| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
a Department of Cardiothoracic Surgery, Mount Sinai School of Medicine, New York, New York
b Department of Anesthesiology, Mount Sinai School of Medicine, New York, New York
Accepted for publication February 24, 2009.
* Address correspondence to Dr Etz, Department of Cardiothoracic Surgery, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029 (Email: christian.etz{at}mountsinai.org).
Presented at the Fifty-fifth Annual Meeting of the Southern Thoracic Surgical Association, Austin, TX, Nov 5–8, 2008.
 |
Abstract |
|---|
 Top Abstract IntroductionPatients and MethodsResultsCommentDiscussionReferences |
|---|
Methods: A catheter was inserted into the distal end of a ligated thoracic segmental artery (SA) (T6 to L1) in 13 patients, 7 of whom underwent descending thoracic and thoracoabdominal aortic aneurysm repair using deep hypothermic circulatory arrest. Spinal cord perfusion pressure was recorded from this catheter before, during, and after serial SA sacrifice, in pairs, from T3 through L4, at 32°C. Somatosensory and motor evoked potentials were also monitored during SA sacrifice and until 1 hour after cardiopulmonary bypass. Target mean arterial pressure was 90 mm Hg during SA sacrifice and after nonpulsatile cardiopulmonary bypass, and 60 mm Hg during cardiopulmonary bypass.
Results: A mean of 9.8 ± 2.6 SAs were sacrificed without somatosensory and motor evoked potential loss. Spinal cord perfusion pressure fell from 62 ± 12 mm Hg (76% ± 11% of mean arterial pressure) before SA sacrifice to 53 ± 13 mm Hg (58% ± 15% of mean arterial pressure) after SA clamping. The most significant drop occurred with initiation of nonpulsatile cardiopulmonary bypass, reaching 29 ± 11 mm Hg (46% ± 18% of mean arterial pressure) before deep hypothermic circulatory arrest. Spinal cord perfusion pressure recovered during rewarming to 40 ± 14 mm Hg (51% ± 20% of mean arterial pressure), and further within the first hour of reestablished pulsatile flow. Somatosensory and motor evoked potentials returned in all patients intraoperatively. Recovery of SCPP began intraoperatively, and in 5 patients with prolonged monitoring, continued during the first 24 hours postoperatively. All but 1 patient, who had remarkably low postoperative SCPPs and experienced paraparesis, regained normal spinal cord function.
Conclusions: This study supports experimental data showing that SCPP drops markedly but then recovers gradually during the first several hours after extensive SA sacrifice. Direct monitoring may help prevent a fall of SCPP below levels critical for spinal cord recovery after surgery and endovascular repair of descending thoracic and thoracoabdominal aortic aneurysms.
|
Introduction |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
|---|
Monitoring of spinal cord function using motor (MEP) or somatosensory evoked potentials (SSEP) is widely accepted in the assessment of intraoperative spinal cord viability during aortic procedures, but is an indirect measurement of the adequacy of spinal cord perfusion [1–6]. If MEPs or SSEPs diminish, the response usually involves anesthetic and hemodynamic maneuvers to improve spinal cord perfusion—chiefly by increasing mean arterial pressure (MAP) and improving cerebrospinal fluid (CSF) drainage—but the assessment of the efficacy of these measures is likewise indirect. It is possible that inadequate spinal cord perfusion may occur even when MEP and SSEP monitoring shows no cause for alarm, and that a more direct, sensitive way of monitoring spinal cord perfusion could be helpful intraoperatively, although the presence of intact MEP and SSEP already provides considerable reassurance of adequate intraoperative spinal cord perfusion.
A recent retrospective study of our clinical cases has suggested, however, that spinal cord vulnerability to inadequate perfusion is likely to be highest not during operation, but in the early postoperative period, and that inadequate perfusion resulting in spinal cord injury may occur with systemic pressures below the individual patient's usual blood pressure even though those systemic pressures fall within limits usually regarded as normal [7]. The major contribution of direct monitoring of SCPP is therefore likely to be in preventing delayed-onset paraplegia. We think that SCPP monitoring during the first 24 hours postoperatively—at a time when monitoring MEPs is not possible, and SSEP monitoring is at best difficult—is likely to prove invaluable.
