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Case Reports  |   May 2002
Unilateral Cerebral Oxygen Desaturation during Emergent Repair of a DeBakey Type 1 Aortic Dissection: Potential Aversion of a Major Catastrophe
Author Affiliations & Notes
  • Gregory M. Janelle, M.D.
    *
  • Stephen Mnookin, M.D.
  • Nikolaus Gravenstein, M.D.
  • Tomas D. Martin, M.D.
    §
  • Felipe Urdaneta, M.D.
    *
  • *Assistant Professor, †Fellow, Cardiothoracic Anesthesia, ‡Professor and Chairman, Department of Anesthesiology, §Associate Professor, Division of Thoracic Surgery, Department of Surgery, University of Florida College of Medicine.
  • Received from the Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida.
Article Information
Case Reports
Case Reports   |   May 2002
Unilateral Cerebral Oxygen Desaturation during Emergent Repair of a DeBakey Type 1 Aortic Dissection: Potential Aversion of a Major Catastrophe
Anesthesiology 5 2002, Vol.96, 1263-1265. doi:
Anesthesiology 5 2002, Vol.96, 1263-1265. doi:
EMERGENT repair of a dissecting or ruptured DeBakey type 1 aortic aneurysm is associated with mortality rates ranging from 17–88%, with adverse neurologic sequelae as a leading cause of major life-altering morbidity. 1 Neurologic monitoring has been advocated to minimize the potential for neurologic damage. The approach at our institution includes a combination of retrograde cerebral perfusion techniques with neurologic monitoring consisting of a two-channel bipolar electroencephalogram along with bifrontal regional cerebral oxygen saturation (rSo2) sensors (INVOS®Cerebral Oximeter 5100; Somanetics, Troy, MI). The Somanetics cerebral oximetry device uses near-infrared spectroscopy to determine the ratio of oxyhemoglobin to deoxyhemoglobin in the underlying frontal cerebral cortical blood. It assumes a relative ratio of 25:75 arterial to venous cerebral blood volume at two predetermined depths from the sensor to determine regional saturation. 2 We report a case in which rSo2monitoring prompted a change in surgical therapy, early detection of hemispheric hypoperfusion, and avoidance of a potentially catastrophic neurologic complication.
Case Report
A 75-yr-old man presented with a presumptive diagnosis of an acute DeBakey type 1 aortic dissection. Eight months earlier, he had undergone three-vessel coronary artery bypass graft surgery. Cardiac catheterization at the referring institution showed 80% stenosis of the vein graft to the right coronary artery and an aortic dissection originating in the proximal aortic root. At the time of arrival at our hospital, a preoperative transesophageal echocardiographic examination revealed a 4.9-cm-diameter aortic root, with an aortic dissection extending from just distal to the left main coronary ostium to as far into the descending aorta as the examination permitted. In addition, moderate aortic insufficiency was noted. The patient was brought to the operating room for redosternotomy, coronary artery bypass graft, aortic valve replacement, and repair of the type 1 aortic dissection. General anesthesia was induced with a combination of midazolam, fentanyl, sodium thiopental, and pancuronium. Hemodynamic monitoring included a left radial artery catheter, an oximetric, pulmonary artery catheter, and continuous transesophageal echocardiography (Hewlett-Packard Omniplane, Sonos 5500; Hewlett-Packard, Andover, MA). Continuous two-channel bipolar electroencephalographic monitoring was performed (A1000; Aspect Medical Systems, Newton, MA) with a ground lead (Fz), a left channel (Fp1–A1), and a right channel (Fp2–A2). In addition, bifrontal rSo2sensors were used for central nervous system monitoring.
Cardiopulmonary bypass was achieved via  left femoral arterial cannulation and two-stage right atrial cannulation. Systemic hypothermia was initiated to reach a target temperature of 18°C, with crushed ice packs surrounding the head to aid in homogenous cooling. To this point, electroencephalographic activity and rSo2values had been bilaterally symmetrical (fig. 1). After approximately 40 min of cardiopulmonary bypass, while the aortic valve was being replaced, profound right hemispheric desaturation occurred abruptly despite a nasopharyngeal temperature of 18°C and an isoelectric electroencephalogram (fig. 1). The surgeon was immediately notified. The aortic valve replacement was temporarily aborted, and hypothermic circulatory arrest was initiated with a subsequent decrease in contralateral rSo2values. The aortic arch was opened, and the dissection was visualized. The false lumen was noted to extend from the ascending aorta through the right innominate artery and into the right common carotid artery. The arch was repaired under retrograde cerebral perfusion, during which no improvement in ipsilateral rSo2values was noted while the contralateral values continued to decrease. After reinstitution of anterograde cardiopulmonary bypass flow via  cannulation of the ascending graft, rSo2values promptly improved symmetrically (fig. 1).
Fig. 1. Cerebral oximetry values during cardiopulmonary bypass. 1 = Begin cardiopulmonary bypass; 2 = begin cooling; 3 = sudden right hemispheric desaturation; 4 = begin deep hypothermic circulatory arrest; 5 = begin retrograde cerebral perfusion; 6 = begin deep hypothermic circulatory arrest; 7 = begin anterograde cerebral perfusion; 8 = begin rewarming.
