Anesthesia Research

Background: Epidural analgesia (EA) is widely used in pancreatic surgery but is associated with hypotension and delayed recovery. The shift towards minimally invasive surgery has led to the exploration of alternative multimodal analgesia strategies. Methadone, with its unique pharmacological properties, may further optimize recovery. Methods: This retrospective cohort study included 213 patients undergoing pancreatic resection, receiving EA (n = 63), multimodal analgesia without methadone (MA; n = 92), or with methadone (MM; n = 58). MA and MM included intravenous ketamine, lidocaine and continuous wound infiltration. Primary outcome was maximum daily postoperative pain scores. Secondary outcomes included opioid consumption, vasopressor use, mobilization, bowel recovery, urinary catheter duration, and ICU/hospital stay. Results: Compared with EA, pain scores were slightly higher in MM (mean difference 2.22; 95% CI 1.22–3.90; p = 0.01) and in MA (mean difference 2.06; 95% CI 0.99–4.30; p = 0.06). Opioid use was comparable between MM and EA (OR 0.99, 95% CI [0.98, 1.00], p = 0.20), and significantly lower in MA (OR 0.97, 95% CI [0.96, 0.98], p < 0.001). Both MA and MM demonstrated reduced vasopressor requirements (both 0 vs. 2.0 median days) and shorter urinary catheterization durations (MA 1.2 MM 1.9 vs. EA 4.0 median days). MA improved mobilization (0 vs. 1 median days; OR 0.52, p = 0.03) and bowel recovery (OR 0.76, p = 0.02). ICU stay was longer in EA due to routine ICU admission for open surgery. Conclusions: Multimodal analgesia, with or without methadone, offers alternative strategies in pancreatic surgery. While EA provides superior pain control, multimodal regimens are associated with improved functional recovery.

Background: Postoperative cognitive dysfunction (POCD) is a significant complication following thoracic surgery. One-lung ventilation (OLV) during these procedures can lead to cerebral desaturation, potentially contributing to POCD. This study investigated the correlation between intraoperative cerebral oximetry, measured by near-infrared spectroscopy (NIRS), and neurocognitive function changes in patients undergoing thoracic surgery. Methods: In this prospective, observational pilot study, 54 adult patients undergoing OLV for thoracic surgery were enrolled. Cerebral oxygen saturation (rScO₂) was monitored continuously using NIRS. Patients were categorized into two groups: Group N (normal NIRS values) and Group D (decreased NIRS values, defined as a drop of ≥20% from baseline or an absolute value <50%). Neurocognitive function was assessed preoperatively, on the 3rd postoperative day, and at 3 months using the Addenbrooke’s Cognitive Examination-Revised (ACE-R) battery. The correlation between intraoperative rScO₂ values, postoperative complications, and neurocognitive outcomes was analyzed. Results: A significant association was found between intraoperative cerebral desaturation and a decline in ACE-R scores. Group D showed a significant decrease in ACE-R scores on the 3rd postoperative day and at 3 months compared to their baseline, while Group N showed no significant change. The most pronounced decline in Group D was observed in the “Fluency” cognitive domain. Interestingly, there was a significant difference in ICU admission rates (p = 0.004) between the two groups, with more admissions in Group D, despite no significant difference in intraoperative hypotension or peripheral desaturation. Patients with pre-existing hypertension were more likely to experience cerebral desaturation. Conclusion: Intraoperative cerebral desaturation, as detected by NIRS, is a strong predictor of both early and late postoperative neurocognitive decline and increased postoperative morbidity in thoracic surgery patients. This underscores the value of NIRS as a sensitive monitoring tool to identify patients at risk and guide timely interventions. These findings suggest a need for further research, including larger randomized controlled trials, to confirm these associations and evaluate the impact of a protocol-driven NIRS intervention strategy on patient outcomes.

Damage-associated molecular patterns (DAMPs) are endogenous molecules released during cellular stress or injury that trigger sterile inflammation. In perioperative settings, common triggers include surgical trauma, ischemia–reperfusion injury, cardiopulmonary bypass, blood transfusion, and mechanical ventilation. When released extracellularly, DAMPs activate innate immune receptors such as Toll-like receptors (TLRs) and the receptor for advanced glycation end products (RAGE), initiating signaling cascades that amplify inflammation, disrupt endothelial integrity, and promote coagulation and metabolic imbalance. This sterile inflammatory response may extend local tissue injury into systemic organ dysfunction, manifesting clinically as acute lung injury, acute kidney injury, myocardial dysfunction, disseminated intravascular coagulation, and perioperative neurocognitive disorders. Recognizing the central role of DAMPs reframes these complications as predictable consequences of endogenous danger signaling rather than solely as results of infection or hemodynamic instability. This understanding supports the use of established strategies such as protective ventilation and restrictive transfusion to minimize DAMP release. Emerging evidence also suggests that anesthetic agents may influence DAMP-mediated inflammation: propofol and dexmedetomidine appear to exert anti-inflammatory effects, whereas volatile anesthetics show variable results. Although clinical data remain limited, anesthetic choice and perioperative management may significantly affect systemic inflammatory burden and recovery. Future research validating DAMPs as biomarkers and therapeutic targets may inform precision anesthetic strategies aimed at modulating sterile inflammation, ultimately enhancing perioperative outcome.