To measure the adequacy of spinal cord perfusion more directly intraoperatively and to enable surveillance into the early postoperative interval, we adapted for clinical use a method of direct measurement of SA pressure that had previously been developed in experimental studies of spinal cord blood flow after SA ligation [8]. The correlation in our experimental studies between the measurement of SCPP and microsphere determinations of spinal cord blood flow as well as functional and histologic outcomes convinced us that this technique would be a valuable guide to hemodynamic management for patients undergoing repair of DTA and TAAA in which spinal cord injury is a concern. What follows is our initial clinical experience with this new monitoring tool.
|
Patients and Methods |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
|---|
|
Bypass Technique
All operations were carried out under moderate hypothermia (32°C), and distal aortic perfusion or, if needed, deep hypothermia was used with circulatory arrest initiated at a bladder temperature of 14°C and jugular bulb cerebral venous saturation of at least 95%.
Hypothermic circulatory arrest
Hypothermic circulatory arrest was effected by surface and perfusion cooling. Adequate cerebral hypothermia was ensured by cooling to an esophageal temperature of 12° to 15°C, and maintaining a jugular venous saturation greater than 95%. The head was packed circumferentially in ice.
The proximal anastomosis was carried out during hypothermic circulatory arrest. A brief period of perfusion by means of the right atrial catheter was used to clear air from the proximal aorta and allow suctioning to remove any putative particulate debris from the area of the anastomosis. Proximal body and coronary perfusion (selective cerebral perfusion) was then restored by perfusion through the axillary artery or a side branch in the aortic graft.
Perfusion warming was performed at the end of the procedure with the gradient between the esophageal and blood temperature maintained at less than 10°C. Warming was maintained until the esophageal temperature reached 35°C and bladder temperature was in excess of 32°C.
Distal aortic perfusion
Distal aortic perfusion was established through femorofemoral cannulation (also using the inferior vena cava, the right atrium, or, in one case, the inferior pulmonary vein for drainage) and an in-line oxygenator (BioMedicus Circuit, Medtronic Biomedicus Inc, Eden Prairie, MN), as previously described. Thereafter, the patient was partially exsanguinated and the aorta clamped above the aneurysm.
Motor Evoked Potential Monitoring
After induction, volatile anesthetics were discontinued, as were muscle relaxants, and narcotic anesthesia was substituted. Motor evoked potentials were elicited by a train of nine transcranial electrical pulses delivered from a Digitimer D185 cortical stimulator (Welwyn, Garden City, United Kingdom). The stimuli were applied through two disposable corkscrew electrodes (Nicolet Biomedical, Madison, WI) anchored in the scalp overlying the left and right motor cortices, respectively, approximately 6 to 8 cm lateral from the vertex. In response to stimulation, MEPs (composed of compound muscle action potentials) were recorded from the skin over the tibialis anterior (leg) and abductor pollicis (hand) muscles through subdermal needle electrodes. The recordings from the hands permit evaluation of the effects of anesthesia and temperature on the amplitudes of the MEPs. The signals were amplified, filtered, digitized, and saved to a hard drive. The stimulation intensity was set to 10% above the level that elicited the maximal MEP amplitude for each patient. A decrease of 50% in amplitude of the leg MEPs in the presence of stable hand MEPs was considered to reflect a lower body ischemic event. In patients in whom hypothermic circulatory arrest was used, MEPs were measured during removal of the aneurysm under moderate hypothermia, before deep cooling, and again after rewarming.
