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Ann Thorac Surg 2007;83:456-461
© 2007 The Society of Thoracic Surgeons
Division of Cardiovascular, Thoracic, and Pediatric Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
Accepted for publication September 15, 2006.
* Address correspondence to Dr Okita, 7–5-2, Kusunoki-Cho, Chuo-Ku, Kobe City, Hyogo, Japan (Email: yokita{at}med.kobe-u.ac.jp).
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Abstract |
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METHODS: Intraoperative tc-MEPs was used in 72 patients who underwent the repair of descending thoracic (n = 24) or thoracoabdominal aortic aneurysms (n = 49) classed as Crawford I in 10 patients, II in 12, III in 23, and IV in 3. There were 52 men and 20 women, and their mean age was 64.9 ± 12.8 years. Tc-MEPs were recorded by transcranial electrical stimulation and compound muscle action potentials.
RESULTS: The hospital mortality rate was 5.6% (n = 4), and the incidence of neurologic deficits was 11.1% (n = 8). All patients whose MEP amplitude recovered to more than 75% of the baseline showed normal spinal function, and 8 of 9 patients whose MEP amplitude decreased to below 75% of the baseline at the end of the procedure showed neurologic deficits postoperatively. The sensitivity of tc-MEPs was 100% and specificity was 98.4%. Latency in patients with postoperative paraplegia was 123% ± 9% and was significantly prolonged at the end of the procedure.
CONCLUSIONS: Tc-MEPs were very sensitive and specific to spinal cord ischemia with reduced amplitude and prolongation of the latency period. Tc-MEPs are considered a useful monitor of spinal cord ischemia during descending thoracic or thoracoabdominal aortic surgery.
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Introduction |
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We investigated whether tc-MEPs after spinal cord ischemia and reperfusion could be used to predict neurologic outcome in a leporine model. We concluded that the amplitude of tc-MEPs at the end of the procedure showed a high correlation with neurologic deficits, and an amplitude that recovered to less than 75% indicated a risk predictor of paraplegia [8]. From this experimental study, recovery to 75% of the baseline in MEP amplitude was considered to be the crucial cutoff point in the repair of thoracoabdominal aortic aneurysms (TAAAs). This study aimed to clarify the usefulness of tc-MEP monitoring, especially its sensitivity and specificity in the detection of spinal cord ischemia.
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Material and Methods |
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The subjects were 52 men (72%) and 20 women (28%), and their mean age was 64.9 ± 12.8 years (range, 18 to 83 years). DTAA were present in 24 patients and were classified as Crawford type I TAAA in 10, type II in 12, type III in 23, and type IV in 3. Aortic dissection was present in 34 patients (47%) and nondissecting aneurysm in 38 (53%). Four patients (6%) had Marfan syndrome. The patient characteristics are summarized in Table 1.
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A CSF drainage catheter was placed in the subarachnoid space the day before operation, and CFS was allowed to drain freely whenever CSF pressure exceeded 10 mm Hg. In patients without a spinal cord deficit, CSF drainage was terminated on postoperative day 2; whereas in those with neurologic injury, the catheter was kept in place beyond 2 days.
Surgical Technique
Intubation was performed with a double-lumen endotracheal tube, allowing collapse of the left lung. Left thoracotomy was performed through the sixth or seventh intercostal space. In some patients with type I and II TAAA, rib-cross thoracotomy was applied, as previously reported [9].
The entire aorta was exposed with dissection of the retroperitoneal space and division of the costal cartilage and diaphragm. Cardiopulmonary bypass was established by means of cannulation of the left femoral artery and the right femoral vein, after the administration of heparin (2 mL/kg). Temperature was decreased actively, reaching rectal temperatures between 31°C and 34°C. Mean radial arterial pressure was maintained between 60 and 100 mm Hg. During cross-clamping, blood pressure was mainly controlled by adjusting the bypass flow of the centrifugal pump.
The proximal descending aorta was clamped with two clamps and completely transected, while distal aortic pressure was kept at more than 60 mm Hg. The proximal aorta was anastomosed in an end-to-end fashion to a gelatin-impregnated knitted Dacron (DuPont, Wilmington, DE) graft with side branches presewn to reattach intercostal, visceral, and renal arteries. After proximal anastomosis, the distal clamp was lowered if the aneurysm allowed segmental clamping.
If cross-clamping of the proximal aorta seemed impossible, deep hypothermic cardiopulmonary bypass and circulatory arrest were applied. Patients were cooled until the tympanic temperature reached 20°C, and circulatory arrest was established with a distal clamp and perfusion. The left side of the heart was vented through the left atrial appendage or the apex of the left ventricle, if necessary. Cardioplegic solution was injected through a balloon catheter. After proximal anastomosis was completed, the graft was clamped just distal to the side branch connected to the second arterial catheter. Flow to the upper body was established after the evacuation of air from the open aorta.
