Ann Thorac Surg 2002;73:1155-1159
© 2002 The Society of Thoracic Surgeons
Original article: cardiovascular
Cold blood spinal cord plegia for prediction of spinal cord ischemia during thoracoabdominal aneurysm repair
Taijiro Sueda, MD*a,
Kenji Okada, MDa,
Kazumasa Orihashi, MDa,
Yuji Sugawara, MDa,
Kazuhiro Kouchi, MDa,
Katsuhiko Imai, MDa
a First Department of Surgery, Hiroshima University, School of Medicine, Hiroshima, Japan
Accepted for publication December 18, 2001.
* Address reprint requests to Dr Sueda, First Department of Surgery, Hiroshima University, School of Medicine, 1-2-3 Kasumi, Minami-ku, Hiroshima 734, Japan
e-mail: sueda{at}hiroshima-u.ac.jp
 |
Abstract
|
|---|
Background. This clinical study was undertaken to evaluate changes in motor evoked potentials (MEPs) during cold blood infusion into a thoracoabdominal aortic aneurysm. We also determined the efficacy of this infusion method for predicting spinal cord injury during thoracoabdominal aortic aneurysmal surgery.
Methods. We monitored descending evoked spinal cord potentials (ESCPs), segmental ESCPs, and MEPs during the prosthetic replacement phase of thoracoabdominal aneurysmal surgery. We perfused cold blood (4°C, 300 to 450 mL) into aneurysms after clamping the aorta, while monitoring spinal cord potentials in 6 cases of thoracoabdominal aortic aneurysm. If the spinal cord potentials decreased during infusion of cold blood, we reconstructed the intercostal arteries in the aneurysm. If the potentials did not change during the infusion of cold blood and after the aneurysmectomy, we did not reconstruct the intercostal arteries and ligated all of them.
Results. Postoperative paraplegia did not occur in any case. The MEPs decreased in amplitude after infusion of cold blood in 3 cases, but amplitude recovered after reconstruction of the intercostal arteries. The other 3 cases did not show any change after infusion of cold blood, and all of the intercostal arteries in the aneurysm were ligated.
Conclusions. Cold blood infusion into the aneurysm while monitoring MEPs was a useful adjunct to detect the presence of critical intercostal arteries and to facilitate thoracoabdominal aortic aneurysmal surgery.
 |
Introduction
|
|---|
The incidence of iatrogenic spinal cord injury remains substantial [1, 2], although improvements in operative techniques and perioperative management have reduced the overall mortality and morbidity for thoracoabdominal aortic aneurysm (TAAA) repair. Evoked spinal cord potentials (ESCPs) or somatosensory evoked cortical potentials reflect the function of the sensory nervous system and the integrity of the white matter of the spinal cord [3, 4]. However, ischemic changes in motor nerves cannot be recorded by this type of monitoring. We have measured the motor evoked potentials (MEPs) elicited by direct transcranial stimulation of the cerebral cortex during thoracoabdominal aortic aneurysm surgery since 1996 [5], and have performed selective intercostal arterial perfusion for spinal cord protection [6]. We have modified our previous method and developed a technique for cold blood infusion into the aneurysm before aneurysmectomy in conjunction with intercostal arterial reconstruction. This article describes a method of cold blood infusion into the aneurysm for prediction of spinal cord ischemia during thoracoabdominal aneurysm repair while monitoring spinal cord potentials.
 |
Patients and methods
|
|---|
A bipolar, flexible, catheter-type platinum electrode (UKG-100-2PM, Unique Medical, Tokyo, Japan) was introduced into the dorsal epidural space through a 17-gauge Tuohy needle in the cervical spinal cord (C5C6) as a stimulating electrode for measuring the ESCPs. A catheter tube with five unipolar electrodes (UKG-100-5PM; Unique Medical) was placed at the level of the lumbar enlargement (T12L1) as a recording electrode for measuring all spinal cord potentials. Both electrodes were inserted on the day before surgery. We recorded the descending ESCPs at the lumbar enlargement after cervical spinal cord stimulation, as well as segmental ESCPs at the lumbar enlargement elicited by left superficial peroneal nerve stimulation delivered by a surface electrode (Vitrode S-200, Nihon Koden, Tokyo, Japan). After induction of anesthesia two bipolar, flexible, catheter-type platinum electrodes were inserted into the subcranial space and placed on the dura mater of both motor cortices through needle puncture holes. Direct transcranial electrical stimulation of the cerebral motor cortices was then performed, and the MEPs were recorded at the lumbar enlargement (Fig 1).
Stimulation and recording were performed using a Nicolet Viking IV stimulator (Nihon Coden). All action potentials were recorded by one of five electrodes at the lumbar enlargements, which recorded the largest amplitude along the trunk.