Somatosensory Evoked Potential Monitoring
Somatosensory evoked potentials were elicited by stimulation of the left and right posterior tibial nerves through two surface disk electrodes placed approximately 2 cm apart below the medial malleolus at the ankle. Recordings were made from the scalp overlying the somatosensory cortex using subdermal needle electrodes placed approximately 3 to 4 cm behind the vertex and referenced to an electrode at frontopolar midline on the forehead. A ground electrode was placed on the shoulder. The recorded signals were amplified, filtered, and saved to a hard drive. The responses to 200 to 300 stimuli were averaged. Ischemic spinal cord dysfunction was defined as a decrease in SSEP amplitude of more than 50%.
Cerebrospinal Fluid Drainage
A catheter for drainage of CSF was placed routinely. Cerebrospinal fluid pressure was monitored during the operation and for the subsequent 72 hours: CSF was drained at a maximum rate of 15 mL/h as long as CSF pressure remained greater than 10 mm Hg.
Postoperative Management
Somatosensory evoked potentials were monitored until the patient awakened. Thereafter, hourly brief neurologic examinations were performed for 72 hours. High normal blood pressures were maintained, aiming for an aortic mean pressure of 90 mm Hg. Cerebrospinal fluid drainage was continued for 72 hours, and methylprednisolone was administered twice a day (125 mg) for 24 to 72 hours.
Segmental Artery Catheter Placement and Spinal Cord Perfusion Pressure Monitoring
The SA in the anticipated center of the aneurysm resection was dissected and divided first. The SA catheter (3F pressure catheter; Medtronic Inc, Minneapolis, MN) for SCPP monitoring was placed into the distal end of the proximally ligated SA (Fig 1A) and connected for intraoperative and postoperative pressure monitoring. The distal end of the catheter was then passed through the muscles of the back using a needle. The SCPP catheter was secured in place with silicone elastomer ties secured with clips (Fig 1B) that occluded the stump of the SA when the catheter was removed postoperatively.
|
Statistical Methods
Data were entered in an Excel (Microsoft Corp, Redmond, WA) spreadsheet and transferred to a SAS (SAS Institute, Cary, NC) file for data description and analysis. Characteristics and risk factors in this sample of patients are described as percentages or as mean and standard deviation. Pressures that were repeatedly measured over time were averaged for the time period. Pressures were compared by paired Student's t tests or independent sample Student's t tests, as appropriate.
|
Results |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
|---|
Clinical data, risk factors, and intraoperative and postoperative details for each of the 13 patients are listed in Table 1 in chronologic order, and summarized for the entire series in Tables 2 and 3.
|
|
Spinal Cord Perfusion Pressure
The SCPP catheter was placed successfully in all 13 patients, as close as possible to the anticipated center of the aneurysm resection. Figure 2
shows the extent of SA sacrifice in each patient and the site of the catheter; the asterisk indicates the 1 patient who developed paraparesis. Spinal cord perfusion pressure readings were recorded from the SA catheter in all patients before, during, and after serial SA sacrifice. In the first 8 patients, the SCPP catheter was removed before the end of the operation. In the subsequent 5 patients (numbers 9 through 13), SCPP monitoring was successfully continued for 24 to 42 hours postoperatively.
|
|
|
Distal aortic perfusion was initiated on average after 23 minutes of lower body ischemia, when the distal anastomosis was completed, and raised the SCPP to 34 ± 13 mm Hg, only 37% ± 15% of MAP. Although distal perfusion increased the SCPP significantly when compared with lower body circulatory arrest (p = 0.05), it did not raise SCPP to the levels seen before proximal clamping (p = 0.02). There was a trend for pulsatile upper body perfusion combined with nonpulsatile distal perfusion to be less efficient in maintaining SCPP (37% ± 15% of MAP) as compared with nonpulsatile CPB, which achieved a pressure of 49% ± 14% of MAP (p = 0.08).
Recovery of SCPP began intraoperatively and, in 5 patients with prolonged monitoring, continued during the first 24 hours postoperatively.
