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Ann Thorac Surg 2007;84:782-788
© 2007 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Role of Somatosensory Evoked Potentials in Predicting Outcome During Thoracoabdominal Aortic Repair

^a Department of Cardiothoracic and Vascular Surgery, The University of Texas Health Science Center at Houston, Memorial Hermann Hospital, Houston, Texas
^b Department of Neuromonitoring, The University of Texas Health Science Center at Houston, Memorial Hermann Hospital, Houston, Texas

Accepted for publication March 21, 2007.

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

Presented at the Forty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 29–31, 2007.

	Abstract

Top Abstract Introduction Material and Methods Results Comment Discussion Acknowledgments References

 
Background: Clinical utility of somatosensory evoked potentials (SSEP) in descending thoracic and thoracoabdominal aortic repair is debated. We reviewed our practical experience with SSEP in descending thoracic and thoracoabdominal aortic repairs.

Methods: Between January 2000 and April 2005, we used SSEP monitoring in 444 patients (270 thoracoabdominal aorta and 174 descending thoracic aorta). Median age was 68 years; 36% were female. Only changes of spinal origin were analyzed. Changes were classified as (1) no change, (2) transient changes that returned to baseline by the end of the procedure, or (3) persistent changes that did not return to baseline by the end of the procedure.

Results: Somatosensory evoked potential changes occurred in 87 (19.6%) patients; 22 (25%) of these did not return to baseline. Immediate neurologic deficit occurred in 8 of 444 patients (1.8%); five deficits (5 of 87; 5.8%) occurred in patients with SSEP changes, compared with three deficits (3 of 357; 0.8%) in patients without changes. Odds ratio for this comparison was 7.2 (p < 0.002). Somatosensory evoked potential was a poor screening tool for neurologic deficit, with a sensitivity of 62.5% and specificity 81.2%. Negative predictive value was 99.2%, indicating a very low event probability in the absence of SSEP changes. Delayed neurologic deficit occurred in 3.2% and was not related to SSEP changes. Somatosensory evoked potential changes were also associated with increased 30-day mortality and low glomerular filtration rate.

Conclusions: Intraoperative SSEP monitoring was reliable in ruling out spinal injury in descending thoracic and thoracoabdominal aortic repair, but had a low sensitivity. It did not predict delayed neurologic deficit. Spinal SSEP change was an independent predictor of mortality and correlated with low preoperative glomerular filtration rate.

	Introduction

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Paraplegia is a devastating complication after descending thoracic aortic (DTA) and thoracoabdominal aortic (TAA) surgery. In the "clamp and sew" era, the overall incidence of neurologic deficit (ND) was 16% and was as high as 31% in extent II TAA repair [1]. This overall incidence dropped dramatically to 3.3% during the past decade with the use of adjuncts (distal aortic perfusion, cerebrospinal fluid drainage, systematic reimplantation of intercostal arteries, and moderate hypothermia) [2–4]. Improved monitoring of the spine and early detection of spinal cord injury have also helped lower the incidence of ND. That can be achieved using either somatosensory evoked potentials (SSEP) or motor evoked potentials. Whether monitoring motor evoked potentials is more reliable than monitoring SSEP in detecting spinal cord ischemia is still debated [5–8]. Although the systematic use of motor evoked potentials is limited by the anesthetic constraints, SSEP monitoring is feasible despite the use of paralytics and can be applied for postoperative neuromonitoring. In consequence, the optimal monitoring technique for spinal cord function during DTA and TAA surgery remains controversial. We reviewed our experience with SSEP monitoring and evaluated the rate of spinal SSEP change and its role in predicting postoperative ND and mortality in DTA and TAA repair.

	Material and Methods

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Data were collected prospectively as approved by the Committee for the Protection of Human Subjects at the University of Texas Houston Medical School. All patients gave their consent for surgery and for entering the data registry at the same time. Between January 2000 and January 2006, we performed 444 consecutive SSEP studies during DTA and TAA repair. Thirty-six percent (158 of 444) were women, with a mean patient age of 68 years (range, 20 to 87 years). The extent of the DTA and TAA repair was classified according to the modified Crawford classification [9].

