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Canadian Journal of Anesthesia 52:335-336 (2005)
© Canadian Anesthesiologists' Society, 2005


Correspondence

Intraoperative neuromonitoring in cardiac surgical patients with severe cerebrovascular disease

Alexander Kulik, MD, Rosendo A. Rodriguez, MD PhD, Howard J. Nathan, MD and Marc Ruel, MD MPH

University of Ottawa, Ottawa, Canada, E-mail: akulik{at}ottawaheart.ca

To the Editor:

Patients with severe cerebrovascular disease are at a high risk of neurologic complications during cardiac surgery, as a result of cerebral embolization or hypoperfusion during cardiopulmonary bypass (CPB). Intraoperative neuromonitoring, including transcranial Doppler ultrasound (TCD) and electroencephalography (EEG), may be particularly useful in patients with cerebrovascular disease.1 We hereby present two cases that illustrate the use of intraoperative neuromonitoring during cardiac surgery in patients with severe cerebrovascular disease.

Patient A suffered a recent right cerebellar stroke and had high-grade obstructing lesions in the right subclavian, right vertebral and mid-basilar arteries, and no posterior communicating arteries. Patient B had a complete occlusion of the right internal carotid artery (ICA) and a 90% stenosis of the left ICA. Both patients were referred for coronary artery bypass graft surgery (CABG) with severe triple vessel coronary disease. Due to the risk of inadequate cerebral perfusion during CPB, intraoperative neuromonitoring techniques were employed for each patient.

After anesthetic induction, electrodes were positioned to continuously record EEG activity. Doppler probes were placed on each temporal window to monitor blood flow in the middle cerebral arteries (MCA). A tight control of cerebral perfusion was ensured with mean systemic blood pressures above 80 mmHg and CPB flows above 5.5 L·min–1. Doppler monitoring of Patient A revealed symmetric flow in both middle cerebral arteries that increased during CPB. A discharge of 53 high-intensity transient signals (HITS) was detected when the aorta was unclamped, followed by a transient period of EEG slowing, but without localized changes on the EEG (FigureGo). Patient B’s Doppler examination revealed flow in both MCA and flow in the opposite direction at the level of the posterior communicating artery, suggesting collateral flow to the anterior circulation from the vertebro-basilar system. No changes indicative of hypoperfusion were identified during Patient B’s surgery. Following CABG, each patient had an uneventful postoperative course free of neurologic injury.



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FIGURE A discharge of high-intensity transient signals (HITS) and brief rise in cerebral blood flow at aortic unclamping (upper figure). This was associated with a transient period of electroencephalography (EEG) slowing (lower figure).

 
Recognition of cerebral hypoperfusion or emboli using neuromonitoring techniques represents an important advance in the prevention of neurologic complications during cardiac surgery. Through the appearance of excessive slow-wave activity, intraoperative EEG can detect a disturbance of cerebrocortical function suggestive of inadequate cerebral perfusion or oxygenation. However, additional monitoring is required to identify the etiology of EEG slowing since cerebrocortical depression resulting from ischemia cannot be discriminated from other causes such as anesthesia or cooling.1 Continuous TCD, on the other hand, provides information regarding the status of the cerebrovasculature, including the direction of blood within the cerebral vessels.2 TCD can also identify the presence, although not necessarily the composition, of HITS, indicative of cerebral emboli.3 Associated with a greater atheromatous burden of the aorta,4 the number of HITS and the location of HITS-related brain damage seem to influence the occurrence of neurologic complications.3

Employed together, a drop in the TCD signal and EEG slowing suggest an evolving ischemic process, providing the surgical team with the opportunity to correct perfusion abnormalities using mechanical or pharmacological support.2 Alternatively, neuroprotective strategies, such as systemic hypothermia and pharmacologic suppression of neuronal activity,5 could be initiated before the development of irreversible injury. Despite the severity of cerebrovascular disease in these two patients, neuromonitoring identified acceptable cerebral flow, and the maintenance of high perfusion pressures likely minimized the risk during surgery. Neuromonitoring-based interventions have previously been demonstrated to reduce postoperative neuropsychologic dysfunction in cardiac surgical patients,5,6 and may therefore prove to be a useful modality for the increasing proportion of high-risk patients undergoing cardiac surgery.

References

1 Edmonds HL Jr, Rodriguez RA, Audenaert SM, Austin EH III, Pollock SB Jr, Ganzel BL. The role of neuromonitoring in cardiovascular surgery. J Cardiothorac Vasc Anesth 1996; 10: 15–23.[Medline]

2 Kochi K, Sueda T, Orihashi K, Matsuura Y. Central retinal artery color Doppler monitoring versus transcranial Doppler monitoring in cardiac surgery. Heart Vessels 2000; 15: 7–10.[Medline]

3 Jacobs A, Neveling M, Horst M, et al. Alterations of neuropsychological function and cerebral glucose metabolism after cardiac surgery are not related only to intraoperative microembolic events. Stroke 1998; 29: 660–7.[Abstract/Free Full Text]

4 Mackensen GB, Ti LK, Phillips-Bute BG, Mathew JP, Newman MF, Grocott HP. Cerebral embolization during cardiac surgery: impact of aortic atheroma burden. The Neurologic Outcome Research Group (NORG). Br J Anaesth 2003; 91: 656–61.[Abstract/Free Full Text]

5 Arom KV, Cohen DE, Strobl FT. Effect of intraoperative intervention on neurological outcome based on electroencephalographic monitoring during cardiopulmonary bypass. Ann Thorac Surg 1989; 48: 476–83.[Abstract]

6 Edmonds HL Jr. Advances in neuromonitoring for cardiothoracic and vascular surgery. J Cardiothorac Vasc Anesth 2001; 15: 241–50.[Medline]





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