Background <p>In preclinical studies, under-assisted respiratory effort has been identified as promoting lung injury, leading to the concept of “<i>patient self-inflicted lung injury”</i> (P-SILI). We aim to characterize this second hit at the ultrastructural level through scanning electron microscopy.</p> Methods <p>In rats, lung injury was induced through surfactant depletion, followed by 3h of standard oxygen therapy or protective mechanical ventilation (MV). The lungs were fixed and removed to be subsequently scanned using a field emission scanning electron microscope. Images were analyzed using a semi-quantitative approach, scoring ten random alveoli for wall discontinuities and hemorrhage, and five small pulmonary vessels for microthrombosis. Computer-assisted morphometric evaluations were performed to quantify loss of lung aeration.</p> Results <p>The standard oxygen therapy group showed higher frequencies of alveolar wall discontinuities, alveolar hemorrhage, and microthrombosis, compared to the MV group (all <i>p</i> &lt; 0.05). The former also resulted in a lower aeration assessed by the aeration/tissue ratio.</p> Conclusions <p>Alveolar wall fractures suggest that unsupported spontaneous breathing induces stress failure in the lung parenchyma. The fractures were associated with hemorrhage and alveolar collapse, as well as with the formation of microthrombi in small pulmonary vessels. This can be caused by regional deformation phenomena as well as by cyclical lung vascular on–off flow.</p>

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What I talk about when I talk about patient self-inflicted lung injury: an ultrastructural perspective

  • Pablo Cruces,
  • Felipe M. Llancalahuen,
  • Carlos González,
  • Juan P. Cruces

摘要

Background

In preclinical studies, under-assisted respiratory effort has been identified as promoting lung injury, leading to the concept of “patient self-inflicted lung injury” (P-SILI). We aim to characterize this second hit at the ultrastructural level through scanning electron microscopy.

Methods

In rats, lung injury was induced through surfactant depletion, followed by 3h of standard oxygen therapy or protective mechanical ventilation (MV). The lungs were fixed and removed to be subsequently scanned using a field emission scanning electron microscope. Images were analyzed using a semi-quantitative approach, scoring ten random alveoli for wall discontinuities and hemorrhage, and five small pulmonary vessels for microthrombosis. Computer-assisted morphometric evaluations were performed to quantify loss of lung aeration.

Results

The standard oxygen therapy group showed higher frequencies of alveolar wall discontinuities, alveolar hemorrhage, and microthrombosis, compared to the MV group (all p < 0.05). The former also resulted in a lower aeration assessed by the aeration/tissue ratio.

Conclusions

Alveolar wall fractures suggest that unsupported spontaneous breathing induces stress failure in the lung parenchyma. The fractures were associated with hemorrhage and alveolar collapse, as well as with the formation of microthrombi in small pulmonary vessels. This can be caused by regional deformation phenomena as well as by cyclical lung vascular on–off flow.