Surgical Technique
The details of our surgical technique have been described previously [3, 4] and are briefly reviewed here. After general anesthesia was induced, the anesthesiologist inserted a cerebrospinal fluid drainage catheter into the third or fourth lumbar space. Cerebrospinal fluid drainage was performed to maintain a pressure of less than 10 mm Hg during the operation and postoperatively for 3 days. Neurologic monitoring included electroencephalogram and SSEP for all patients. The patient was positioned in the right lateral decubitus position with the hips flexed 60 degrees for accessibility to the left and right groin. The incision was tailored to complement the extent of the aortic repair. The diaphragm was preserved, exposing only the aortic hiatus. After the patient was anticoagulated with heparin (1 mg/kg), distal aortic perfusion was established by cannulating the left common femoral artery and the left inferior pulmonary vein. A Bio-Medicus pump (Minneapolis, MN) with an inline heat exchanger was used for distal aortic perfusion and visceral perfusion. Aortic reconstruction involved sequential aortic cross-clamping. Reattachment of patent lower intercostal arteries (T8 to T12) was performed routinely. With completion of intercostal artery reattachment, the abdominal aorta was opened, and the visceral vessels were perfused using 13F or 9F balloon-tipped perfusion catheters. Core body temperature was maintained between 32° and 34°C. Before completion of the distal anastomosis, the graft was flushed proximally and the aorta distally. The patient was weaned from partial bypass once the core temperature had reached 36°C. Protamine was then administered, and the atrial and femoral cannulas were removed. Neurologic monitoring (SSEP, electroencephalogram) was discontinued at the end of the surgical procedure. During surgery, any sign of spinal cord dysfunction on SSEP monitoring triggered a series of corrective measures aimed at restoring and optimizing oxygen delivery to the spine: reimplantation of additional patent intercostal arteries, lowering of cerebrospinal fluid pressure by free drainage, increase of hemoglobin level by transfusion, and increase of distal aortic perfusion pressure by either adding volume to the pump to increase flow or the use of vasoconstrictors or both. If the SSEP change occurred while reimplanting the intercostal arteries, one of the priorities would be to finish the anastomosis and reestablish pulsatile flow to the spine. If it occurred later during surgery, any additional patent intercostal artery was reimplanted using a 10-mm separate graft that was reattached to the descending aortic graft using a partial cross-clamp.

Anesthetic Protocol
Induction was standardized for all patients and consisted of a balanced narcotic, benzodiazepine, hypnotic, and relaxant technique. The agents used were fentanyl (10 µg/kg), midazolam (0.05 mg/kg), pancuronium (0.1 mg/kg), propofol (40 to 70 mg), and pancuronium (10 mg). Anesthesia was then maintained using a minimal alveolar concentration of isoflurane. Fenoldopam (0.05 to 0.08 µg · kg^–1 · min^–1) was started at the beginning of the procedure and maintained throughout the first postoperative day.

Neurophysiologic Monitoring
An eight-channel electroencephalogram monitoring was performed during the surgical procedure. The SSEP stimulatory electrodes were placed bilaterally at the level of the malleolus. Recording electrodes were bilaterally placed at three levels: popliteal fossa, cervical spine (C5), and vertex (Fig 1). Evoked potentials were induced using a Digitimer generator and stimulator (Digitimer, Hertfordshire, UK). The right and left posterior tibial nerves were alternatively stimulated at the ankle (rate, 4.7 Hz; stimulus duration, 0.05 to 0.7 seconds; stimulus intensity, 0.3 A) to get a sustained waveform. Somatosensory evoked potentials were bilaterally recorded on three channels: popliteal, cervical, and cortical. A baseline SSEP tracing was obtained before the beginning of the procedure (Fig 2A). All the subsequent SSEP tracings were superimposed and compared with the baseline tracing (Fig 2B). The "traditional" 10/50 rule was considered to define SSEP abnormalities: 10% increase in latency or a 50% reduction in amplitude. The simultaneous interpretation of the three channels enabled us to distinguish SSEP changes related to spinal cord injury from those related to peripheral nerve ischemia or cerebral injury. Peripheral nerve ischemia (secondary to cannulation of the femoral artery or interruption of distal aortic perfusion) would result in a change or loss of SSEP signals in all three channels (Fig 3). Spinal cord injury or dysfunction would result in a change or loss of SSEP signals in the cervical and cortical channels, with normal popliteal signals (Fig 4). A cerebral injury would translate into a change or loss of SSEP signals in the cortical channel as well as in the electroencephalogram recording, with normal popliteal and cervical SSEP signals.

