Obesity is associated with unique and compounding perioperative challenges in otolaryngologic surgery. This review summarizes evidence-based guidance on preoperative risk stratification, airway management, intraoperative anesthetic and ventilatory strategies, and procedure-specific postoperative care for patients with obesity undergoing otolaryngologic surgery, with emphasis on the emerging phenotype of sarcopenic obesity, the shared airway, and individualized monitoring frameworks.

Neuropathic pain arises from complex pathological processes involving oxidative stress and neuroinflammation. Excessive production of reactive oxygen species (ROS) contributes critically to the initiation and persistence of neuropathic pain following nerve injury and inflammatory insults, and antioxidant-based interventions have shown consistent efficacy across multiple preclinical models. This study investigated the analgesic effects of 4-(phenylsulfanyl)butan-2-one (4-PSB-2), a compound with known anti-inflammatory properties, using the chronic constriction injury (CCI) rat model. Intrathecal administration of 4-PSB-2 significantly alleviated CCI-induced thermal hyperalgesia and mechanical allodynia from postoperative days 3 to 28, without affecting baseline nociceptive responses in naïve rats. In the ipsilateral spinal cord dorsal horn (SCDH), 4-PSB-2 reduced oxidative stress, evidenced by decreased expression of tyrosinase and nitrotyrosine, particularly in astrocytes. Additionally, 4-PSB-2 modulated the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling pathway, as demonstrated by enhanced nuclear expression of Nrf2 and upregulation of HO-1 expression, along with reduced Kelch-like ECH-associated protein 1 (Keap1), phosphorylated P38 (p-P38), and tumor necrosis factor-alpha (TNF-α) levels. Glial cell activation was also attenuated. Notably, co-administration with zinc protoporphyrin (ZnPP), a pharmacological inhibitor of heme oxygenase activity, attenuated the analgesic, antioxidant, and anti-inflammatory effects of 4-PSB-2, suggesting that activation of the Nrf2/HO-1 pathway contributes to the protective effects of 4-PSB-2. These findings indicate that 4-PSB-2 confers sustained neuropathic pain relief by regulating oxidative stress and neuroinflammation via astrocytic Nrf2/HO-1 pathway activation, highlighting its potential as a promising therapeutic candidate for neuropathic pain management.

Postpartum depression is a major maternal and child health concern, but evidence regarding prenatal exposure to ultrafine particles (UFPs) remains limited. This prospective two-center pregnancy cohort in Shanghai included 2,647 pregnant women. Residential prenatal exposures to UFPs and PM2.5 were estimated for the first, second, and third trimesters and the full pregnancy. Depressive symptoms were assessed at 6-10 weeks postpartum using the Edinburgh Postnatal Depression Scale, with a score ≥10 defined as positive screening for postpartum depression. Associations were evaluated using multivariable logistic regression, two-pollutant models, joint-trimester logistic regression, exploratory stacked logistic generalized estimating equations, restricted cubic splines, and interaction analyses. The prevalence of positive screening for postpartum depression was 20.4%. After adjustment for potential confounders, an IQR increase in first-trimester UFPs exposure was associated with higher odds of screen-positive postpartum depression (OR = 1.252, 95% CI: 1.065-1.471), as was an IQR increase in full-pregnancy UFPs exposure (OR = 1.104, 95% CI: 1.047-1.164). These associations persisted after adjustment for PM2.5, whereas PM2.5 showed no stable independent association. Sensitive-window analysis supported the first trimester as the main window of association, and infant-sex interaction analysis suggested a stronger association among pregnancies with male infants. These findings suggest that prenatal UFPs exposure, particularly during early pregnancy, may be associated with higher odds of positive screening for postpartum depression, highlighting the potential relevance of ultrafine particle number concentration in perinatal environmental health research.

