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Ann Thorac Surg 2002;74:S1867-S1869
© 2002 The Society of Thoracic Surgeons
a Cliniques Universitaires St-Luc, Catholic University of Louvain, Brussels, Belgium
b Leids Universitair Medisch Centrum, Leiden, The Netherlands
* Address reprint requests to Dr Guérit, Service "Potentiels Evoqués," Cliniques Universitaires Saint-Luc, Avenue Hippocrate, 10, B-1200 Brussels, Belgium
e-mail: guerit{at}nchm.ucl.ac.be
Presented at the Aortic Surgery Symposium VIII, May 2–3, 2002, New York, NY.
Abstract
BACKGROUND: The prevention of immediate and delayed paraplegia after thoracoabdominal aorta surgery relies on hemodynamic maneuvers (aimed at restoration of an adequate spinal cord perfusion pressure) and cytoprotective measures (hypothermia, drugs).
METHODS: The indications for implementing these measures can be provided by motor-evoked potential (MEP) or somatosensory-evoked potential (SEP) monitoring.
RESULTS: Intraoperative interactions between the surgeon and the neurophysiologist can be described by algorithms to be applied in the presence or absence of intraoperative MEP or SEP changes.
CONCLUSIONS: It should be noted that normal SEPs or MEPs at the end of surgery do not systematically guarantee the nonoccurrence of delayed paraplegia, especially when segmental arteries have been ligated, in which case postoperative SEP monitoring is indicated.
Proposed methods to prevent both immediate and delayed paraplegia after descending aorta surgery can be subdivided into those aimed at restoring an adequate spinal cord perfusion pressure (SCPP: maintenance of sufficient systemic blood pressure, atrio-femoral shunting, reimplantation of critical arteries, cerebrospinal fluid drainage) and those protecting the spinal cord against cytotoxic damage when SCPP is insufficient (drugs, local or systemic hypothermia) [1–3]. Even if all these measures are theoretically justified, none of these has as yet been independently proven fully efficient, and most have possible adverse effects [1, 3, 4]. That means that they should only be used when actually needed. This justifies neuromonitoring, whose value resides in its ability to detect ischemic penumbra, that is, the pathophysiological state occurring in acute ischemia in which neurons are nonfunctional but still alive and salvageable by appropriate measures [5]. Nevertheless, even if there is increasing evidence that neuromonitoring has helped prevent paraplegia in several cases, some issues are still a matter of debate: the choice between somatosensory-evoked potentials (SEPs) [6, 7] and motor-evoked potentials (MEPs) [8]; the time period (intra- or postoperative) over which neuromonitoring must be performed; and the rules of the interaction between the surgeon and the neurophysiologist. The aim of this paper is to reexamine these issues in light of the pathophysiology of immediate and delayed paraplegia.
Pathophysiology of spinal cord ischemia
Ischemic penumbra just means that the energy supply of the involved tissue is no longer adapted to its metabolic needs. Thus, even if a marked decrease in SCPP always causes dysfunction irrespective of the current metabolic needs of the spinal cord, a milder decrease may remain compatible with intact function as long as metabolic needs are relatively low, but may be associated with ischemia if they subsequently increase. Recent evidence has challenged the concept of a unique Adamkiewicz artery whose occlusion would totally compromise spinal cord blood supply, so segmental spinal cord ischemia can no longer be considered an "all-or-none" phenomenon [9, 10]. Moreover, the intraoperative metabolic needs of the spinal cord are likely to be relatively low, owing to relative hypothermia, optimal oxygenation and O2 transport, and patient immobility. Taken together, these considerations imply that the absence of intraoperative signs of ischemia in a patient in whom segmental arteries were excluded does not guarantee that ischemia will not occur postoperatively, particularly in the event of relative hypotension, hypoxia, anemia, or patient agitation [6, 11]. It should be evident that intraoperative monitoring can only reveal the concurrent status of spinal pathways, but may be unable to predict postoperative complications, and that neuromonitoring should, therefore, be pursued postoperatively [6, 7].
MEPs or SEPs?
We have previously discussed the values of SEPs and MEPs in terms of feasibility, sensitivity, and specificity [12].
Regarding sensitivity, any given test becomes more sensitive as it evaluates neural structures that are more exposed to ischemia. That is, monitoring must always aim at assessing the most sensitive structures. Both metabolic and hemodynamic factors explain that the central gray matter of the lumbar enlargement is most exposed to ischemia, as confirmed by magnetic resonance imaging studies of patients with paraplegia of vascular origin [13]. The central gray matter of the spinal cord is assessed by both SEPs and MEPs, which are therefore likely to complement each other. Indeed, MEPs depend on motor neuron integrity in the anterior horns, which cannot be assessed by SEPs, and the SEP lumbar N24 depends on the dorsal horn of the spinal cord, which cannot be assessed by MEPs. Therefore, and to increase safety by redundancy, it is highly recommended to combine SEPs and MEPs whenever possible. It should be noted that the argument that SEPs only test the posterior columns whereas MEPs are more sensitive because they test the pyramidal tracts is an oversimplification, because both structures belong to white matter, which is not the most sensitive neural tissue, and both structures are equally exposed, owing to the anatomy of spinal cord blood supply [14]. The expected equivalence of MEPs and SEPs has also been confirmed statistically, without any definitely proven superiority of either technique [13].
Test feasibility depends on both the anesthetic constraints and the preoperative neurologic factors liable to interfere with MEPs or SEPs. Reliable MEP recording actually requires the combination of special anesthetic regimens (ketamine or etomidate/fentanyl); special stimulation techniques (paired electrical stimuli of high intensity), and partial neuromuscular blockade [8]. This anesthestic regimen is fully compatible with reliable SEP recording. It is noteworthy that electrical stimulations are particularly painful, and therefore cannot be used postoperatively in awake, sedated patients. Because magnetic MEPs are unreliable in sedated patients [15], only SEPs are usable in the postoperative period.
