Abstract Information

O-162

Intravesicular Lidocaine: Pharmacodynamics and Effects on Autonomic Dysreflexia Prevention

Solinsky R
Spaulding Rehabilitation Hospital, Boston, MA, United states

Objective: Lidocaine gel is commonly used in urologic procedures to decrease noxious stimulation. In patients with SCI at risk for autonomic dysreflexia (AD), this potentially has more serious implications than just pain (AD). Unfortunately, based on clinical experience, published pharmacodynamic parameters of intravesical lidocaine overestimate the time to onset of action (15 min) given the subjective nature of sensory experience. Coupled with minimal research literature regarding the effects of lidocaine in the SCI population, intravesical lidocaine’s role remains unclear (despite its mention in AD management consortium guidelines).[1] The goal of this study was to elucidate more accurate pharmacodynamics of intravesicular lidocaine, leveraging unique SCI physiology, and also to determine any role lidocaine may play in prevention of AD.

Design/Method: In this prospective, observational cohort study, the time to onset of intravesical lidocaine was estimated by administering 10 ml of 2% intravesical lidocaine through the indwelling catheter of SCI patients at risk for AD as they presented for routine catheter change. It was postulated that given potential low grade sympathetic tone from the bladder, decreasing these afferent signals may manifest as a decrease in systolic blood pressure (SBP).[1,2] Without position change or catheter manipulation, serial blood pressures were recorded for up to 6 minutes. The time to onset of action was noted as the time to achieve a 10 mmHg decrease in SBP.[3,4] Comparing those patients who received pretreatment with lidocaine prior to catheter change with a second group of patients without pre-procedure lidocaine, the rate of AD and magnitude of SBP change was monitored immediately after routine catheter change.

Results: Twenty-seven consecutive SCI patients at risk for AD were pretreated with lidocaine, with 44% experiencing a 10 mmHg decrease in SBP without further intervention. This occurred at a mean time of 94.4 seconds – an objective timepoint for onset of clinical action. An additional 23 SCI patients underwent catheter change without lidocaine pretreatment. The rate of AD in patients who were pretreated with lidocaine was 14.8% vs 47.8% in those without (p= 0.011). Patients pretreated with lidocaine also demonstrated a significantly attenuated increase in SBP immediately after catheter change (9.5 mmHg vs 26.9 mmHg, p= 0.014).

Conclusion: Evidence demonstrates time to onset of intravesicular lidocaine is significantly less than has been reported, approximately 90 seconds. Pretreatment with lidocaine prevents AD and attenuates the magnitude of SBP increase in SCI patients undergoing routine indwelling catheter change.

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