Laryngoscopy mediated stress response induces opposite effects on cerebral and paraspinal oxygen saturation

Abstract

Background: Intraoperative sympathetic stimulation induces a cascade of metabolic and hormonal changes. It increases perfusion of vital organs, but also causes vasoconstriction of blood vessels supplying less vital organs, potentially leading to organ injury. To date, it is unknown how an endogenous stress reaction affects the spinal cord blood supply. Near-infrared spectroscopy (NIRS) can be applied paravertebrally to monitor the oxygenation of the collateral network, which contributes to the spinal cord blood supply. It has already been demonstrated that regional cerebral oxygen saturation (rScO2) increases following sympathetic stimulation.

Objectives: We hypothesized that laryngoscopy would cause an increase in cerebral and paraspinal regional tissue saturations (rScO2 and rSpsO2, respectively).

Design: Retrospective analysis of a previous conducted randomized trial.

Setting: Laryngoscopy in the operating room.

Methods: Data of 28 patients, scheduled for arterial dilation of the lower limb, were retrospectively analyzed. Before induction of anesthesia, standard monitoring, BIS and 8 NIRS sensors were applied (two on the forehead, six bilaterally on the back at T3-T4, T9-T10 and L1-L2). Sympathetic stimulation was induced by laryngoscopy.

Main outcome measures: Changes in rStO2 following sympathetic stimulation induced by laryngoscopy.

Results: Following laryngoscopy, rScO2 significantly increased and rSpsO2 significantly decreased at T9-T10 and L1-L2. The relative changes (regional tissue oxygen saturation (rStO2) after intubation-rStO2 before intubation)/ rStO2 before intubation), at cerebral level, T9-T10 and L1-L2 were 9%, -5% and -3%, respectively (p < 0.01). rSpsO2 at T3-T4 did not change significantly. Changes (Δ) in mean arterial pressure following laryngoscopy were weakly correlated with ΔrScO2 and moderately correlated with ΔrSpsO2 at T9-T10 and L1-L2.

Conclusions: Intraoperative sympathetic stimulation may decrease the oxygen supply to the spinal cord.

Trial registration: The trial was registered at ClinicalTrials.gov (NCT 03767296).