Lidocaine-Induced Systemic Jitters

Mechanism of CNS Toxicity

The American Society of Anesthesiologists notes that lidocaine has an extremely narrow therapeutic window, with CNS toxicity beginning at plasma levels only slightly above therapeutic concentrations, affecting multiple receptor systems in a concentration-dependent manner 1, 2
At therapeutic concentrations, lidocaine blocks muscarinic and NMDA receptors, while at near-toxic concentrations, many additional receptor types become affected, including Nav1.8/1.7, nicotinic cholinergic receptors, and voltage-gated calcium channels 1, 2
The correlation between plasma levels and toxicity symptoms is not linear, making toxicity unpredictable even with appropriate dosing, as stated by the American College of Medical Toxicology 1, 2

Early neurologic symptoms of lidocaine toxicity include lightheadedness, dizziness, perioral numbness, tinnitus, metallic taste, visual disturbances, confusion, and disorientation, according to the World Federation of Neurosurgical Societies 6
The oral cavity presents unique risks for systemic absorption due to highly vascular tissues, inadvertent intravascular injection, and non-standardized oral infiltration techniques, as reported by the American Dental Association 3, 4, 5

Inadvertent intravascular injection during oral procedures can deliver the entire dose directly into systemic circulation, bypassing first-pass metabolism and immediately achieving toxic plasma levels, as warned by the American Society of Anesthesiologists 4
The American Heart Association recommends always aspirating before injection and using the lowest effective dose, as the therapeutic index is inherently low regardless of technique 1, 2
Lipid emulsion 20% should be readily available wherever lidocaine is used, and all staff must know its location for immediate treatment of systemic toxicity, as advised by the American College of Emergency Physicians 8, 9