Perioperative use of intravenous lidocaine infusion (1.5 mg/kg bolus then 1.5–2 mg/kg/hr) is increasingly used as part of multimodal analgesia. Which analgesic mechanism, beyond simple sodium channel blockade, is responsible for its anti-hyperalgesic effect?

• A Competitive inhibition of mu-opioid receptors at spinal dorsal horn
• B Inhibition of cyclooxygenase-2 in inflamed peripheral tissue
• C Activation of descending inhibitory noradrenergic pathways from locus coeruleus
• D Reduction of central sensitisation by antagonising NMDA receptors and blocking G protein-coupled inflammatory mediators ✓

Explanation

IV lidocaine's analgesic effects extend beyond peripheral sodium channel blockade. At subanatomic plasma concentrations achieved during infusion, lidocaine inhibits NMDA receptor-mediated central sensitisation in the dorsal horn (reducing windup and hyperalgesia), blocks glycine receptors, suppresses inflammatory G protein-coupled receptor signalling, and has anti-inflammatory effects by reducing neutrophil-endothelial adhesion. This explains its efficacy in reducing postoperative pain scores, opioid consumption, and facilitating return of bowel function particularly in abdominal surgery. COX-2 inhibition is the mechanism of NSAIDs. Noradrenergic descending pathways are activated by tramadol/tricyclic antidepressants.

Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.

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