Can Intraoperative Neurological Preconditioning Occur After Intraoperative Hypotensive Episodes?

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Ischemic preconditioning has been proven experimentally, especially in animal studies to improve tolerance of neuronal tissue to subsequent ischemic insults. A Chinese study in subarachnoid hemorrhage patients showed intraoperative short-term controlled temporary clipping of cerebral vessel to be beneficial. It reduces decline of cerebral oxygen tension and pH in patients whose aneurysm structure required temporary clipping of vessel.1 We report a case of internal carotid artery (ICA) giant aneurysm with evidence of intraoperative preconditioning due to periods of spontaneous hypotension related to blood loss.
Written consent of the patient was obtained before writing this report. The case was a 62-year-old gentleman, with symptoms of sudden-onset headache consistent with subarachnoid hemorrhage. Contrast-enhanced CT scan of the brain showed a thrombosed right cavernous ICA aneurysm, confirmed by cerebral digital subtraction angiography. Endoscopic transnasal transethmoidal clipping of aneurysm was planned with neuronavigation.
Because of requirement of temporary clipping of ICA intraoperatively, the anesthetic plan involved monitoring of bilateral frontotemporal electroencephalography montages FP 1/2 to T3/4 (EEG) and frontal cerebral oximetry (SctO2). EEG and SctO2 probes were applied after induction, positioning the patient and registering the facial landmarks in neuronavigation. The baseline EEG showed low amplitude α and δ activity with spectral edge frequency of 7 to 8 Hz on both sides with baseline SctO2 of 68% to 72% bilaterally and systolic blood pressure (SBP) of 140 mm Hg. After dissecting through the bone, ICA was visualized with aneurysm and the ICA was temporarily clipped. The ipsilateral SctO2 reduced to 64% (contralateral 71%) within 10 minutes, whereas the EEG did not show any amplitude or frequency changes. Thus, collaterals were presumed to be adequate and the surgeon was informed.
During aneurysm dissection, aneurysm ruptured with acute blood loss of approximately 0.5 L, and SBP decreased to 100 mm Hg. At this pressure level, the ipsilateral SctO2 was noticed to reduce to 55% with contralateral maintaining 70% and spectral edge frequency decreasing slightly to 6 to 7 Hz bilaterally. Rapid fluid infusion and blood transfusion improved SBP to 120 mm Hg and SctO2 was seen to improve to prehypotension levels of 64. We surmised the SBP threshold for ipsilateral hypoperfusion to be 100 mm Hg. Blood loss continued at a rapid rate, and 15 minutes later, the SBP decreased to 90 mm Hg despite replacement, and the SctO2 declined below 90 mm Hg. As noted previously, it improved when blood pressure was brought up to 120 mm Hg. Thirty minutes later SBP reduced to 80 mm Hg temporarily, but the SctO2 was seen to stay stable at 62% to 64%. After multiple clipping attempts, bleeding was stopped and blood pressure stabilized at SBP 130 mm Hg with ipsilateral SctO2 being 64% and contralateral 70% (Fig. 1). EEG did not show noticeable difference between the 2 sides. The patient was shifted for angiography and ICA was seen to be partially clipped with sluggish flow inside the aneurysm as well as ipsilateral hemisphere. Unfortunately, the patient developed hemispheric infarct and expired despite decompressive craniectomy performed afterward.
The decrease of threshold of SBP for cerebral oximetric desaturation points to either an improvement of blood supply by recruitment of collaterals or a cellular level change causing decreased utilization of oxygen. Chan et al1 proved a preconditioning effect in humans, confirmed by cerebral oxygen tension and pH, after temporary artery occlusion for 2 minutes and reperfusion for 30 minutes. Similarly, Wegener et al2 showed that stroke patients with history of transient ischemic attacks tended to have smaller initial diffusion defects and final infarct volumes on MRI than those without.

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