A Correlational Study to Analyze the Effect of Decrease in Mean Arterial Pressure on Cerebral Oxygen Saturation in Hypertensive Patients during Hypotensive Anesthesia for Transsphenoidal Surgery

Abstract Controlled hypotension is employed for transsphenoidal surgeries (TSS) to provide a bloodless surgical field carries the potential risk of cerebral hypoperfusion and neurological injury. Pituitary adenoma may present with a high incidence of hypertension due to associated acromegaly and Cushing's disease. The risk of cerebral hypoperfusion increases with a decrease in blood pressure in chronic hypertensive patients due to a rightward shift of the autoregulation curve. This observational study aimed to correlate the changes in cerebral oxygenation (ScO2) with reduction in mean arterial pressure (MAP) in hypertensive patients undergoing TSS to determine the safety limit of permissive hypotension. Thirty hypertensive patients undergoing transsphenoidal pituitary surgery under hypotension anesthesia (targeted MAP 60–70 mm Hg) were included. Calibrated near-infrared spectroscopy was used to record continuous ScO2. A decrease in the absolute value of ScO2 <50 or ≥20% drop from baseline was considered significant. Patients were monitored after surgery for hemodynamic instability, cognitive dysfunction, and any neurological complications. Eleven out of 30 patients showed a significant drop in ScO2. A decrease in MAP < 70 mm Hg or more than 30% from baseline was associated with a significant reduction in ScO2. A fair positive correlation between decrease in MAP and drop in ScO2 (rho = 0.6, p < 0.001) was observed. The duration of hypertension and ventricular hypertrophy was also associated with a decrease in ScO2. Postoperative cognitive score was low on day 1 after surgery in patients having deceased ScO2 (p = 0.045). Our study showed that ScO2 monitoring can play a pivotal role in managing MAP during hypotensive anesthesia. It can provide an early warning sign of decreased ScO2, enabling rapid intervention to prevent postoperative neurological deficit.