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Daily Anesthesiology Research Analysis

3 papers

Analyzed 102 papers and selected 3 impactful papers.

Summary

Three anesthesia-focused studies stood out today: a randomized trial showed that non-intubated anesthesia for VATS lung surgery halved postoperative pulmonary complications and reduced diaphragmatic dysfunction; a mechanistic study revealed that isoflurane impairs SERCA-dependent calcium removal via mitochondrial complex I inhibition, linking ATP depletion to early neurotoxicity signals; and a randomized trial demonstrated that driving pressure–guided tidal volume titration during one-lung ventilation lowered dependent-lung IL-6, indicating reduced biotrauma.

Research Themes

  • Non-intubated anesthesia in thoracic surgery improves pulmonary outcomes
  • Mechanistic insights into anesthetic-induced neurotoxicity (calcium handling, mitochondrial ATP)
  • Driving pressure–guided ventilation reduces biotrauma during one-lung ventilation

Selected Articles

1. Effect of non-intubated anaesthesia video-assisted thoracoscopic surgery on postoperative diaphragm function and pulmonary complications in patients undergoing lung surgery: a randomized clinical trial.

75.5Level IRCTInternational journal of surgery (London, England) · 2025PMID: 41416613

In a single-center randomized trial of 160 VATS patients, non-intubated anesthesia significantly reduced diaphragmatic dysfunction at 24 hours and halved postoperative pulmonary complications compared with intubated anesthesia. These benefits suggest NIVATS may be a superior option for selected thoracic surgical patients.

Impact: Provides randomized evidence that a non-intubated anesthetic strategy yields clinically meaningful reductions in PPCs and diaphragmatic dysfunction after lung surgery.

Clinical Implications: Consider NIVATS in appropriate VATS candidates to reduce PPCs and preserve diaphragmatic function; implement careful patient selection, surgical/anesthesia team expertise, and conversion readiness.

Key Findings

  • PDD at 24 h: 35.0% (NIVATS) vs 57.5% (IVATS); RR 0.61 (95% CI 0.43–0.87); P<0.001
  • PPCs within 7 days: 17.5% (NIVATS) vs 33.8% (IVATS); RR 0.52 (95% CI 0.29–0.91); P=0.019
  • Randomized 160 VATS patients to NIVATS vs IVATS with ultrasound-defined diaphragm excursion threshold (<10 mm)

Methodological Strengths

  • Randomized allocation with prespecified, clinically relevant outcomes (PDD and PPCs)
  • Objective diaphragm function assessment by ultrasound and defined PPC follow-up window (7 days)

Limitations

  • Single-center design; generalizability may be limited
  • Blinding not feasible; selection limited to suitable VATS candidates

Future Directions: Multicenter RCTs with standardized conversion criteria and longer-term outcomes (e.g., readmissions, functional recovery) to define patient selection and implementation frameworks.

2. The Effects of Isoflurane Inhibition of Mitochondrial Complex I on Calcium Removal in Mouse Neuronal Cultures.

73Level VBasic/Mechanistic researchAnesthesiology · 2025PMID: 41417580

Isoflurane dramatically prolonged presynaptic calcium decay (t1/2 ~14 s to ~160 s) by impairing ATP-dependent SERCA-mediated calcium removal; ATP supplementation or SERCA activation rescued this defect. Isoflurane also reduced mitochondrial dye uptake and increased cleaved caspase, linking mitochondrial complex I inhibition to early neurotoxicity signaling.

Impact: Clarifies a mechanistic pathway for anesthetic-induced neurotoxicity by pinpointing ATP-dependent SERCA dysfunction as the proximal driver of calcium dysregulation under isoflurane.

Clinical Implications: While preclinical, the findings motivate strategies to preserve mitochondrial ATP or enhance SERCA activity during exposure to volatile anesthetics, and inform risk assessments in vulnerable populations (e.g., developing brain).

Key Findings

  • Isoflurane increased presynaptic Ca2+ decay half-life from 14 s (10) to 160 s (77) in wildtype neurons (p=0.001)
  • ATP maintenance (30 mM glucose) rescued Ca2+ removal defect (t1/2 ~16 s; p=0.001), and SERCA activation reduced t1/2 to ~36 s (p=0.002)
  • Isoflurane decreased MitoView uptake (SERCA-dependent) and increased cleaved caspase, indicating early cellular toxicity

Methodological Strengths

  • Use of genetically encoded calcium indicators and targeted pharmacologic modulation (ATP supply, SERCA activation)
  • Convergent readouts (Ca kinetics, mitochondrial dye uptake, caspase activation) across wildtype and mutant cultures

Limitations

  • In vitro neuronal culture model; in vivo validation is needed
  • Anesthetic concentrations and exposure conditions may not fully mirror clinical scenarios

Future Directions: Test mitochondrial-support or SERCA-enhancing interventions in in vivo models and assess neurodevelopmental and functional outcomes under clinically relevant anesthetic exposures.

3. Driving Pressure-Guided Tidal Volume Titration Reduces Lung Injury in Thoracic Surgery With One-Lung Ventilation: A Randomized Clinical Trial.

72.5Level IRCTJournal of cardiothoracic and vascular anesthesia · 2025PMID: 41412843

This single-center RCT (n=96) found that driving pressure–guided tidal volume titration targeting 8–10 cm H2O during OLV reduced dependent-lung IL-6 versus a fixed 8 mL/kg PBW strategy. The protocol resulted in lower tidal volumes (~4.6 mL/kg PBW), suggesting reduced biotrauma.

Impact: Provides randomized evidence supporting driving pressure–guided ventilation during OLV to mitigate inflammatory lung injury, aligning with lung-protective principles.

Clinical Implications: Adopting driving pressure–guided tidal volume titration during OLV may reduce intraoperative biotrauma; protocols should incorporate real-time monitoring of driving pressure with careful oxygenation and CO2 targets.

Key Findings

  • Driving pressure–guided group achieved tidal volumes ~4.6 mL/kg PBW during OLV (15 and 45 min)
  • Dependent-lung IL-6 after OLV was significantly lower with driving pressure guidance (5.31 [3.62]) vs control (7.37 [5.21])
  • Targeting driving pressure 8–10 cm H2O was feasible and altered ventilatory dosing compared with fixed 8 mL/kg

Methodological Strengths

  • Randomized controlled design with a prespecified physiologic biomarker endpoint (IL-6 in dependent lung)
  • Clear ventilatory protocol linking driving pressure targets to delivered tidal volume

Limitations

  • Single-center with modest sample size; surrogate endpoint may not translate directly to clinical outcomes
  • Details on postoperative clinical endpoints and longer-term outcomes were not primary

Future Directions: Larger multicenter trials powered for clinical outcomes (PPCs, oxygenation trajectories, length of stay) comparing driving pressure–guided vs conventional OLV strategies.