergoing aortic repair using the same operative techniques (ie, left heart bypass and not circulatory arrest), we believe that the occurrence of delayed paraplegia or paraparesis even weeks postoperatively supports aggressive intercostal vessel reimplantation and maintenance of adequate blood pressure in all thoracoabdominal aneurysm repair patients.
We encourage a tailored approach to the postoperative care of these patients, including assiduous maintenance of blood pressure in excess of that routinely accepted after cardiac operations. We found that the institution of a printed set of guidelines posted in the patient’s room emphasizing these special needs facilitated patient care and minimized confusion between team members at change of shift. We believe that this simple intervention reduced the "latent conditions for failure" in the system [32] and improved patient safety. We further encourage a gradual and stepwise approach to the institution of oral antihypertensive medications before discharge.
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Acknowledgments |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Discussion |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Since the initiation of surgical treatment of extensive thoracic aortic aneurysms, the postoperative complication of paraplegia and its prevention have received enormous amounts of attention. As pointed out by the authors, far less focus has been placed on the development and the treatment of delayed paraplegia following similar reconstructions.
It is truly devastating to have a patient wake up following an extensive thoracoabdominal aortic aneurysm repair moving their legs, only to later develop loss of function of their lower extremities, on occasion combined with loss of bladder control, impotence, and other problems associated with the nemesis of the development of paraplegia.
The authors are to be congratulated for drawing our attention to this problem and suggesting some possible solutions. Albeit with an overall occurrence of only five patients, the development of conclusions with regard to the treatment was simply not feasible. I am pleased to see that the authors substantiate our approach and experience regarding the use of left heart bypass, intercostal artery reattachment, and cerebrospinal fluid drainage.
(Slide) Over a 15-year period we reviewed 2,059 descending and thoracoabdominal aortic aneurysm repairs: 1,667 of these were thoracoabdominals and 392 were descendings. In their report, the authors combine paraparesis and paraplegia together under the single grouping of paraplegia. We have chosen to separate these—paraplegia being those patients with simply no function of their lower extremities and paraparesis with substantial weakness. There was a fairly even split, with the incidence of paraplegia and paraparesis, with a total of 16 patients with delayed paraplegia out of an overall 79 patients who had developed paraplegia and/or paraparesis—3.8% of the total group.
(Slide) In contradistinction to the authors, we found that most of our problems occur in the Crawford extent I and extent II groups. Interestingly enough, we have applied postoperative insertion of drains for cerebrospinal fluid drainage in 10 of the 11 patients in these two particular groups and had an improvement in 50% of these patients.
The authors specifically draw our attention to the basic tenets of preventing spinal cord ischemia intraoperatively as well as certain strategies postoperatively, including the continuation of cerebrospinal drainage for a period of 48 hours postoperatively, steroids, hemodynamic stabilization, volume expansion, avoiding episodes of postoperative hypotension, etc.
In addition to these strategies, we have used, albeit with mixed success, mannitol, increased blood pressure, optimization of oxygen delivery, increased hemoglobin, and increased cardiac output, as well as attempts to prevent and treat hyperthermia. Techniques for postoperative spinal cord monitoring to detect early malperfusion, even before a patient awakes, need to be developed, as well as strategies to treat the problem. For the authors, I have a number of questions.
It is stated in their manuscript and alluded to in the presentation that circulatory arrest was frequently used for their more complex reconstructions in the earlier portion of the series, but then this has evolved to a group of patients in which this is applied only when proximal aortic cross-clamping is not possible. Please elaborate on the reasoning for this trend.
Additionally, there is some controversy with the use of heparin in patients, particularly with and without the use of left heart bypass, and I ask them to expand on their strategy.
Regarding cerebrospinal fluid drainage, what were the volume targets? What were the pressure targets? Also, do the authors have a strategy or a perspective on the role of treatment with regard to postoperative hyperthermia in the development of delayed paraplegia?
Thank you. I appreciate the opportunity to discuss this manuscript.
DR NICHOLAS T. KOUCHOUKOS (St. Louis, MO): Did you observe a difference in the rates of paraplegia between the patients in whom hypothermic circulatory arrest was used and those in whom left heart bypass and lesser degrees of hypothermia were used?
DR MANIAR: Thank you Dr Coselli for your comments and questions. As this study has demonstrated, the majority of thoracoabdominal aortic reconstructions performed at our institution now incorporate a distal perfusion technique with either femorofemoral bypass or, more commonly, partial left heart bypass. We believe that there is now convincing evidence that these perfusion strategies may be protective against the development of short-term postoperative paraplegia. As such, partial left heart bypass represents an alternative to profound hypothermia and circulatory arrest. We have also found this strategy somewhat simpler to use. At Washington University we have adopted a collaborative approach toward thoracoabdominal aneurysms and perform all of these procedures in collaboration with members from the division of vascular surgery. Together, over the past several years, our team has gravitated as a matter of consensus to this approach and has found it satisfactory. We remain uncomfortable, however, in placing aortic clamps between the carotid and subclavian out of concern for dislodging atheroembolic material. Therefore, when a proximal neck is not apparent beyond the subclavian artery we still use circulatory arrest.
Our approach to anticoagulation with left heart bypass has been low-dose heparin (5,000 U) to maintain an activated clotting time of approximately 250 seconds. We believe some level of anticoagulation is needed to reduce the risk of clots forming around the left atrial cannula. We have not formally studied this however. At the same time, we are aggressive about factor replacement even during left heart bypass as it is easy to fall behind and impossible to catch up with these patients after discontinuation of bypass. Although this may seem a mixed strategy, it has worked well for us.
With regard to spinal drainage, we maintain a spinal drain for at least 48 hours postoperatively targeting a cerebrospinal fluid pressure less than 10 cm H2O rather than targeting the volume of cerebrospinal fluid drained.
Doctor Kouchoukos, given the very small size of this series and the even smaller number of patients undergoing operation with circulatory arrest, I do not believe that I can answer your question satisfactorily. In this study group, none of the patients undergoing operation with circulatory arrest suffered delayed paraplegia; however, 1 patient undergoing total aortic replacement from the sino-tubular junction to the iliac bifurcation using circulatory arrest did experience delayed paraplegia. Although this is anecdotal, on the basis of this experience we do not think that circulatory arrest protects one in an absolute way from this devastating complication.
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