View larger version (14K):
[in this window]
[in a new window]
|
Fig 1. Spinal cord monitoring. Descending evoked spinal cord potentials (ESCP) after cervical spinal cord stimulation and segmental ESCP elicited by left peroneal nerve stimulation were recorded at the lumbar enlargement. Two bipolar electrodes were inserted into the subcranial space and placed on the dura mater for direct transcranial electrical stimulation of the cerebral motor cortex, and motor evoked potentials (MEP) were recorded at the lumbar enlargement. (C = cervical; L = lumbar; S-ESCP = segmental evoked spinal cord potentials; Th = thoracic.)
|
|
Aneurysmectomy was performed by means of a left thoracotomy using a paramedian retroperitoneal approach. A femoro-femoral partial cardiopulmonary bypass was established (mean pump flow 2,000 to 2,600 mL/min), and the body temperature was maintained at 32°C, measured rectally. An aortic cross clamp was then placed at the proximal aorta above the aneurysm and at the distal aorta below the aneurysm. Cold blood (4°C) was infused into the aneurysm through a 12-gauge needle by gradual infusion (100 to 150 mL/min, total 300 to 500 mL) while observing the spinal cord potentials. The amount of blood infused was determined by the size of the aneurysm. If the aneurysm was large, such as a Crawford type I or type II, 450 to 500 mL of cold blood was infused. If the aneurysm was smaller, about 300 to 350 mL of cold blood was infused. We then observed the amplitude changes of the ESCPs and MEPs during the cold blood infusion and after the aneurysmectomy.
If there was a significant decrease in the amplitude of these potentials, the aneurysm was opened, and two or three pairs of intercostal arteries were reconstructed. There were usually six or seven pairs of intercostal arteries in the posterior wall of the aneurysm. The reconstruction of the intercostal arteries was typically initiated from the 9th intercostal artery to the 11th intercostal artery in this segment, because the critical intercostal artery was usually situated between the 9th intercostal artery and the L1 lumbar artery. The reconstruction of the intercostal arteries was performed using a small piece of a Dacron (CR Bard; Haverhill, PA) prosthesis (diameter 10 mm). The reconstructed intercostal artery was reperfused immediately with warm blood at a constant flow rate (40 to 50 mL/min) and perfusion pressure (100 mm Hg) for each intercostal artery pair through a small prosthesis (Fig 2).
If the recovery of the amplitude of the spinal cord potentials was not satisfactory, we continued to reconstruct the 11th or 12th intercostal artery and the L1 lumbar artery, and perfused these intercostal arteries in the same manner. If the amplitude of the MEPs recovered to the preoperative value after the reconstruction of two or three pairs of intercostal arteries (usually the 9th, 10th, and 11th intercostal arteries), we ligated the other intercostal arteries without further reconstruction. After completing the prosthetic replacement of the aneurysm, each small Dacron graft of the intercostal arteries was anastomosed to the main tube graft and perfused segmentally.

