Patient self-inflicted lung injury an important phenomenon

Mechanical ventilation is essential in acute hypoxemic respiratory failure (AHRF), yet excessive respiratory drive and inspiratory effort may aggravate injury, a phenomenon termed patient self-inflicted lung injury (P-SILI). This review summarizes mechanistic insights, preclinical and clinical evidence, and current strategies to prevent P-SILI while preserving diaphragmatic function.

Preclinical experimental studies show that vigorous inspiratory efforts amplify pleural pressure swings, regional overdistension, pendelluft, and inflammation, with damage involving both lung and diaphragm. positive end-expiratory pressure (PEEP) and continuous positive airway pressure (CPAP) can homogenize ventilation, reduce strain-rate, and protect diaphragmatic mechanics, whereas uncontrolled effort worsens outcomes. Clinical investigations confirm that high drive and effort increase total lung stress despite protective tidal volumes and are linked to mortality, ventilator dependence, and complications such as pneumomediastinum. Emerging approaches include titrated pressure support and sedation and ventilatory assistance, neuromuscular blockade, phrenic nerve block, pharmacological drive modulation, prone positioning, and extracorporeal CO 2 removal. Strategies aimed at preserving diaphragm activity, such as electrical phrenic stimulation or inspiratory muscle training, further broaden protective options.

P-SILI arises when excessive inspiratory effort translates into injurious lung and diaphragm stress. Preventive strategies should not abolish but shape effort, integrating ventilatory settings, sedation, and drive-modulating interventions across the continuum from the acute phase to weaning and rehabilitation.