Perioperative neurocognitive disorders (PND), including postoperative delirium (POD), delayed neurocognitive recovery (DNR), and postoperative neurocognitive disorder, are common after surgery in older adults, and the gut-brain axis has been proposed as a contributing pathway. Most mechanistic support rests on rodent behavioral assays, yet these endpoints and human clinical diagnoses are routinely treated as interchangeable. This critical narrative review examines that translational boundary. PND is used here as a clinically consequential test case for a broader behavioral-neuroscience problem: how animal behavioral phenotypes, microbiome-associated signals, and intervention effects should be translated into human diagnostic constructs. A structured search identified and appraised the principal evidence rather than an exhaustive synthesis; no formal risk-of-bias or certainty-of-evidence assessment was performed. Evidence was separated into human perioperative studies reporting a neurocognitive outcome with either a measured gut-brain exposure or a gut-directed intervention; those reporting gut-brain change without a cognitive outcome; perioperative preclinical evidence; and indirect non-perioperative evidence. The retrieved human perioperative evidence spans observational cohorts across gastric, orthopedic, spinal and cardiac surgery, multi-omic and metabolomic cohorts, and randomized perioperative probiotic trials reporting lower rates of study-defined cognitive outcomes. It nonetheless remains heterogeneous and largely single-center, with modest event numbers, inconsistent sampling and assessment, and limited external validation. Mechanistic support still comes mainly from perioperative rodent models using water maze, fear-conditioning, recognition-memory, and delirium-like readouts, which measure narrow, species-specific capacities and are not diagnostic equivalents of POD, DNR, or postoperative neurocognitive disorder. Microbiome-mediated causation is unproven, and cross-species endpoint alignment remains a central route to improved translation.

In children with multiple organ dysfunction syndrome (MODS), vancomycin dosing is frequently guided by population-based approaches followed by therapeutic drug monitoring that requires considerable blood volumes. We sought to develop a population pharmacokinetic (PK) model and describe vancomycin exposures using blood-sparing, whole-blood volumetric absorptive microsampling (VAMS). In this multicentre prospective observational study, up to 15 PK samples were collected per subject over 3 days. Individual whole-blood areas under the concentration-time curve during 0-24 hours (AUC0-24h) and 24-48 hours (AUC24-48h) after treatment initiation were estimated. Simulations explored exposures across weight and renal function strata. Sixty-five subjects were included in the final model cohort (median age, 10 years [range, 1 month-17 years]; median weight, 30 kg [3-214 kg]). A two-compartment, allometrically scaled model incorporating renal function best described vancomycin PK. The median dose preceding the first PK sample was 380 mg (15 mg/kg), with most subjects receiving vancomycin every 6 hours. In the fully paired analysis set (n=46), median whole-blood AUC0-24h and AUC24-48h were 475 mg·h/L (range, 232-1,749) and 594 mg·h/L (range, 188-2,157), respectively. Simulations demonstrated substantial exposure variability across weight and renal function strata. These findings demonstrate substantial interindividual exposure variability despite population-based dosing. The model provides a foundation for prospective evaluation of individualized exposure estimation using sparse VAMS sampling. Whole-blood VAMS AUC therapeutic targets remain unvalidated, and direct interpretation against established plasma-based targets is an important future effort.

This technical note is meant to be complementary to the recently published Professional Practice Guidelines of the SFAR-ADARPEF. The limits of using blood pressure as a surrogate for changes in cardiac output and the variable accuracy of its non-invasive measurement are reminded. As clearcut population-based threshold values based on measurements obtained in awake or anaesthetised children cannot be provided, an adaptation based on the child's baseline blood pressure, comorbidity and surgical context is necessary to prevent unnecessary treatment of an acceptable low blood pressure or tolerating a too low blood pressure. The measurement of a baseline awake blood pressure, although often difficult to achieve in children, is therefore very helpful. If a low intraoperative MAP is measured, the presence of hypotension should be confirmed by repeat measurement and the simultaneous evaluation of clinical and paraclinical signs, and the observation of the surgical field. The treatment should then be adapted to the cause: anaesthetic overdose, hypovolaemia, positioning, surgical action, anaphylaxis, etc.