Postoperative spinal cord perfusion pressure recordings
Five patients (8 ± 3 SAs sacrificed) underwent SCPP monitoring for up to 42 hours postoperatively. Although 4 patients completely recovered spinal cord function, 1 patient experienced permanent paraparesis within the first 24 hours postoperatively despite intact MEPs and SSEPs intraoperatively.
Figure 5 shows postoperative recordings of what we have termed the "corrected" SCPP—the directly measured SCPP in the SA stump minus the CSF pressure—in the 4 patients who recovered compared with the patient who suffered paraparesis. The postoperative corrected SCPP was markedly lower in the subsequently paraparetic patient than in the 4 patients who recovered (p = 0.02). It is particularly of note that during the first 24 hours postoperatively, all 5 patients had similar systemic arterial pressures: there was no statistically significant difference in MAP between the 4 recovered patients (96 ± 7 mm Hg) and the patient who experienced paraparesis (100 ± 6 mm Hg; Fig 6C). There was also no significant difference between the average postoperative CSF pressure between the recovered patients (13 ± 5 mm Hg) and the paraparetic patient (19 ± 3 mm Hg; Fig 6B).
|
|
All patients without spinal cord injury recovered SCPP postoperatively (72 ± 9 mm Hg), reaching 99% of their baseline SCPP level before SA sacrifice (73 ± 13 mm Hg) within 24 hours.
Postoperative paraparesis
Postoperative paraparesis occurred in a 41-year-old man with a history of an acute type B dissection 6 years earlier, who underwent urgent operation after presenting with chest pain associated with a 7.2-cm descending thoracic aneurysm. The patient's body mass index was more than 40; he had a past medical history of hypertension, a pacemaker secondary to congenital third-degree atrioventricular block, and sleep apnea treated with continuous positive airway pressure and home oxygen therapy. Intraoperatively, the SSEPs remained intact during SA sacrifice from T6 through T12; they disappeared during hypothermic circulatory arrest (for 20 minutes at 15.5°C) and remained absent during selective cerebral perfusion. After rewarming was instituted, the SSEPs began reappearing at 28°C, and the somewhat depressed MEPs, which reappeared only toward the end of the procedure, were attributed to a very low core body temperature in this exceptionally obese individual. Nevertheless, continuously elevated mean aortic pressures were instituted and maintained throughout the postoperative period. (The recordings of his corrected postoperative SCPP—as compared retrospectively with those of the patients who recovered spinal cord function—are seen in Fig 5.) The patient's course was additionally complicated by reintubation on postoperative day 4, with computed tomographic evidence of acute parenchymal hemorrhage in the left occipital lobe, as well as possible intraventricular and subdural hemorrhages. The patient has subsequently recovered and returned to work as a computer programmer, but requires a walker and braces to ambulate.
|
Comment |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
|---|
Clinical and experimental studies have made clear that maintenance of a high normal MAP is not always a guarantee of adequate SCPP, which even under baseline conditions is only 70% of MAP. Systemic pressures during recovery from SA sacrifice may need to be even higher than currently recommended in the presence of antecedent hypertension [7]. It has been shown that an elevated CVP as well as an elevated CSF pressure, can interfere with adequate spinal cord perfusion [7, 11–13]. The persistence of a seemingly irreducible incidence of delayed-onset paraplegia in an era when immediate paraplegia rates have been falling has put the focus on the first 24 hours after SA sacrifice. Electrophysiologic monitoring during those first few hours postoperatively is difficult; we know from experimental data that SCPP falls to very low levels before recovering, and that clinical hemodynamic instability is a frequent threat [7, 8]. For all these reasons, direct monitoring of SCPP, especially postoperatively, is potentially very valuable.