Fig. 1. Cerebral oximetry values during cardiopulmonary bypass. 1 = Begin cardiopulmonary bypass; 2 = begin cooling; 3 = sudden right hemispheric desaturation; 4 = begin deep hypothermic circulatory arrest; 5 = begin retrograde cerebral perfusion; 6 = begin deep hypothermic circulatory arrest; 7 = begin anterograde cerebral perfusion; 8 = begin rewarming.
Fig. 1. Cerebral oximetry values during cardiopulmonary bypass. 1 = Begin cardiopulmonary bypass; 2 = begin cooling; 3 = sudden right hemispheric desaturation; 4 = begin deep hypothermic circulatory arrest; 5 = begin retrograde cerebral perfusion; 6 = begin deep hypothermic circulatory arrest; 7 = begin anterograde cerebral perfusion; 8 = begin rewarming.
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The total time from right hemispheric cerebral desaturation to restoration of anterograde blood flow with consequent resaturation was approximately 35 min and occurred during deep hypothermia with 22 min of retrograde cerebral perfusion. The aortic valve was replaced, and the remainder of the operation continued without incident. The patient emerged from anesthesia in the intensive care unit without obvious neurologic deficits. He was discharged on the 11th hospital day.
Discussion
Cerebral oximetry is a relatively new monitoring modality that has undergone much criticism since its advent. Both the confounding contribution of external carotid flow and variations in the ratio of cerebral arterial/venous blood flow have been reported to result in inaccurate absolute rSo2values. 2,3 In fact, normal values have been reported in brain-dead patients, presumably because of either the contribution of external carotid flow or because of the decrease in cerebral oxygen consumption. 3 Interpretation of low rSo2values remains controversial as well. Using somatosensory evoked potential changes as a control, Beese et al.  4 determined no critical threshold value after carotid cross clamping that would reliably indicate the need for shunting. Similarly, Samra et al.  5 reported that in a group of awake patients undergoing carotid endarterectomy, no consistent relative change from baseline rSo2values reliably accompanied neurologic changes. In addition, abnormal rSo2values with simultaneously normal mean velocity flows—documented by transcranial Doppler insonation of the middle cerebral artery during ipsilateral carotid occlusion—could potentially result in an increased number of unnecessary shunts during carotid surgery. 6 In fact, rSo2values have even been reported in a pumpkin species (presumably from pigments present in the pumpkin). 7 
Although absolute values may not be accurately measured, decreasing rSo2trends seem to reliably reflect decreasing cerebral hemoglobin oxygen saturation. 8 Significant intraoperative cerebral oxygen desaturations have been related to postoperative cognitive dysfunction as well as prolonged hospital and intensive care unit durations of stay. 9,10 A recent interventional study showed an 80% reduction in the incidence of stroke by optimization of the oxygen supply/demand ratio during bypass to maintain baseline rSo2values. 11 Cerebral oximetry has previously been advocated as a helpful neurophysiologic monitor during cases necessitating hypothermic circulatory arrest and retrograde cerebral perfusion to assure optimal brain cooling and bihemispheric delivery of retrograde perfusion. Blas et al.  12 recently reported such a case during which rSo2monitoring detected suboptimal global retrograde cerebral perfusion due to a loose retrograde cannula suture, which resulted in leakage of perfusate into the right atrium and inferior vena cava.
At our institution, advocates of cerebral oximetry tend to use the device during cardiopulmonary bypass, especially as a trend monitor when the procedure involves retrograde cerebral perfusion to assess the balance of cerebral oxygen supply and demand in much the same fashion that mixed venous oximetry readings from a pulmonary artery catheter can be used to assess global oxygen supply and demand. We apply bilateral sensors to diagnose hemispheric differences that may occur during bypass, including embolic events, aortic cannula malposition, unilateral venous obstruction, or, as in this case, extension of a false lumen into a carotid artery resulting in inadequate hemispheric cerebral blood flow. Despite uncertainty as to the absolute values that should be cause for alarm, the sudden precipitous and unilateral rSo2decrease prompted sufficient alarm to change the sequence of the surgery. It is our belief that the cerebral oximeter enabled early detection of hemispheric ischemia and prevented what could have been a prolonged ischemic insult if the course of the operation had not been altered.
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Fig. 1. Cerebral oximetry values during cardiopulmonary bypass. 1 = Begin cardiopulmonary bypass; 2 = begin cooling; 3 = sudden right hemispheric desaturation; 4 = begin deep hypothermic circulatory arrest; 5 = begin retrograde cerebral perfusion; 6 = begin deep hypothermic circulatory arrest; 7 = begin anterograde cerebral perfusion; 8 = begin rewarming.
Fig. 1. Cerebral oximetry values during cardiopulmonary bypass. 1 = Begin cardiopulmonary bypass; 2 = begin cooling; 3 = sudden right hemispheric desaturation; 4 = begin deep hypothermic circulatory arrest; 5 = begin retrograde cerebral perfusion; 6 = begin deep hypothermic circulatory arrest; 7 = begin anterograde cerebral perfusion; 8 = begin rewarming.
Fig. 1. Cerebral oximetry values during cardiopulmonary bypass. 1 = Begin cardiopulmonary bypass; 2 = begin cooling; 3 = sudden right hemispheric desaturation; 4 = begin deep hypothermic circulatory arrest; 5 = begin retrograde cerebral perfusion; 6 = begin deep hypothermic circulatory arrest; 7 = begin anterograde cerebral perfusion; 8 = begin rewarming.
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