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Prevention of Ischemic Neurologic Injury with Intraoperative Neurol Clin 24 (2006) 631–645 Prevention of Ischemic Neurologic Injury With Intraoperative Monitoring of Selected Cardiovascular and Cerebrovascular Procedures: Roles of Electroencephalography, Somatosensory Evoked Potentials, Transcranial Doppler, and Near-Infrared Spectroscopy Michael A. Sloan, MD, MSa,b,* aDivision of Neurology, Neuroscience and Spine Institute, Carolinas Medical Center, Charlotte, NC, USA bUniversity of North Carolina at Chapel Hill, Chapel Hill, NC, USA The United States Census estimates that there will be 40 million Ameri- cans ages 65 and older in 2010 [1]. The aging population undoubtedly will result in an increased occurrence of chronic diseases, such as cardiovascular (coronary and aortic) and cerebrovascular (carotid artery) diseases, which will lead to an increasing number of surgical and interventional procedures. The American Heart Association estimates that of 709,000 open-heart pro- cedures performed in 2002, 515,000 were coronary artery bypass grafting (CABG) procedures [2]. Postoperative neurologic complications, including cerebral infarction and encephalopathy, occur in up to 15% of patients who undergo CABG surgery. In addition, neuropsychologic testing can doc- ument behavioral abnormalities in up to 70% of patients [3–11]. The risk of stroke after CABG can be predicted based on characteristics known before surgery [8,11–16]. Carotid endarterectomy (CEA) is the noncardiac vascular procedure performed most frequently, with 134,000 procedures performed * Carolinas Medical Center, Neuroscience and Spine Institute, Division of Neurology, 1010 Edgehill Road North, Charlotte, NC 28207. E-mail address: [email protected] 0733-8619/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.ncl.2006.05.002 neurologic.theclinics.com 632 SLOAN in the United States in 2002. The complication rate after CEA should be maintained at an extremely low rate (between 5% and 6% for symptomatic and !3% for asymptomatic internal carotid artery [ICA] disease) by sur- geons to maintain the beneficial effects of CEA over medical therapy [17]. The number of CEAs likely will increase because of aging of the population and the results of the Asymptomatic Carotid Atherosclerosis Study and the Asymptomatic Carotid Surgery Trial [17]. Neurologic injury is a significant problem during repairs of the ascending and transverse aortic arch repairs and during repairs of the acute type A aortic dissection [18,19]. For the acute type A aortic dissection, the incidence of focal neurologic injury ranges from 1% to 11% and is associated with increased early and late mor- tality [20–23]. In addition, postoperative confusion, agitation, or delirium, collectively known as temporary neurologic dysfunction, varies in incidence from 9% to 32% [24,25], with detrimental long-term consequences [26]. The occurrence of adverse neurologic outcomes after diverse cardiovas- cular and cerebrovascular procedures has fostered the development of methods to monitor the brain and cerebral circulation noninvasively in an attempt to identify electrophysiologic, hemodynamic, and other ab- normalities that may be ameliorated by changes in operative technique or treatment. The ideal neuromonitoring system should provide continuous, real-time information about the cerebral circulation and cerebral function. Currently available functional neuromonitoring methods include electroen- cephalography (EEG) [27] and somatosensory evoked potentials (SSEP) [28], whereas circulatory/hemodynamic information can be provided by transcranial Doppler ultrasonography (TCD) [29,30] and near-infrared spectroscopy (NIRS) [30]. Each of these methods has advantages and disad- vantages, and no one technique has perfect sensitivity, specificity, or dis- criminating value in a specific setting. This article has two objectives. First, the capabilities of each noninvasive technique are described briefly. Second, data on the use of these techniques, often applied in combination, in the settings of CABG, CEA, and aortic sur- gery, are presented. Noninvasive neuromonitoring methods Electroencephalography Cerebral ischemia produces neuronal dysfunction, leading to slowing of frequencies or reduced amplitude in the EEG tracing. These changes may be generalized (global ischemia) or regional (focal ischemia). The depth of ischemia is associated with the severity of EEG changes. EEG cannot assess the whole cerebral cortex, however, and is less reliable at assessing subcor- tical structures. In the setting of CEA, the focal EEG changes after cross clamping the carotid artery may be defined as none, mild (increase in theta waves !25% or decrease in amplitude O50%), moderate (increase of theta PREVENTION OF ISCHEMIC NEUROLOGIC INJURY 633 waves