The SCPP catheter was successfully placed in all 13 patients during dissection of the aneurysm; it required about 15 minutes of additional time before CPB and proximal aortic cross-clamping, and no catheter-related complications ensued. After an average of 10 SA pairs had been sacrificed (constituting two thirds of all SAs supplying the thoracic and lumbar spinal cord), the SCPP catheter detected a 9-mm Hg fall (a decrease in SCPP relative to MAP of 18%), indicating a high sensitivity in detecting even small pressure differences. The moderate fall in SCPP after sacrifice of the majority of thoracoabdominal SAs not only demonstrates the presence of a rich collateral paraspinal network capable of providing immediate compensatory flow—as also documented in recent animal studies [8, 14]—but once again challenges the theory that there is a dominant artery of Adamkiewicz that is essential for spinal cord perfusion: all but 2 patients had all the SAs from T7 to T11 sacrificed. The restoration of SCPP to greater than 90% of the level before SA sacrifice within 24 hours postoperatively in 4 of 5 patients supports the notion that the human paraspinal collateral network—in the few patients studied—is at least as resilient as had been predicted from experimental animal studies [8, 14].
Although MEP and SSEP monitoring are likely sufficient safeguards to assure adequate spinal cord perfusion, we have gained valuable insights from the direct monitoring of SCPP during operation. We were surprised to find that SCPP is only 70% to 80% of MAP even before SA sacrifice. In operations using hypothermic circulatory arrest, SCPP falls to very low levels after SA sacrifice during CPB and cooling, recovering with rewarming and with the reinstitution of pulsatile flow. In patients who underwent DTA and TAAA repair using distal aortic perfusion, the SCPP dropped immediately after proximal clamping to very low levels, corresponding to only 24% of radial MAP. Distal aortic perfusion was initiated on average after 23 minutes of lower body arrest, when the distal anastomosis was completed. During this time, the measured SCPP leveled off at average pressures of less than 25 mm Hg, with CSF pressures between 10 and 15 mm Hg, providing a corrected SCPP less than 15 mm Hg. This pressure is arguably less than what is required to sustain spinal cord perfusion at a body core temperature of 32°C (Fig 4B), risking spinal cord injury if distal perfusion is not initiated in a timely fashion. Recent experimental flow studies have demonstrated an increased risk of lumbar spinal cord damage during prolonged lower body arrest at mild-to-moderate hypothermia [15].
Interestingly, initiation of distal aortic perfusion—widely expected "to exploit the rich collateral network that likely is present in most patients" [16]—only raised the SCPP to 34 ± 13 mm Hg (37% of MAP) in this cohort of patients. This may explain our recent finding—previously also suggested by others [17]—that the incidence of spinal cord injury after extensive SA sacrifice is lower with deep hypothermic circulatory arrest than with other perfusion methods. In the current study, however, the presence of intact MEPs and SSEPs in all patients suggests that perfusion pressures were high enough to prevent intraoperative spinal cord injury.
The unfortunate occurrence of one case of paraparesis among the patients who had extended SCPP monitoring afforded us the opportunity to examine the possible role of inadequate postoperative SCPP in precipitating spinal cord injury. The patient who exhibited paraparesis had postoperative MAP within the normal range, with an elevated CVP. Apart from the maintenance of a high systemic pressure, specific additional measures to raise the SCPP were, in the absence of reference values, not undertaken, although aggressive CSF drainage was used. With the advantage of hindsight, we now recognize that this patient's postoperative values for SCPP were unacceptably low. If we calculate what we have termed corrected SCPP (SCPP minus CSF pressure), the values for the first 24 hours postoperatively in the subsequently paraparetic patient were significantly less than those of the patients who recovered normal spinal cord function (Fig 5).
In retrospect, we can see that the subsequently paraparetic patient's CVP was significantly higher than the postoperative values in the patients who recovered. This underscores our observation in a recent retrospective study that an elevated CVP is a risk factor for delayed paraplegia after extensive SA sacrifice [7]. The injured patient had a body mass index far above average, requiring continuous positive airway pressure therapy even before the operation, and necessitating high airway pressure postoperatively to provide adequate ventilation and oxygenation, perhaps explaining an elevated postoperative CVP refractory to conventional treatment.