View larger version (26K):
[in this window]
[in a new window]
|
Fig 2. Cold blood infusion and selective intercostal arterial perfusion. Cold blood was infused into the aneurysm before aneurysmectomy. If the amplitude of motor evoked potentials decreased, the critical intercostal arteries were reconstructed. Reconstruction of the intercostal artery was initiated from the 9th to 11th intercostal artery. These arteries were reconstructed using a small piece of Dacron prosthesis, then reperfused immediately with warm blood (blood flow, 40 to 50 mL/min) for each artery pair.
|
|
If there was no diminution of the amplitude of the spinal cord potentials during the infusion of cold blood into the aneurysm and after the aneurysmectomy, all intercostal arteries in the aneurysm were ligated. We then continued to reconstruct the distal part of the aneurysm with visceral arterial reconstruction using a branched graft under visceral arterial perfusion (150 mL/min for each visceral artery).
Six patients with thoracoabdominal aortic aneurysms were operated on using this monitoring protocol and selective cold blood infusion. All of these cases were atherosclerotic aneurysms. Approval for this monitoring and perfusion protocol was obtained from our institutional review board. We informed the patients as to the proposed instrumentation, and all gave written consent.
 |
Results
|
|---|
This procedure was performed on 6 patients with atherosclerotic thoracoabdominal aneurysms (3 with Crawford type I, and 3 with Crawford type III). There were no complications associated with the spinal cord monitoring either during or after surgery.
Three patients showed a decrease in their MEPs during the infusion of cold blood into the aneuryms and underwent intercostal arterial reconstruction. Patent intercostal arteries from the 9th to 12th intercostal arteries were principally reconstructed; however, small and occlusive intercostal arteries were sacrificed. The mean number of intercostal arteries reconstructed was 2.7 pairs (Table 1).
The mean partial femoro-femoral bypass time was 82 min in these patients (Table 2).
The amplitudes of all MEPs returned to normal after the completion of the intercostal arterial reconstruction. The MEP was the most sensitive and responsive indicator among the spinal cord potentials during cold blood infusion into the aneurysm and after reconstruction of the intercostal arteries. The amplitude of the MEPs decreased significantly within 3 min after the infusion of cold blood into the thoracoabdominal aorta (Fig 3).
Reconstruction of each intercostal artery required between 8 and 12 minutes. Once the critical intercostal artery was reconstructed and reperfused, the amplitude of the MEP recovered quickly. The amplitude of the ESCPs and S-ESCPs did not change significantly during either the infusion of cold blood into the aneurysm or the reconstruction of the intercostal arteries. Reconstruction of two to three pairs of intercostal arteries was usually enough to achieve full recovery of the MEP amplitude. If full recovery of the MEP was obtained by reconstructing two or three pairs of intercostal arteries (usually T9, T10, and T11), we presumed that the critical spinal cord artery had been reconstructed. After the reconstruction of the intercostal arteries, the MEPs recovered to their preoperative levels in all patients. None of the patients experienced any spinal neurologic deficits postoperatively (Table 2).

