Perioperative Prophylactic Positive Pressure Ventilation Reduces Postoperative Pulmonary Complications.

Perioperative Prophylactic Positive Pressure Ventilation Reduces Postoperative Pulmonary Complications.

The incidence of postoperative pulmonary complications (PPCs) ranges from 5% to 33%. PPCs significantly prolong hospital stay, increase the economic burden, and are associated with postoperative mortality at 30 days and 1 year. The occurrence of PPCs is associated with multiple perioperative factors. A multimodal approach may provide better prevention against PPCs. We hypothesize that perioperative prophylactic positive pressure ventilation can reduce the incidence of PPCs in patients undergoing high-risk abdominal surgery.

Globally, over 313 million surgical procedures are performed annually. The incidence of postoperative pulmonary complications (PPCs) ranges from 5% to 33%. PPCs include respiratory tract infection, respiratory failure, pleural effusion, atelectasis, pneumothorax, bronchospasm, and aspiration pneumonia, representing the second most common postoperative complication, second only to surgical site infection. PPCs significantly prolong hospital stay, increase economic burden, and are associated with 30-day and 1-year postoperative mortality.

The occurrence of PPCs is associated with multiple perioperative factors. General anesthesia induction can alter the distribution of gas within the lungs, shifting ventilation toward the ventral and left regions, resulting in decreased dorsal ventilation and varying degrees of atelectasis. This leads to ventilation inhomogeneity and ventilation-perfusion mismatch, impairing systemic oxygenation. Studies have shown that during mechanical ventilation, mechanical stress increases in atelectatic areas, potentially causing tissue hypoxia, while adjacent areas may experience overdistension and hyperoxia. Hyperoxia and overdistension promote the release of pulmonary pro-inflammatory factors, reactive oxygen species, and increased leukocyte infiltration. Research indicates that local tissue hypoxia and altered mechanical stress due to atelectasis can induce lung injury. An experimental study reported ultrastructural evidence of microvascular endothelial disruption in atelectatic lung tissue, suggesting that such damage may increase pulmonary vascular permeability and protein leakage. Furthermore, the systemic inflammatory response triggered by the nociceptive stimuli of major thoracic or abdominal surgery, combined with airway hyperreactivity, can collectively disrupt the alveolar epithelial barrier and impair mucociliary clearance. After extubation at the end of surgery, the risk of atelectasis and hypoxemia persists due to residual anesthetic effects, pain-induced suppression of the cough reflex, among other factors. These elements, combined with patient-related factors (e.g., advanced age, smoking, pre-existing lung disease), collectively contribute to the development of PPCs.

Lung-protective ventilation strategies, including low tidal volume, application of PEEP, and intermittent recruitment maneuvers, are now widely used clinically to prevent PPCs. Some scholars posit that the primary principle of lung-protective ventilation is the prophylactic perioperative use of positive pressure ventilation (P.O.P-ventilation), aimed at minimizing the reduction in lung volume throughout the perioperative period. Evidence suggests that prophylactic positive pressure ventilation applied before anesthesia induction, during surgery, and after tracheal extubation can reduce the incidence of adverse postoperative respiratory events. Although lung-protective ventilation is increasingly adopted, critical gaps in evidence remain. How to best implement a multimodal, perioperative prophylactic positive pressure ventilation strategy to reduce PPCs requires further investigation. Therefore, in a preliminary study, we divided 120 patients scheduled for elective non-cardiac surgery under general anesthesia with endotracheal intubation into three groups, applying 0, 5, or 10 cm H₂O of positive end-expiratory pressure (PEEP) during anesthesia induction, respectively, and observed the incidence of post-induction atelectasis. Our results showed that 10 cm H₂O of PEEP significantly reduced the occurrence of atelectasis following induction. However, this preliminary study did not follow up on the incidence of postoperative PPCs.

Building upon our preliminary findings, and to further evaluate the safety and efficacy of perioperative prophylactic positive pressure ventilation in reducing PPCs, we propose the following strategies for our new clinical study: (1) Increase the sample size and enroll patients undergoing abdominal surgery at intermediate-to-high risk for PPCs (Assessement of Respiratory Risk in Surgical Patients in Catalonia score, ARISCAT score ≥ 45); (2) Implement a multimodal strategy for prophylactic positive airway pressure. This includes using 10 cm H₂O PEEP during anesthesia induction, applying electrical impedance tomography (EIT)-guided individualized PEEP during surgery, and utilizing high-flow nasal cannula (HFNC) oxygen therapy after tracheal extubation to maintain positive end-expiratory pressure. (3) Follow up and assess PPCs occurring within 7 days postoperatively during the hospital stay. Through these strategies, we aim to further establish the protective role of a perioperative prophylactic positive pressure ventilation strategy on postoperative lung outcomes, thereby providing an enhanced empirical foundation for optimizing the clinical prevention of PPCs.

Inclusion Criteria:

• Patients who have signed the informed consent form and are willing to comply with the study protocol;
• Age ≥ 18 years and ≤ 90 years;
• ASA physical status classification I to III;
• Scheduled for major elective abdominal surgery;
• Undergoing general anesthesia with endotracheal intubation;
• ARISCAT (Assessement of Respiratory Risk in Surgical Patients in Catalonia) score ≥ 45;
• Anticipated surgery duration ≥ 2 hours.

Exclusion Criteria:

• Untreated ischemic heart disease; severe cardiovascular or cerebrovascular disease;
• Severe asthma, pulmonary bullae/bullous lung disease, pneumothorax, bronchopleural fistula, etc.;
• Severe underlying hepatic or renal disease;
• Age < 18 years or > 90 years;
• Refusal to participate in the clinical study.