Patent intercostal arteries at the Th4 to Th7 level were closed, and below Th8 level in the excluded segment they were reattached individually with presewn branches and immediately reperfused. Significant back-bleeding from segmental arteries was managed by inserting balloon catheters or external clamping of the segmental arteries to reduce the stealing effect from the anterior spinal artery during attachment. Rewarming was started after the lowest intercostal or lumbar arteries were reattached and reperfused.
For type II, III, and IV TAAA, abdominal branch reconstruction was routinely performed with selective perfusion of the celiac, superior mesenteric, and renal arteries with 10F and 12F balloon cannulas. Each artery was perfused at a flow rate of approximately 200 mL/min. Distal anastomosis of the graft and reconstruction of the visceral and renal vessels were completed during rewarming. The visceral and renal vessels were also reconstructed individually with presewn branches.
Measurement of Transcranial Motor Evoked Potentials
Tc-MEPs are elicited by using a multiple electrical transcranial stimulator (Digitimer D185 cortical stimulator; Digitimer Ltd, Welwyn Garden City, UK). Stimuli are applied to the skull with the anode placed in the C3 position and the cathode in the C4 position (International 10-20 system for the placement of electroencephalogram electrodes). The stimulus consists of a series of five pulses. Each individual stimulation lasts 50 ms, and the interstimulus interval between pulses is 2.0 ms. The output voltage is set at 500 V.
Compound muscle action potentials are recorded from the skin over the right flexor hallucis brevis muscle and the right flexor pollicis brevis muscle using adhesive gel Ag/AgCl electrodes. Tc-MEPs are recorded on the right side of the body because the left lower limb is not perfused continuously owing to cannulation of the left femoral artery. Signals are recorded every 100 ms, passed through a bandpass filter of 10 to 1000 Hz, and amplified 5000 to 20,000 times (Fig 1). Data acquisition, processing, analysis, and saving require a personal computer system (Neuropak MEB-2200, Nihon Koden, Tokyo, Japan).
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At the end of the procedure, a MEP amplitude of more than 75% of the baseline is considered to demonstrate adequate spinal function in accordance with our animal experiment [8].
Interventions Based on Motor Evoked Potentials Changes
When tc-MEPs demonstrate ischemic changes during aortic cross-clamping, attempts first focus on increasing distal aortic flow and proximal mean arterial pressure. Second, CSF pressure is decreased to 5 to 8 mm Hg. When exclusion of an aortic segment results in ischemic MEP change, the intercostal or lumbar arteries in that segment are considered critical to spinal cord blood supply and are immediately reimplanted and reperfused. When no segmental arteries can be identified, endarterectomy of the aortic wall is rapidly performed. Even when no MEP changes are observed, segmental arteries are also reimplanted if possible.
Statistical Analysis
Data were processed using StatView J-5.0 (SAS Institute, Cary, NC) software. All values are expressed as the mean ± standard deviation. Statistical analysis was performed with the Mann-Whitney U test to compare MEP amplitude and onset latency between patients with and without postoperative neurologic deficits. Differences were considered statistically significant at p < 0.05.
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Results |
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Changes in Transcranial Motor Evoked Potential During Operation
Tc-MEP changes and neurologic outcome are summarized in Table 3. Among 54 patients who underwent surgery under mild hypothermia, after aortic cross-clamping, the MEP amplitude remained normal in 27 patients (50.0%), resulting in no paraplegia. In 27 patients (50.0%), the change of MEP amplitude demonstrated spinal cord ischemia. Two of 27 patients had type I TAAA, 4 had type II, 13 had type III, 1 had type IV, and 7 had DTAA. Of these, 19 patients maintained distal aortic pressure and mean arterial pressure above 60 mm Hg, although efforts to increase pressure were made in all patients. At the same time, CSF pressure was decreased to 5 to 8 mm Hg, which resulted in MEP amplitude above 50% of the baseline in 5 patients. In these 5 and in another 8 patients, tc-MEPs recovered after reperfusion of intercostal or lumbar arteries. Aortic declamping achieved tc-MEP recovery in 8 patients, but tc-MEPs disappeared again in 1 patient after coming off cardiopulmonary bypass because of serious hypotension, resulting in paraplegia. In the 6 remaining patients, MEP amplitudes remained absent or below 75% of the baseline at the end of the procedure, and 5 showed neurologic deficits.
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All patients whose MEP amplitude recovered to more than 75% of the baseline at the end of the procedure showed normal spinal function, and 8 of 9 patients whose MEP amplitude decreased to below 75% of the baseline showed neurologic deficits postoperatively. MEP amplitude and onset latency of each patient at the end of the procedure are shown in Figure 2. The patients with MEP amplitude above 69% of the baseline at the end of the procedure showed no neurologic deficits.
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Comment |
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Tc-MEPs are widely used, and many clinical outcomes justify this technique [13–15] because they are reported to provide superior sensitivity and specificity against anterior horn ischemia compared with SSEPs [11, 16]. Because they mainly monitor signal transmission through the dorsal columns, SSEPs might not provide precise information about motor function and blood supply to the anterior horn, which are most likely to suffer ischemic injury.