The analysis of direct SCPP monitoring in these few patients, although illuminating, still leaves many questions unanswered. We have not ascertained what is likely to be the minimal SCPP to prevent spinal cord injury at a given temperature, and whether this is more sensitive as an absolute value or a minimum percent of MAP. We are not sure whether the adequacy of the collateral network is affected by the etiology of the aneurysm, the duration of the problem, or by other patient characteristics, such as the presence of diabetes. We suspect that pulsatile flow may be important for the collateral network to maintain its perfusion pressure early after SA sacrifice, as the proportional SCPP (% MAP) fell after initiation of CPB and leveled off at values during distal aortic perfusion that were significantly lower than before proximal aortic clamping. We have also already seen that both CSF and CVP have an impact on SCPP, but we have not accumulated sufficient experience to know how to manipulate these factors most effectively [7]. How various pharmacologic agents affect spinal cord perfusion also remains to be explored.
We do know enough to suggest that direct monitoring of SCPP is a promising new technique that will likely contribute directly or indirectly to further reduction in the incidence of spinal cord injury after surgical or endovascular repair of DTA and TAAA. Monitoring of spinal cord function is impractical during the first 24 hours after surgery, making direct SCPP assessment in the postoperative period an appealing way to bridge the gap between intraoperative MEP and SSEP monitoring and the possibility of clinical evaluation of spinal cord function. Direct measurement of SCPP is likely to be especially valuable to guide management during a time when hemodynamic instability is frequent and spinal cord perfusion has been shown to be precarious, to ensure that SCPP does not fall below levels critical for spinal cord recovery. Determination of the minimum safe levels of perfusion pressure at various points during aneurysm operation and recovery will require monitoring of additional patients, and correlating directly measured SCPP with antecedent systemic blood pressures, with concurrently measured intraoperative and postoperative MAP and CVP, and with MEP and SSEP measurements and clinical recovery of neurologic function.
|
Discussion |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
|---|
Here you present a new technique to even more directly assess adequacy of spinal cord perfusion during these difficult operations. This clinical study seems well founded in your basic investigations; however, I must point out to the audience, this is at best a very preliminary study. To date, you utilized this technique in only 13 patients over the last 2 years. Certainly your group has done more thoracic aortic operations than that. In only 5 of the 13 did you keep the catheter in for as long as 42 hours after surgery. So basically my first question is, why have you utilized this technique to this point in so few patients? In addition, I would like to point out that in this small series, 1 of the 13 patients did indeed suffer paraparesis, and that yields a spinal cord injury rate of 8%.
So while I appreciate that this is primarily a new technique paper, I guess the next step is really to generate observational data and then decide if you can pinpoint and give us parameters as to what is the optimal corrected spinal cord perfusion pressure, and so on. So my next question then is, how are you going to intervene on your next patient when you see some of these changes?
I want to finish up by saying I still have an uneasy feeling of measuring adequacy of total spinal cord perfusion through a catheter in one small select intercostal artery. Indeed, the spinal cord is supplied by a rich collateral network, and there are no valves in these collaterals, but flow is certainly resistance-dependent and collaterals are not uniform. So is it not still possible to have areas of ischemia develop even though you feel comfortable the spinal cord perfusion is adequate as measured by the catheter?
Which brings me to the catheter and the monitoring system itself. Are there risks associated with this technique? We know from the historical days of aortography and trying to find the glorified artery of Adamkiewicz it is possible to do just as much harm as good. So my scenario is this. You are up in the unit and you have this catheter in place and someone is not sure it is working, is it not possible that as the catheter is flushed, microemboli—particulate or air—can be introduced and cause spinal cord injury?
Finally, you touched on this in your last slide; given the potential important information that this technique can provide, how can you see it extrapolated to endovascular patients? Because very likely, 10 years from now we are not going to be doing these open operations anymore.
Thank you.
DR ETZ: Thank you very much, Dr Kern, for these very important questions.