View larger version (30K):
[in this window]
[in a new window]
|
Fig 3. Changes in evoked spinal cord potentials (ESCP) during cold blood infusion into aneurysm. Amplitude of motor evoked potentials (MEPs) decreased significantly during infusion of cold blood into the aneurysm. Once intercostal arteries were reconstructed and reperfused, the amplitude of the MEP recovered quickly. (ICA = intercostal artery; min = minute(s); Th = thoracic; S-ESCP = segmental evoked spinal cord potentials.)
|
|
Three patients who showed no decrease in the amplitude of their MEPs during or after the infusion of cold blood underwent a ligation of the intercostal arteries in the aneurysm, which was quickly replaced by the tube prosthesis. The spinal cord potentials did not change during or after surgery in these 3 cases, nor did they show any spinal cord damage after surgery (Table 2).
 |
Comment
|
|---|
Prevention of paralysis after repair of thoracoabdominal aortic aneurysm remains an ultimate goal. Many methods of reducing the degree and duration of spinal cord ischemia during aortic crossclamping, including distal perfusion, hypothermia, spinal fluid drainage, segmental repairs of intercostal arteries, and use of pharmacological agents have been reported [711]. Svensson and colleagues [12, 13] have reported important work such as reattachment of segmental intercostal arteries from T-7 to L-1 and accuracy of MEPs to identify segmental arteries that supply the spinal cord. They also reported a local infusion of a single dose of cold crystalloid with lidocaine as a type of "spinoplegia" was found to be effective in reducing the severity of ischemia during aortic crossclamping, but was apparently less effective in reducing neurologic deficits [14]. These studies differ on how best to manage intercostal and lumbar arteries at the time of aortic repairs. Because the duration of aortic crossclamping is the most significant predictor of risk of spinal cord damage, the time required to reattach intercostal vessels may increase the risk of paralysis. Although reattachment of none of the intercostal arteries can shorten the period of aortic crossclamping, there is higher incidence of paralysis. In that case, we usually perform reattachment of the intercostals from T-7 down to and including L-1, which are most likely to supply the artery of Adamkiewcz on the basis of anatomic studies [15, 16].
We tried to identify existence of the segmental arteries by infusing cold blood into the aneurysm under MEP monitoring in this study. Using reductions in the amplitude of the MEP signal to detect ischemic damage to the thoracic spine during aortic occlusion, we previously reported the superior sensitivity of the MEP in predicting approximately 90% of the incidence of spinal cord damage in an animal model [5]. In this study, the amplitude of the MEP decreased immediately and diminished significantly within 3 min after the infusion of cold blood. This means that cold blood infusion promotes a decrease in MEP amplitude. A single bolus infusion of cold fluid (4°C saline) into the intercostal arteries decreased the temperature of the spinal cord by 6° to 7°C below body temperature in an experimental study [17]. We used mild hypothermia at a body temperature of 32°C during partial extracorporeal circulation, in addition to cold blood infusion (4°C) into the aneurysm. Therefore, the spinal cord temperature might be cooled to less than 26°C. Hypothermia induces a depression of the electrophysiologic response of both cerebral and peripheral neurologic activity [18, 19]. The quick decrease in the MEP amplitude is thought to be induced by cold blood infusion into the spinal cord [17]. The dissociation of the evoked response between the MEPs and ESCPs during cold blood infusion might depend on the temperature sensitivity of each evoked potential, as well as its sensitivity to ischemia [18, 19]. An encephalogram is more easily depressed than somatosensory evoked potentials by hypothermia [18]. This means that MEPs are more sensitive to hypothermia as well as to ischemia. A decrease in the MEP amplitude during cold blood infusion suggests the presence of a critical spinal cord artery in the aneurysm. We could diagnose a decrease in the MEP amplitude during cold blood infusion and quickly reconstruct two or three pairs of intercostal arteries in the aneurysm. In addition, we could decide whether the intercostal arteries in the aneurysm could be ligated by this method. We could safely ligate all of the intercostal arteries in the aneurysm in those patients who showed no change in their MEP during cold blood infusion or after the aneurysmectomy.