View larger version (25K): [in this window] [in a new window]   Fig 1. Patient in the surgical position, with the different electroencephalogram (EEG) and somatosensory evoked potential leads in place. (A = somatosensory evoked potential stimulatory leads to posterior tibialis nerve at the level of malleolus; B = somatosensory evoked potential recording leads at the level of the popliteal fossa; C = somatosensory evoked potential recording leads at the level of the cervical spine (C5); D = somatosensory evoked potential recording leads at the level of the vertex; E = electroencephalogram leads.)

View larger version (25K): [in this window] [in a new window]   Fig 2. Normal somatosensory evoked potential tracing. (A) Baseline somatosensory evoked potential tracing, obtained just before the beginning of the surgical procedure, showing normal bilateral signals at all three levels (popliteal, cervical, and cortical) after peroneal stimulation. (B) Normal somatosensory evoked potential tracing obtained during the surgical procedure. The actual somatosensory evoked potential tracing (represented by full line) is comparable to the baseline somatosensory evoked potential (represented by dotted line).

View larger version (38K): [in this window] [in a new window]   Fig 3. Left leg cannulation. Somatosensory evoked potential tracing shows a loss of all signals in the left leg secondary to cannulation of the left femoral artery. On the right side, the right popliteal signal is present (A); there are also normal signals in the cervical and cortical channels (B and C, respectively).

View larger version (38K): [in this window] [in a new window]   Fig 4. Spinal change. All signals on the left side were already lost after femoral artery cannulation. On the right side, the right popliteal signal is normal (A), whereas both cervical and cortical signals are lost (B and C, respectively).

Statistical Analysis
Analyses of risk factors for these outcomes were conducted first by univariate analysis using contingency table methods, and then by multivariable analysis using multiple logistic regression analysis. All computations were performed using SAS software version 8.2 (SAS Institute, Inc, Cary NC).

	Results

Top Abstract Introduction Material and Methods Results Comment Discussion Acknowledgments References

 
Eighty-seven patients (87 of 444; 19.6%) presented signs of spinal cord dysfunction (groups 2 and 3) on the SSEP. The incidence of spinal changes according to the extent of the aortic repair is depicted in Table 1. Corrective measures were immediately instituted in all these cases, leading the normalization of spinal cord SSEP in 65 of 87 patients (75%; group 2). In 22 of 444 patients (5%), the spinal cord signals remained abnormal at the end of the procedure (group 3). The incidence of ND and the 30-day mortality according to the type of spinal SSEP change are depicted in Table 2.

The incidence of immediate ND in the study group was 8 of 444 patients (1.8%); 5 of these patients (62.5%) had shown signs of spinal cord dysfunction on SSEP compared with 3 of 357 patients (0.8%) without changes. The odds ratio for this comparison was 7.2 (p < 0.002). Despite the significant difference, SSEP was a poor screening tool for immediate ND, with a sensitivity of 62.5% and a specificity of 81.2%. The negative predictive value of SSEP monitoring for immediate ND was 99.2%, which indicated a very low event probability in the absence of SSEP changes.

The incidence of delayed ND was 14 of 436 patients (3.2%); only 3 patients (21.4%) showed signs of spinal cord dysfunction on the SSEP study. The negative predictive value of SSEP monitoring for delayed ND was 96.9%.