O25% or increase of delta waves !25%), or severe (increase of delta waves O25%, severe flattening of amplitude or isoelectric curve). In patients who receive thiopental narcosis to induce burst suppression, only asymme- tries between the hemispheres can be used [31]. Somatosensory evoked responses Cerebral ischemia results in delay in the arrival of or reduction in ampli- tude of evoked responses, as measured by peak-peak amplitudes of the cer- vical potential N14-P18 and the primary cortical response N20-P25 from the postcentral region on the side that is operated on. Critical ischemia leading to cerebral hypoperfusion is assumed if the N20-P25 peak on the side oper- ated on is not identifiable [32]. Transcranial Doppler ultrasonography TCD uniquely measures local blood flow velocity (BFV) (speed and di- rection) in the proximal portions of large intracranial arteries [29], based on the assumption that the angle of insonation between the ultrasound beam and the direction of arterial flow is 0 to 30. As long as fluctuations in arterial blood pressure and arterial CO2 content are small, changes in flow velocity reflect changes in cerebral blood flow [33,34]. TCD monitoring of the middle cerebral artery (MCA) does not provide information about he- modynamic changes occurring in arteries that may serve as collateral path- ways supplying ischemic brain. Hemodynamic compromise is inferred when there is reduction in mean flow velocities or when there is slow flow acceler- ation. In addition, TCD can detect cerebral microembolic signals, reflecting the presence of gaseous or particulate matter in the insonated cerebral ar- tery. Particulate (solid or fat) or gaseous (gas or air) materials in flowing blood are larger and of different composition and, thus, have different acoustic impedance than surrounding red blood cells. The Doppler ultra- sound beam, thus, is both reflected and scattered at the interface between the embolus and blood, resulting in an increased intensity of the received Doppler signal. Microembolic signals are detected in patients who have or do not have symptoms, in patients who have diverse cardiovascular or cere- brovascular diseases, and in patients undergoing a wide variety of surgical and interventional procedures. There often is considerable overlap of inten- sities and velocities corresponding to particles of different compositions and sizes. A completely accurate and reliable characterization of embolus size and composition, however, is not yet possible with current technology [29]. Near-infrared spectroscopy In brain tissue, the venous oxygen saturation predominates (70%–80%), and cerebral oximetry relies on this fact. NIRS uses light optical spectros- copy in the near-infrared range to evaluate brain oxygen saturation by 634 SLOAN measuring regional cerebral venous oxygen saturation (rCVOS) [30]. As- suming constant metabolism, the change of hemoglobin is directly propor- tional to the change of CBF. A reduction in rCVOS is believed to reflect the occurrence of cerebral ischemia. Clinical applications of cerebral oximetry have relied on relative changes expressed as percent deviation from baseline [30]. TCD can be used to localize the embolic source or monitor the effects of antithrombotic treatment in patients who have atherosclerotic cerebrovas- cular disease [35–39]. In patients who have high-grade carotid stenosis, sour- ces of asymptomatic microembolic signals may include ulcerated plaques [40,41] and microscopic platelet aggregates and fibrin clots [42]. Asymptom- atic cerebral microembolization is reported to be associated with an increased risk of further cerebral ischemia (odds ratio 8.10; 95% CI, 1.58– 41.57) in this setting [40]. Recently, cessation of microembolic signal detec- tion after institution or modification of antiplatelet but not anticoagulant therapy has been reported in patients who have arterioembolic cerebrovas- cular disease [40]. Perioperative and periprocedural monitoring Coronary artery bypass graft surgery During cardiopulmonary bypass (CPB), the brain is subjected to marked changes in systemic and cerebral hemodynamics, temperature, oxygenation, and hematocrit. Although the etiology and reversibility of neurologic injury after CABG are not understood completely, there is evidence that hypo- and hyperperfusion with consequent compromise of oxygen delivery and focal occlusion by microemboli or macroemboli may play a role [29,30]. TCD monitoring can show MCA BFV changes in all phases of the op- eration. Flow velocities decrease after induction of anesthesia and during initiation of CPB and increase during rewarming; changes correlate best with temperature and arterial CO2 content [43,44]. Flow velocity changes typically remain within a relatively narrow range and do not correlate with
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