However, it is questionable whether a single bolus infusion of cold blood could prevent postoperative paraplegia after a long period of ischemia to the spinal cord. The infusion of a hypothermic solution leads to an abrupt drop in spinal cord temperature during the initial phase of ischemia [17], but the spinal cord temperature rose again quickly because of collateral circulation. Therefore, a single bolus infusion of cold blood is useful for detecting critical intercostal arteries but is not sufficient for the prevention of spinal cord ischemic injury.
Although it seems complicated to perform our procedure and more research will be necessary, we conclude that cold blood infusion into an aneurysm under MEP monitoring is an effective method for predicting the presence of critical spinal cord arteries, and for simplifing thoracoabdominal aneurysmal repair.
 |
References
|
|---|
-
Crawford E.S., Crawford J.L., Safi J.H., et al. Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operation of 605 patients. J Vasc Surg 1986;3:389-404.[Medline]
-
Laschinger J.G., Izumoto H., Kouchoukus N.T. Evolving concepts in prevention of spinal cord injury during operation on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 1987;44:667-674.[Abstract]
-
Cunningham J.N., Jr, Laschinger J.C., Spencer F.C. Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta: IV. Clinical observations and results. J Thorac Cardiovasc Surg 1987;94:275-285.[Abstract]
-
Yamamoto N., Takano H., Kitagawa H., Kawaguchi Y., Tsuji H., Uozaki Y. Monitoring for spinal cord ischemia by use of the evoked spinal cord potentials during aortic aneurysm surgery. J Vasc Surg 1994;20:826-833.[Medline]
-
Tanaka S., Fujimoto Y., Sasaki M., Oka S., Ikuta Y., Sueda T. Effect of spinal cord ischemia on spinal cord evoked potentials. J Electrodiagn Spinal Cord 1997;19:21-24.
-
Sueda T., Morita S., Okada K., et al. Selective intercostal arterial perfusion during thoracoabdominal aortic aneurysm surgery. Ann Thorac Surg 2000;70:44-47.[Abstract/Free Full Text]
-
Svensson L.G., Hess K.R., Coselli J.S., Safi H.J. Influence of segmental arteries, extent, and atrio-femoral bypass on post-operative paraplegia after thoracoabdominal aortic aneurysm repairs. J Vasc Surg 1994;20:255-262.[Medline]
-
Kouchoukos N.T., Daily B.D., Rokkas C.K., et al. Hypothermic bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 1995;60:67-77.[Abstract/Free Full Text]
-
Safi H.J. Neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysm: the role of cerebral spinal fluid drainage and distal aortic perfusion. J Vasc Surg 1994;20:434-443.[Medline]
-
Crawford E.S., Svensson L.G., Hess K.R., et al. A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery on the thoracoabdominal aorta. J Vasc Surg 1991;13:36-45.[Medline]
-
Acher C.W., Wynn M.M., Hoch J.R., Popic P.M., Turnipseed W.D. Combined use of spinal fluid drainage and naloxone reduces risk of neurologic deficit in the repair of thoracoabdominal aneurysms. J Vasc Surg 1994;19:236-248.[Medline]
-
Svensson L.G., Crawford E.S., Hess K.R., Coselli J.S., Safi H.J. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993;17:357-370.[Medline]
-
Svensson L.G., Patel V., Robinson M.F., Ueda T., Roehm J.O., Jr, Crawford E.S. Influence of preservation or perfusion of intraoperatively identified spinal cord blood supply on spinal motor evoked potentials and paraplegia after aortic surgery. J Vasc Surg 1991;13:355-365.[Medline]
-
Svensson L.G., Crawford E.S., Patel V., McLean T.R., Jones J.W., DeBakey M.E. Spinal oxygenation, blood supply localization, cooling, and function with aortic clamping. Ann Thorac Surg 1992;54:74-79.[Abstract]
-
Kieffer E., Richard T., Chiras J., Godet G., Cormier E. Preoperative spinal cord arteriography in aneurysmal disease of the descending thoracic and thoracoabdominal aorta: preliminary results in 45 patients. Ann Vasc Surg 1989;3:34-46.[Medline]
-
William G.M., Perler B.A., Burdick J.F., et al. Angiographic localization of spinal cord blood supply and its relationship to postoperative paraplegia. J Vasc Surg 1991;13:23-33.[Medline]
-
Ueno T., Furukawa K., Katayama Y., et al. Protection against ischemic spinal cord injury: one-shot perfusion cooling and percutaneous topical cooling. J Vasc Surg 1994;19:882-887.[Medline]
-
Stecker M.M., Cheung A.T., Pochettino A., et al. Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials. Ann Thorac Surg 2001;71:14-21.[Abstract/Free Full Text]
-
Stecker M.M., Cheung A.T., Pochettino A., et al. Deep hypothermic circulatory arrest: II. Changes in electroencephalogram and evoked potentials during rewarming. Ann Thorac Surg 2001;71:22-28.[Abstract/Free Full Text]
This article has been cited by other articles:

|
 |

|
 |
 
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]
|
 |
|

|
 |

|
 |
 
T. Fleck, C. Hamilton, M. P. Ehrlich, D. Hutschala, H. Koinig, E. Wolner, and M. Grabenwoger
Thoracoabdominal Aortic Aneurysm Repair: Reducing Adverse Outcome with Left Heart Bypass, Selective Visceral Perfusion and Renal Protection
Seminars in Cardiothoracic and Vascular Anesthesia,
December 1, 2002;
6(4):
287 - 291.
[Abstract]
[PDF]
|
 |
|