The sensitivity and specificity of intraoperative SSEP monitoring in predicting combined ND (immediate and delayed) were 30.0% and 80.9%, respectively. The negative predictive value of SSEP monitoring for combined ND was 96.1%.

The presence of spinal cord dysfunction on SSEP was an independent predictor for mortality on multivariable analysis (Table 3). There was a significant correlation between low preoperative glomerular filtration rate and spinal cord dysfunction on SSEP monitoring (Fig 5).

View larger version (11K): [in this window] [in a new window]   Fig 5. Graph showing the correlation between low preoperative glomerular filtration rate (GFR) as assessed by Cockroft-Gault formula and spinal cord dysfunction on somatosensory evoked potential (SSEP) monitoring. The correlation equation was exp((–0.7684) + (GFR – 0.00970)/(exp((–0.7684) + (GFR – 0.00970)) + 1, with p < 0.05.

	Comment

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Somatosensory evoked potential was a poor screening tool for immediate ND, with a sensitivity of 62.5%. One fifth of the patients presented signs of spinal cord dysfunction on SSEP. This proportion is even higher in other studies [11]. The utility of SSEP monitoring should not be underestimated according to these results. In fact, the number of true-positive SSEP studies, reflecting a real ischemia to the spine, is always hard to assess. Somatosensory evoked potentials changed the intraoperative management in 20% of the cases, which is in accordance with other reports [6, 11]. Every time there was a sign of spinal dysfunction on SSEP, a series of measures was undertaken to improve the spinal perfusion by increasing the perfusion pressure and the delivery of oxygen to the spine, thus reversing the ischemic insult. In other words, SSEP monitoring has surely helped detect numerous cases of spinal ischemic penumbrae and prevented some cases from becoming permanent injuries. Therefore, the true sensitivity of this test in detecting spinal cord injury cannot be assessed accurately. The only way to do so would be not to react nor change the surgical strategy in case of SSEP change; that would be unethical toward the patient.

In our experience, SSEP was useful in ruling out spinal injury. The negative predictive value of SSEP monitoring for immediate ND was 99.2%, which indicated a very low event probability in the absence of SSEP changes. If the SSEP was negative for spinal cord changes, the risk of developing immediate ND was less than 0.8%. Guerit and associates [11] reported similar findings. The risk of immediate ND increased to 3.1% in case of temporary changes and to 13.6% in case of permanent changes. Immediate ND in the setting of permanent SSEP changes might have been higher than what is reported. Half of these patients (group 3) presented to surgery with ruptured aneurysms or experienced acute myocardial infarction intraoperatively or in the immediate postoperative period. They died subsequently without being assessed for neurologic integrity. Thus, the real number of paraplegic outcomes in this group of patients might have been underestimated. A postoperative SSEP monitoring while the patient was still sedated would have helped identify those patients with ND.

Somatosensory evoked potential was not a good predictor of delayed ND. This finding has already been reported by other groups [11, 12]. The pathophysiology of delayed ND is different from that of immediate ND. Even if the initial insult happens during surgery, it can still be too small to be detected by SSEP. Postoperatively, this spinal cord insult worsens (edema, loss of collaterals, hypotension, low spinal perfusion pressure, hemodilution, and so forth) and leads to delayed ND [13, 14]. Such dysfunction could eventually be detected by postoperative SSEP monitoring.

Spinal SSEP change was a predictor for mortality on multivariable analysis (Table 3). Low perfusion states could affect the spinal cord as well as other vital organs and could lead to death owing to multiple organ failure. Therefore, persistent SSEP change can either be a sign of spinal cord ischemia or a sign of imminent death as a result of low perfusion states.

The present study showed a correlation between low glomerular filtration rate, as assessed by Cockroft-Gault formula, and spinal SSEP changes. Indeed, renal insufficiency is known to be associated with a higher incidence of postoperative complications in different types of surgeries. Low preoperative glomerular filtration rate has been reported by our group to correlate with postoperative mortality and with immediate and delayed ND [15–19]. Renal insufficiency can be a marker for diffuse atherosclerotic disease, and perhaps also a marker for a precarious spinal cord vascularization, and thus a risk factor for intraoperative spinal dysfunction.

