[Patient Self-inflicted Lung Injury (P-SILI): pathophysiology and clinical implications].
Source: PubMed, NCBI / U.S. National Library of Medicine
Patient self-inflicted lung injury (P-SILI) describes a pathophysiological concept in which patients with acute hypoxemic respiratory failure (AHRF) may exacerbate lung injury through excessive respiratory drive and vigorous spontaneous breathing efforts, thereby perpetuating respiratory failure. Spontaneous breathing-related lung injury is thought to be mediated by 4 main mechanisms: 1. increased mechanical stress on lung tissue, 2. heterogeneous ventilation with intrapulmonary gas redistribution (pendelluft), 3. augmented pulmonary blood flow leading to microvascular injury, and 4. Patient-ventilator asynchrony (PVA) in the setting of non-invasive ventilation (NIV). All of these mechanisms are closely linked to an elevated respiratory drive, which primarily arises from the underlying lung pathology, particularly alveolar flooding due to plasma leakage. Clinical monitoring of respiratory effort and neural respiratory drive is possible using techniques such as esophageal pressure measurement. However, these methods are often invasive, not fully validated, time- and resource-intensive, costly, and may be associated with reduced patient comfort.In the management of acute respiratory failure, including acute respiratory distress syndrome (ARDS) and AHRF, prevention of P-SILI is essential. Recent evidence suggests that late failure of NIV followed by delayed intubation is associated with the highest mortality rates. Consequently, the choice of ventilatory support must be individu
Abstract
Patient self-inflicted lung injury (P-SILI) describes a pathophysiological concept in which patients with acute hypoxemic respiratory failure (AHRF) may exacerbate lung injury through excessive respiratory drive and vigorous spontaneous breathing efforts, thereby perpetuating respiratory failure. Spontaneous breathing-related lung injury is thought to be mediated by 4 main mechanisms: 1. increased mechanical stress on lung tissue, 2. heterogeneous ventilation with intrapulmonary gas redistribution (pendelluft), 3. augmented pulmonary blood flow leading to microvascular injury, and 4. Patient-ventilator asynchrony (PVA) in the setting of non-invasive ventilation (NIV). All of these mechanisms are closely linked to an elevated respiratory drive, which primarily arises from the underlying lung pathology, particularly alveolar flooding due to plasma leakage. Clinical monitoring of respiratory effort and neural respiratory drive is possible using techniques such as esophageal pressure measurement. However, these methods are often invasive, not fully validated, time- and resource-intensive, costly, and may be associated with reduced patient comfort.In the management of acute respiratory failure, including acute respiratory distress syndrome (ARDS) and AHRF, prevention of P-SILI is essential. Recent evidence suggests that late failure of NIV followed by delayed intubation is associated with the highest mortality rates. Consequently, the choice of ventilatory support must be individualized and continuously reassessed, taking into account the risk of both P-SILI and ventilator-induced lung injury. Non-invasive ventilation, high-flow nasal cannula therapy, pharmacological interventions, and prone positioning during spontaneous breathing all have therapeutic limits that require continuous, round-the-clock evaluation. To date, robust evidence from large clinical trials regarding their impact on the prevention and treatment of P-SILI, as well as the optimal timing of intubation, remains lacking.