Regional Alveolar Damage Despite Lung Protective Ventilation Settings During Robotic-Assisted Laparoscopic Surgery

Robotic-assisted laparoscopic surgery (RALS) in a steep Trendelenburg position creates conditions conducive to cyclical alveolar collapse when using standard lung protective ventilation settings (LPV). The magnitude of force induced by alveolar collapse and expansion is predicted to cause a localized injury, but biological evidence of perioperative atelectrauma is lacking. We hypothesized that the negative transpulmonary pressures and increased dissipated power of ventilation encountered during RALS lead to injury of the dependent (apical) lung despite the use of LPV settings.

We conducted a single-center, observational study of lung mechanics and injury in 15 subjects (8 M/7F; mean ± standard deviation: 59.5 ± 7.4 years) without lung disease undergoing RALS with LPV at an academic hospital in the United States. Subjects had a median body mass index of 32.5 kg/m2 with a range of 24.3 to 50.9 kg/m2. We continuously measured lung mechanics, including transpulmonary pressures. Bronchoalveolar lavages (BAL) were obtained from apical and anteromedial subsegments after intubation and from contralateral subsegments before extubation. During RALS, the apical lung is dependent and the anteromedial lung in nondependent. BAL analyses included total protein concentrations, proteomics, lipidomics, and leukocyte counts.

Lung mechanics were impaired, with elevated respiratory elastance and driving pressures, and negative end-expiratory transpulmonary pressures, despite standard LPV settings (tidal volume 7.0 ± 0.8 mL/kg ideal body weight; positive end-expiratory pressure 8.7 ± 3.4 cm H2O). Increases in total protein (median [interquartile range], 131 [27-193] µg/mL), extracellular matrix components (fibulin-1: 2.1 [1.6-4.0] fold; microfibril-associated glycoprotein-4: 2.2 [1.3-4.0] fold), and procoagulants (prothrombin: 1.7 [1.3-4.8] fold; plasminogen: 3.2 [1.9-4.5] fold) were observed in apical BAL after surgery (adj. P < .001 for all), but not in anteromedial BAL (adj. P > .05). No differences in percent leukocyte composition were observed among lavages (P > .287 for all cell types). Phosphatidylglycerol abundance was increased in apical BAL after surgery in unadjusted analyses (5.8 [1.9-7.9] %, P = .021), but no changes in phospholipid abundance were noted in adjusted analysis. Increases in apical BAL total protein were positively correlated with the dissipated mechanical power of ventilation (r2 = 0.434, P = .014).

In this focused biomechanical study, we found molecular evidence for alveolar-capillary damage in the dependent apical lobes, consistent with localized atelectrauma. Regional atelectrauma from impaired lung mechanics can occur in the positionally dependent lung while using LPV settings during RALS, most likely from insufficient end-expiratory pressure.