This study should be viewed with certain limitations. Although data were collected prospectively, analysis was retrospective and is associated with its inherent biases. Furthermore, the sensitivity of SSEP monitoring could not be assessed accurately because of the corrective measures taken, which might have helped prevent ND. On the other hand, the true incidence of ND could not be determined in a subgroup of patients because some of the patients died before they could be assessed for neurologic integrity.

In conclusion, intraoperative SSEP monitoring was reliable in ruling out spinal injury in DTA and TAA repair, but had a low sensitivity. Somatosensory evoked potential did not predict delayed ND. Spinal SSEP change was an independent predictor for mortality in DTA and TAA repair and correlated with low preoperative glomerular filtration rate.

	Discussion

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DR FRANK W. SELLKE (Boston, MA): Is there any evidence that manipulations you do to normalize SSEP (somatosensory evoked potentials) will have an effect on outcome? It is a good predictor, but are things you do to normalize the SSEP going to change the condition of the patient?

DR ACHOUH: That is really an important question, Dr Selke. As I stated earlier in my presentation, in 20% of our cases, positive somatosensory evoked potentials led us to change our operative strategy by increasing blood pressure, transfusing packed red blood cells, draining the CSF (cerebrospinal fluid), and reimplanting more intercostal arteries. In our experience, these maneuvers have been shown to reduce the risk of paraplegia. So basically, the real sensitivity of somatosensory evoked potentials in predicting neurologic deficit cannot be accurately assessed, because we have surely been able to prevent some of the paraplegia cases from happening by changing our operative strategy. Somatosensory evoked potentials have indeed changed our operative strategy in at least 20% of the cases, and that number has also been reported by other groups.

DR SELLKE: I think the way you would have to do that is ignore the SSEP in certain cases. I am not sure you would consider that ethical.

DR MICHAEL T. JANUSZ (Vancouver, British Columbia, Canada): Congratulations on a very impressive clinical series.

We have been doing sensory and motor potentials routinely for descending thoracic and thoracoabdominal aneurysms and have published that previously. What we found is that in every case the motor is much more sensitive. And when sensory changes have occurred, they have been quite a bit delayed or did not occur at all despite prominent motor changes.

Have you any experience with motor monitoring and how does this compare with your sensory findings?

DR ACHOUH: Thank you for your question. In fact, when we reviewed the literature, we did not find any consensus on the optimal monitoring technique for the spinal cord in aortic surgery. We started using motor evoked potentials in addition to the somatosensory in January 2006. Since that date, we have been using both somatosensory and motor evoked potentials on all our patients. We are actually reviewing this group of patients and trying to compare the two monitoring techniques. We will have the results soon.

DR ROBERT S. KRAMER (Portland, ME): I have a question regarding one of your remedies for spinal cord ischemia. At Maine Medical Center in Portland, Maine, the average unit of bank blood has been stored for at least 21 days. As you know, hemoglobin in old blood has a high affinity for oxygen and will not release it to the tissues.

Unless you have access to fresh blood, how do you suppose that blood transfusions would help your patients with spinal cord ischemia?

DR ACHOUH: Well, we have the advantage in our institution to have a very good relationship with the blood bank, and we have never had any problem getting fresh blood products. The protocol for volume expansion in thoracoabdominal surgery in our institution is to avoid crystalloids and to preferentially give colloids and blood products (packed red blood cells and fresh-frozen plasma). We try to keep the hemoglobin levels in our patients strictly higher than 10 g/dL. That is one of our strategies to decrease the risk of paraplegia. So we do not hesitate to transfuse the patients if their hemoglobin is less than 10 g/dL. And fortunately, in our institution, we have never had any problems getting fresh blood products. And I think all this helps.

	Acknowledgments

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The authors would like to thank Chris Aker, medical illustrator, for his valuable assistance.

	References

Top Abstract Introduction Material and Methods Results Comment Discussion Acknowledgments References

 

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