Few data are available on the relationship between MEP amplitude and spinal cord perfusion or neurologic outcome, although tc-MEP amplitude below 25% of the baseline is considered spinal cord ischemia in some institutes [17, 18]. Van Dongen and colleagues [14] demonstrated that the relative risk of paraplegia after thoracic aneurysm repair was 31-fold that of MEP of more than 50%, if MEP amplitude was 50% of the baseline or less during skin closure [14]. To prevent spinal dysfunction, spinal cord ischemia should be detected as early as possible, and protective procedures must be applied before irreversible neuronal damage has occurred. This explains why a reduction of amplitude less than 50% of the baseline was adopted as spinal cord ischemia in this study.
We have also investigated whether we could predict neurologic outcome after transient spinal cord ischemia with MEPs in a rabbit model [8]. In that experiment, MEP amplitude at the end of the procedure showed high correlation with neurologic deficits, and in particular, recovery of MEP amplitude to less than 75% indicated a risk of paraplegia. We applied these results to our clinical practice and tc-MEP monitoring with a cutoff value of 75% predicted postoperative neurologic deficits with a high sensitivity of 100% and specificity of 98.4%. To limit false-negative results, the cutoff value should be lowered. Both sensitivity and specificity will be 100% if 60% is regarded as normal spinal function (Figs 2 and 3). Further investigation is required, especially of a final MEP amplitude between 50% and 70% of the baseline, to distinguish patients suffering from spinal cord injury.
Kakinohana and colleagues [17] reported in an experimental study that MEPs could be recorded clearly after spinal interneurons were damaged, which would result in spastic paraplegia. They also reported a clinical case of spastic paraplegia, in which postoperative MEP amplitude seemed almost normal. We should, perhaps, remain aware of this possibility, but many reports, including this study, have demonstrated that MEP monitoring is a useful adjunct [14, 15].
Onset latency has not been considered a reliable predictor of spinal cord ischemia compared with amplitude. De Haan and colleagues [18] reported that no changes in onset latency were observed, even when amplitude fell below 25% of the baseline. Although latency had a tendency to be prolonged in accordance with amplitude reduction in our study, there is not enough evidence to regard onset latency as a monitor of spinal cord ischemia.
One might insist that we do not need to reattach intercostal arteries unless tc-MEPs show ischemic change. It was reported that the sacrifice of all segmental arteries caused a high paraplegia rate of 15%, even if tc-MEPs remained above 25% of the baseline [18, 19]. In a later report, the paraplegia rate had improved to less than 2% with intercostal arteries reattached under tc-MEP monitoring [13]. On the other hand, it can be debated whether tc-MEP monitoring is necessary if all patent segmental arteries are to be reattached. Judging from our experience, we can decide not only which segmental arteries should be attached but also the sites of segmental clamping or order of reattaching intercostal arteries in accordance with tc-MEP monitoring and preoperative spinal magnetic resonance angiography or computed tomography angiography, which provide information about the artery of Adamkiewicz. Furthermore, tc-MEPs are useful to undertake additional procedures such as endarterectomy to restore spinal cord blood supply.
We used tc-MEPs even for operations performed under deep hypothermia [19]. We might have to exclude these patients because MEP amplitude disappears under deep hypothermia, and this subgroup is quite different from patients who underwent just cardiopulmonary bypass. In this study, however, we would like to emphasize that MEP amplitude at the end of the procedure can predict the neurologic results and that we can perform additional procedures on the basis of these findings. Tc-MEP is therefore useful even when the operation is performed under deep hypothermia because MEP amplitude will recover with rewarming unless the spinal cord suffers ischemia. If the MEP amplitude remains absent, a further attempt to maintain spinal cord perfusion, such as the reattachment of intercostal or lumbar arteries with endarterectomy, might prevent paraplegia.
This study is not a randomized or comparative study. This is because patients who were not monitored with tc-MEP mainly had ruptured aneurysms and they were quite different from patients monitored with tc-MEP. To examine the usefulness of tc-MEP during TAAA surgery, it is preferable to compare the results between patients with and without tc-MEP. It is certain that tc-MEP is a reliable monitor of spinal ischemia, but this study does not show whether the application of tc-MEP would really reduce the incidence of paraplegia.
In conclusion, Tc-MEP monitoring was very sensitive and specific for spinal cord ischemia with amplitude reduction and prolongation of latency. Furthermore, MEP amplitude at the end of the procedure could predict postoperative spinal function. Tc-MEP monitoring is considered useful for detecting of spinal cord ischemia and helpful as a guide to surgical strategies to prevent paraplegia in the repair of thoracoabdominal aortic aneurysm.
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References |
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  M. Hamaishi, K. Orihashi, S. Takahashi, M. Isaka, K. Okada, and T. Sueda Transcranial motor-evoked potentials following intra-aortic cold blood infusion facilitates detection of critical supplying artery of spinal cord Eur. J. Cardiothorac. Surg., April 1, 2008; 33(4): 695 - 699. [Abstract] [Full Text] [PDF]
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