Bispectral index and detection of acute brain injury during cardiac surgery.

EDITOR: Stroke, encephalopathy and cognitive disorders following cardiac surgery remain devastating problems as a result of macroor micro-embolic phenomena or global cerebral hypoperfusion [1]. Besides, more sophisticated neuromonitoring systems (i.e. raw electroencephalogram (EEG), evoked potential, near infra-red spectroscopy), the bispectral index (BIS) derived from a single channel frontal EEG may serve as a simple and less-expensive tool, which affords the unique opportunity to gauge the hypnotic level while detecting cortical dysfunction [2]. Herein, we report a case of severe depression of the BIS index and discuss a multimodal approach for early diagnosis of neurological dysfunction. A 62-yr-old female with an aneurysm of the ascending aorta and stable aortic insufficiency was scheduled for elective valve replacement and aortic prosthetic graft insertion. The patient was chronically treated for diabetes, hyperlipidaemia and hypertension. Four weeks previously, she had suffered a stroke associated with atrial fibrillation. Preoperative cardiac investigations demonstrated normal ventricular function, patent coronary arteries and a 50% stenosis on the left carotid artery with a hypoplastic right vertebral artery. At arrival in the operating room – in addition to standard equipment – a 4-electrodes BIS sensor was placed on the forehead and connected to the AXP-2000 monitoring system (software version 4.0; Aspect Medical, Newton, MA, USA). After intrathecal injection of 0.7 mg morphine, general anaesthesia was induced and maintained with a propofol infusion targeted to BIS values between 40 and 60. After endotracheal intubation and mechanical lung ventilation, transoesophageal echocardiography (TOE) demonstrated the absence of patent foramen ovale and intracardiac thrombi, whereas the ascending aorta appeared free from calcification, atheromatous plaque, intimal flap or false lumen suggestive of dissection. After heparinization, normothermic cardiopulmonary bypass (CPB) was instituted with cannula inserted in the right subclavian artery and the right atrium. After aortic cross-clamping, myocardial protection was accomplished by antegrade infusion of hyperkalaemic blood solution; 2 min later, haemodynamic and blood parameters were unchanged, but the BIS value abruptly decreased from 40 to 0 along with a steep increase in the burst suppression index to 100% (Fig. 1). While any cause of technical artefacts was excluded, the infusion of propofol was slightly decreased and the surgeons were asked to verify the position of the cannulas. Using a transthoracic 4–8 MHz echographic probe at the right temporal acoustic window, colour and pulsed Doppler failed to demonstrate blood flow in the middle and anterior cerebral arteries. While the subclavian arterial cannula was slightly withdrawn, direct puncture of the innominate artery revealed a non-pulsatile pressure value equal to the monitored radial pressure (55–60 mmHg). Although the BIS index persisted at ‘near-zero’ values with the raw EEG resembling a flat line (burst suppression ratio of 100), the surgeons completed the intervention (aortic cross-clamp time of 60 min) by inserting a 24-mm St Jude stentless valve and a 24-mm collagen impregnated Dacron graft. After ventricular de-airing, the patient was weaned from CPB without pharmacological support. Postoperatively, no clinical sign of awakening was noticed and magnetic resonance imaging documented severe and diffuse cortical lesions consistent with anoxic encephalopathy. The patient remained in a persistent coma and active life support was withdrawn on the eleventh postoperative day. Autopsy examination confirmed global brain ischaemic injuries and documented a common origin of right and left carotid arteries. Although BIS index is not designed as a tool for neurological monitoring during cardiac surgery, the sudden and sustained decrease in BIS concurrent with a flat EEG line in our case was highly suspicious for global ischaemic-induced cortical dysfunction at the time of aortic cross-clamping. Among likely causes leading to severe brain damage, one should consider malposition of the subclavian cannula (advanced too proximally) and/ or disruption of atheromatous plaque due to a ‘sandblasting’ effect generated by a high-velocity flow pattern at the orifice of the CPB cannula. Intraoperative TOE and autopsy ruled out arterial Correspondence to: Marc Licker, Service d’Anesthésiologie, Hôpital Universitaire, Rue Micheli-du-Crest, CH-1211 Geneva. E-mail: marc-joseph.licker@ hcuge.ch; Tel: 141 22 3827439; Fax: 141 22 38 27 403