We should emphasize that these patients represent a pilot study of our initial experience. Doctor Griepp started putting in the catheter 2 years ago, and, as you point out, there are potential risks. But at the same time, we realized from our laboratory work that this catheter might enable very important data to be gathered in the clinical setting. So we started slowly. At this point, however, catheter placement has become more and more routine, and we expect it to become a regular monitoring technique in our institution.
You also make the important point that we cannot expect the spinal cord perfusion pressure to be at the same level along the entire spinal cord. We picked a position for the catheter in the middle of the resected area because that is the region which we know from our laboratory experiments in pigs that usually shows the lowest pressure. We published a study about 2 years ago in the European journal in which we showed that we can sacrifice all the segmental arteries in the pig model, and, with microsphere flow measurements, we can determine where the lowest flow occurs: that is where we put our catheter. We hope in all cases that we put the catheter in the area that shows us the lowest pressure so that we can prevent the devastating consequence of having inadequate perfusion. But one cannot be sure.
The handling of the catheter is restricted to people who know how to deal with it: in the ICU (intensive care unit) only specially instructed personnel. We have not seen any complications yet. We have not had any bleeding, which is obviously our most serious concern. Flushing-induced embolization is a frightening potential complication, but likely to be avoided by our policy of never flushing a nonfunctioning catheter.
I would like to show you in more detail the pressures in the single case of paraparesis we encountered. In this patient, in retrospect, what would we have done differently? What measures could we have taken if we had known that this patient would develop paraparesis? At baseline, this patient's SCPP (spinal cord perfusion pressure) was well within the range of the other patients who recovered. After sacrifice, the patient was somewhat at the lower end of the spectrum with regard to SCPP pressure, but still within the same range as patients that recovered. But within the first 5 hours postoperatively, the mean aortic pressure of this patient was only 87% of his preoperative mean aortic pressure. This confirms a finding from a retrospective study we published a year ago: that the mean aortic pressure seems to play a very important role, but must be considered in relation to the patient's own baseline. This patient's aortic pressure relative to his antecedent pressure was significantly lower than the same measurement in all of his peers, and that obviously affects the SCPP. Since we can show that SCPP after segmental artery sacrifice is at best only 60% of MAP (mean arterial pressure), one would have to raise the MAP significantly to get an increase in SCPP.
In future, the measures we would take if SCPP fell would be aimed at trying to raise the MAP, lower the CSF (cerebrospinal fluid) pressure, and lower the CVP (central venous pressure).
DR JOSEPH S. COSELLI (Houston, TX): I congratulate you on an excellent presentation, and congratulate Randy Griepp and your institution, Mount Sinai, for your many contributions to this area. I was very impressed by your illustration showing the plethora of circulation to the spinal cord and the surrounding area. There is, of course, a great deal of anatomic data showing that the blood supply to the spinal cord is indeed very limited in many individuals.
My concern stems from the problem that in about 30% of the patients in whom paraplegia develops, the onset of paraplegia is delayed. I am glad that your own data highlights the fact that although an individual may fall within normal parameters, that specific individual's spinal cord perfusion is not necessarily adequate, particularly when you have altered it by ligating so many intercostal arteries.
So my question is, if, according to your hypothesis, a given intercostal artery reflects the spinal cord perfusion pressure (because the artery is a directly related to spinal perfusion and is responsible for maintaining that pressure), then how do you justify ligating such a significant artery?
Thank you.
DR ETZ: Thank you, Dr Coselli. As you know, this technique was developed by Dr Griepp over decades, with the belief that the collateral network would take over spinal cord perfusion after segmental arteries were ligated. We have shown in our animal laboratory that it takes about 5 days in pigs to completely restore spinal cord perfusion after extensive segmental artery sacrifice, and from what we see here, we believe that it may happen even more quickly in humans.
