Intraoperative Ultrasonic Atomization of Lidocaine and Postoperative Pulmonary Complications

Overview

There is high incidence of postoperative pulmonary complications (PPCs) in patients undergoing major abdominal surgeries.PPCs significantly prolongs the hospital stay of patients, increases their economic burden, and raises the mortality rates within 30 days and 1 year after surgery. The inflammatory response during the perioperative period plays an important role in the occurrence and development of PPCs. The anti-inflammatory effect of lidocaine has a potential lung protection mechanism. The purpose of this study is to explore the effect of ultrasonic atomization of lidocaine on the incidence of PPCs. The investigators hypothesized that intraoperative ultrasonic atomization of lidocaine could reduce the incidence of PPCs.

Introduction Globally, over 313 million surgical procedures are performed annually, with postoperative pulmonary complications (PPCs) occurring in 5-33% of cases. PPCs, the second most common postoperative complication after surgical site infections, encompass conditions such as respiratory infections, respiratory failure, pleural effusion, atelectasis, pneumothorax, bronchospasm, and aspiration pneumonia. These complications significantly prolong hospital stays, increase healthcare costs, and elevate 30-day and 1-year mortality rates. Pathophysiology of PPCs PPCs are closely linked to perioperative pulmonary inflammatory responses. Mechanical ventilation during general anesthesia alters pulmonary ventilation distribution, leading to atelectasis in over 90% of patients. Atelectasis increases mechanical stress and hypoxia in collapsed lung regions while causing hyperinflation and hyperoxia in adjacent areas. These conditions promote the release of pro-inflammatory cytokines, reactive oxygen species, and leukocyte infiltration. Additionally, atelectasis-induced hypoxia and mechanical stress contribute to endothelial damage, increasing vascular permeability and protein leakage. Major abdominal and thoracic surgeries further exacerbate systemic inflammation and airway hyperreactivity, impairing alveolar epithelial barrier function and mucociliary clearance. Lidocaine's Anti-Inflammatory and Lung-Protective Mechanisms Lidocaine has emerged as a potential therapeutic agent due to its anti-inflammatory properties. Studies indicate that it inhibits neutrophil infiltration and reduces pro-inflammatory cytokines (e.g., IL-6, TNF-α) by blocking Toll-like receptor 4/NF-κB signaling. Inhaled lidocaine has shown efficacy in murine asthma models by suppressing GATA-3 expression, eosinophilic inflammation, mucus overproduction, and airway hyperreactivity. It has also been explored as an adjunct therapy for severe COVID-19 respiratory symptoms, mitigating cytokine storms and improving outcomes. In pediatric patients, lidocaine reduces postoperative cough incidence. Current Challenges and the Promise of Ultrasonic Nebulization Despite its potential, lidocaine's clinical application for lung protection remains inconsistent. Intravenous administration poses risks due to narrow therapeutic windows, with fluctuating plasma concentrations potentially causing neurotoxicity or cardiotoxicity. Conventional nebulizers produce particles \>5 μm, depositing primarily in the upper airways, with less than 15% reaching the lung parenchyma. In contrast, ultrasonic nebulization generates 1-5 μm aerosol particles, enhancing lower respiratory tract deposition to 40-60%. Animal studies demonstrate that nebulized lidocaine achieves lung tissue concentrations 8-10 times higher than plasma levels, suggesting targeted efficacy. Research Objective and Hypothesis The role of ultrasonic nebulized lidocaine in reducing PPCs remains underexplored. This study aims to evaluate its impact on PPC incidence within seven days post-surgery. The hypothesis is that intraoperative ultrasonic nebulized lidocaine administration will decrease PPC rates, offering a safer and more effective approach to perioperative lung protection.