Several key issues must be noted in determining postoperative analgesic efficacy of intercostal nerve block for thoracoscopic surgery.

The letter to the editor was written in response to "The effect of ultrasound-guided intercostal nerve block on postoperative analgesia in thoracoscopic surgery: a randomized, double-blinded, clinical trial", which was recently published by Li et al. (J Cardiothorac Surg 18(1):128, 2023). In this article, Li et al. showed that addition of a preoperative intercostal nerve block to the multimodal analgesic strategy significantly reduced the pain scores within 48 h after surgery. However, we noted several issues in this study that were not well addressed. They were no use of a standard opioid-sparing multimodal analgesic strategy recommended in the current Enhanced Recovery After Surgery protocols for thoracic surgery, the lack of clear description for reasonable selection of rescue analgesics, the interpretion of between-group differences in the postoperative pain scores based on only statistical differences rather than clinically meaningful differences, inclusion of patients who were not blinded to study intervention, not reporting cumulative opioid consumption and complications of intercostal nerve block. We believe that clarification of these issues is not only useful for improving design quality of randomized clinical trials which assess postoperative analgesic efficacy of nerve blocks, but also is helpful for the readers who want to use an opioid-sparing multimodal protocol including a nerve block in patients undergoing thoracoscopic surgery.

Lidocaine pretreatment attenuates inflammatory response and protects against sepsis-induced acute lung injury via inhibiting potassium efflux-dependent NLRP3 activation.

OBJECTIVE: Sepsis may often result in acute lung injury (ALI), with a high mortality and morbidity. Available evidence indicates that activation of NLRP3 inflammasome to induce macrophage inflammation plays a crucial role in the inflammation progression of ALI and lidocaine can attenuate inflammatory responses. We hypothesized that lidocaine may attenuate inflammatory response and sepsis-induced ALI by inhibiting potassium efflux-dependent NLRP3 activation. METHODS: C57BL/6N mice were randomized and divided into six groups (n = 6) receiving different treatments. Lung vascular permeability and histological changes in the lungs were evaluated by Evans blue dye, bronchoalveolar lavage analysis and hematoxylin and eosin staining. J774A.1 macrophages were divided into 12 groups receiving different treatments. The expression of both NLRP3 inflammasome activation-related protein and P2X7 in the macrophages was measured by immunofluorescence staining and Western blots. The whole cell currents were determined by a voltage-patch clamp technique. RESULTS: Challenge with LPS led to ALI in mice with an increased lung injury score (0.54 ± 0.09), which was significantly attenuated by lidocaine pretreatment (0.20 ± 0.08, P < 0.0001). Lidocaine pretreatment significantly decreased the NLRP3 activation and IL-1ß release in the macrophages. Furthermore, lidocaine pretreatment down-regulated the expression of P2X7 receptors, inhibited LPS- and ATP-induced sodium (Na+) inward flow, and maintained the intracellular K+ level in the macrophages. In addition, activation of Na+ influx did not eliminate anti-inflammatory effect of lidocaine. The activation of NLRP3 could be suppressed by extracellular K+ level in a dose-dependent model. However, lidocaine pretreatment eliminated NLRP3 activation and IL-1ß release induced by K+ efflux, and decreased outward K+ current and extracellular K+ level in the macrophages challenged by LPS/ATP. CONCLUSIONS: Lidocaine pretreatment can attenuate the sepsis-induced ALI by an anti-inflammatory mechanism of inhibiting K+ efflux-dependent NLRP3 activation.