I have a slide which shows the similarity of the collateral circulation in man and in the pig. This is a human cast (which we obviously didn't produce) from which you can see how closely pig and humans resemble one another. From our laboratory experiments, we think it is possible to provide adequate spinal cord perfusion from the collateral network after segmental artery sacrifice, and that this is the only practical way to enable safe endovascular therapy of extensive aortic aneurysms in the future. That is why we think this question is of such great interest.
|
References |
|---|
|
TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  M. S. Bischoff, G. Di Luozzo, E. B. Griepp, and R. B. Griepp Spinal Cord Preservation in Thoracoabdominal Aneurysm Repair Perspectives in Vascular Surgery and Endovascular Therapy, September 1, 2011; 23(3): 214 - 222. [Abstract] [PDF]
|
|
|
|
 |
|
 M. S. Bischoff, J. Scheumann, R. M. Brenner, D. Ladage, C. A. Bodian, G. Kleinman, S. H. Ellozy, G. Di Luozzo, C. D. Etz, and R. B. Griepp Staged Approach Prevents Spinal Cord Injury in Hybrid Surgical-Endovascular Thoracoabdominal Aortic Aneurysm Repair: An Experimental Model Ann. Thorac. Surg., July 1, 2011; 92(1): 138 - 146. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. D. Etz, F. A. Kari, C. S. Mueller, D. Silovitz, R. M. Brenner, H.-M. Lin, and R. B. Griepp The collateral network concept: A reassessment of the anatomy of spinal cord perfusion. J. Thorac. Cardiovasc. Surg., April 1, 2011; 141(4): 1020 - 1028. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. D. Etz, F. A. Kari, C. S. Mueller, R. M. Brenner, H.-M. Lin, and R. B. Griepp The collateral network concept: Remodeling of the arterial collateral network after experimental segmental artery sacrifice. J. Thorac. Cardiovasc. Surg., April 1, 2011; 141(4): 1029 - 1036. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. D. Etz, S. Zoli, M. S. Bischoff, C. Bodian, G. Di Luozzo, and R. B. Griepp Measuring the collateral network pressure to minimize paraplegia risk in thoracoabdominal aneurysm resection J. Thorac. Cardiovasc. Surg., December 1, 2010; 140(6_suppl): S125 - S130. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Zoli, F. Roder, C. D. Etz, R. M. Brenner, C. A. Bodian, H.-M. Lin, G. Di Luozzo, and R. B. Griepp Predicting the Risk of Paraplegia After Thoracic and Thoracoabdominal Aneurysm Repair Ann. Thorac. Surg., October 1, 2010; 90(4): 1237 - 1245. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Zoli, C. D. Etz, F. Roder, R. M. Brenner, C. A. Bodian, G. Kleinman, G. Di Luozzo, and R. B. Griepp Experimental Two-Stage Simulated Repair of Extensive Thoracoabdominal Aneurysms Reduces Paraplegia Risk Ann. Thorac. Surg., September 1, 2010; 90(3): 722 - 729. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. D. Etz, S. Zoli, C. S. Mueller, C. A. Bodian, G. Di Luozzo, R. Lazala, K. A. Plestis, and R. B. Griepp Staged repair significantly reduces paraplegia rate after extensive thoracoabdominal aortic aneurysm repair. J. Thorac. Cardiovasc. Surg., June 1, 2010; 139(6): 1464 - 1472. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. D. Etz, M. Luehr, F. A. Kari, H. M. Lin, G. Kleinman, S. Zoli, K. A. Plestis, and R. B. Griepp Selective cerebral perfusion at 28 {degrees}C -- is the spinal cord safe? Eur J Cardiothorac Surg, December 1, 2009; 36(6): 946 - 955. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. D. Etz, S. Zoli, F. A. Kari, C. S. Mueller, C. A. Bodian, G. Di Luozzo, K. A. Plestis, and R. B. Griepp Redo Lateral Thoracotomy for Reoperative Descending and Thoracoabdominal Aortic Repair: A Consecutive Series of 60 Patients Ann. Thorac. Surg., September 1, 2009; 88(3): 758 - 767. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