Regarding test specificity, we have demonstrated that, although cortical SEP alterations are not specific for spinal cord ischemia, multilevel SEP recordings have always allowed us to disentangle these alterations due to distal or segmental spinal cord ischemia from those resulting from peripheral nerve or brain ischemia [6]. Although MEPs are also able to differentiate spinal cord ischemia (bilateral MEP alterations) from unilateral peripheral nerve ischemia or ischemia in the left carotid artery territory (unilateral MEP alterations), they do not allow differentiation of distal from segmental ischemia. Thus, although the sensitivities of cortical SEPs and MEPs look similar, multilevel SEPs allow one more easily to pinpoint precisely the type of spinal cord ischemia.
Rules of the interactions between the surgeon and the neurophysiologist
Whereas the prevention of immediate paraplegia should only rely on intraoperative strategies (restoration of SCPP through shunting; reimplantation of culprit vessels in case of segmental ischemia or CSF drainage; and intraoperative prevention of cytotoxic damage whenever transient ischemia cannot be avoided), avoidance of delayed paraplegia must rely on both intraoperative (reimplantation of as many segmental arteries as technically feasible) and postoperative strategies, especially in cases of increased risk of spinal cord ischemia. In the presence of developing delayed ischemia, strategies should include CSF drainage and spinal cord protection (oxygenation, sedation, and elevation of blood pressure). It should be noted that the reimplantation of "all" arteries increases the risk of immediate lesions if it is association with too long a period of intraoperative ischemia in the absence of spinal cord protection. And spinal cord "over-protection" may increase the risk of delayed paraplegia if the absence of signs of intraoperative ischemia is inappropriately interpreted as indicating sufficient perfusion in a patient in whom several segmental arteries have been ligated.
Intraoperative interaction
Alterations of MEPs or brain stem or cortical SEPs (Fig 1) first raise the issue of their origin: peripheral nerve, spinal cord, or brain (ischemia in the territory of one carotid artery, or a consequence of systemic hypoperfusion). Several criteria may help disentangle these alterations. These include: MEP or SEP comparison to stimulation of left/right, upper/lower limbs; differential recording of peripheral nerve, lumbar, brain stem, and cortical SEP components; dynamics of changes (alterations of peripheral origin are usually slower to develop [> 15 minutes] than alterations due to the spinal cord [< 15 minutes] or to brain ischemia [< 7 minutes]); and temporal relationships with intraoperative events (carotid, aortic or segmental artery cross-clamping, drop in blood pressure) [6]. Alterations of brain or spinal cord origin must always be promptly corrected (blood pressure restoration, removal of a carotid cross-clamp, atrio-femoral shunting if not systematically performed, reimplantation of segmental arteries) in order to avoid more than a 30-minute loss of cortical components [16]. If a longer delay is expected for technical reasons, measures for spinal cord protection should be started (systemic or local cooling, cerebrospinal fluid drainage, drugs), taking into account that the efficacy of these measures spans just the period of their application.
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Postoperative interaction
Whenever there is any risk of delayed ischemia (ligation of intercostals or lumbar arteries, or need for intraoperative supplementary measures for spinal cord protection), monitoring must be continued until the patient can be evaluated clinically. Owing to the painful character of electrical brain stimulation and the variability of magnetic transcranial stimulation in sedated patients [15], only SEPs can be used. These should be recorded according to an automatic predetermined schedule (for example, one recording every 30 minutes), with the possibility of immediate recording whenever there is any risk of delayed ischemia (relative hypotension, anemia, agitation). If present, SEP alterations must be corrected (blood pressure restoration, cerebrospinal drainage, or prevention of cytotoxic damage).
References
This article has been cited by other articles:
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  P. E. Achouh, A. L. Estrera, C. C. Miller III, A. Azizzadeh, A. Irani, T. L. Wegryn, and H. J. Safi Role of Somatosensory Evoked Potentials in Predicting Outcome During Thoracoabdominal Aortic Repair Ann. Thorac. Surg., September 1, 2007; 84(3): 782 - 788. [Abstract] [Full Text] [PDF]
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 A. Winnerkvist, R. E. Anderson, L.-O. Hansson, L. Rosengren, A. E. Estrera, T. T.T. Huynh, E. E. Porat, and H. J. Safi Multilevel somatosensory evoked potentials and cerebrospinal proteins: indicators of spinal cord injury in thoracoabdominal aortic aneurysm surgery Eur. J. Cardiothorac. Surg., April 1, 2007; 31(4): 637 - 642. [Abstract] [Full Text] [PDF]
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 S. A. LeMaire, L. N. Ochoa, L. D. Conklin, R. A. Widman, F. J. Clubb Jr, A. Undar, Z. C. Schmittling, X. L. Wang, C. D. Fraser Jr, and J. S. Coselli Transcutaneous near-infrared spectroscopy for detection of regional spinal ischemia during intercostal artery ligation: preliminary experimental results. J. Thorac. Cardiovasc. Surg., November 1, 2006; 132(5): 1150 - 1155. [Abstract] [Full Text] [PDF]
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E. Weigang, M. Hartert, M. P. Siegenthaler, K. Pitzer-Hartert, M. Luehr, R. Sircar, P. von Samson, and F. Beyersdorf Neurophysiological monitoring during thoracoabdominal aortic endovascular stent graft implantation Eur. J. Cardiothorac. Surg., March 1, 2006; 29(3): 392 - 396. [Abstract] [Full Text] [PDF]
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