Sodium-glucose cotransporter 2 (SGLT2) inhibitors are widely used for type 2 diabetes, heart failure, and chronic kidney disease, including in patients without diabetes. Their ketogenic effects may be amplified perioperatively by fasting, surgical stress, and volume loss, resulting in ketoacidosis without marked hyperglycemia. Reported frequencies depend on ascertainment. Where ketones were measured against a diagnostic threshold, cohorts reported 0–1.8% in non-cardiac and mixed populations and 0–15.1% in cardiac surgery; one prospective study using a lower threshold (≥ 0.6 mmol/L) reported a far higher figure, and studies without ketone measurement reported surrogate metabolic-acidosis endpoints of 30–41%. None of these are comparable incidence estimates. Severe and fatal cases have been reported. Because plasma glucose may be normal, diagnosis requires attention to acid–base status and ketones. Quantitative blood β-hydroxybutyrate is preferred when SGLT2 inhibitor (SGLT2i)-associated ketoacidosis is suspected; urine ketone tests may screen when blood testing is unavailable, but a negative result does not exclude it. Perioperative guidance remains inconsistent: some bodies recommend withholding SGLT2i for 3 days (4 days for ertugliflozin), whereas others support risk-stratified continuation in selected patients under specified fasting and dietary conditions. No randomized trial has compared continuation with discontinuation using perioperative ketoacidosis as an endpoint; observational evidence remains limited and conflicting, and ketone thresholds and monitoring intervals lack prospective validation. This review summarizes evidence on recognition, diagnosis, withholding, monitoring, and postoperative restart.
Liver transplantation is an established treatment for children with end-stage liver disease, acute liver failure, and selected metabolic and malignant conditions. Small circulating volume, limited thermoregulatory and metabolic reserve, interruption and recovery of hepatic function, and graft-recipient size mismatch affect perioperative care. This narrative review examined how these features inform preoperative assessment, anesthetic preparation, management across the operative phases, and recovery. Cardiopulmonary assessment identified associated anomalies and functional impairment that affect tolerance of induction and reperfusion. Intraoperative management combined assessment of blood loss, vascular tone, and ventricular function with serial evaluation of temperature, electrolyte and glucose levels, and hemostasis. Systemic hemodynamic measurements were interpreted alongside graft-specific inflow and outflow assessment, and fluid responsiveness was distinguished from a clinical need for fluid. Postoperative management included respiratory readiness, unresolved metabolic and circulatory disturbances, renal function, and analgesia. The evidence was interpreted according to population, design, and setting. Pediatric guidelines chiefly addressed candidate evaluation and postoperative care, while much intraoperative evidence came from small observational cohorts or extrapolation from pediatric intensive care and adult transplantation. The recipients with the smallest body size and children with acute liver failure, metabolic disease, or repeat grafts require further adaptation. This review emphasized preparation for predictable disturbances and reassessment after intervention, while avoiding the application of study-specific thresholds or protocols.
Population aging has increased the number of patients aged 65 years or older with cancer undergoing surgery; however, chronological age alone does not adequately capture perioperative vulnerability. Inflammaging, a chronic low-grade inflammatory state that accompanies aging, may provide a biological framework for understanding the heterogeneity of perioperative risk. Senescent-cell accumulation and the senescence-associated secretory phenotype contribute to persistent inflammatory signaling, while age-related immune remodeling produces an "immune paradox" involving heightened inflammatory signaling despite impaired immune effector function. Surgical stress may act as a second hit in this pre-existing state by amplifying damage-associated molecular pattern signaling, neuroendocrine activation, and perioperative immune dysfunction. These changes provide plausible links to impaired antitumor immune surveillance, infection, pulmonary complications, delirium, and delayed recovery but do not establish an inflammaging-mediated causal pathway to clinical outcomes. In this review, established perioperative care is discussed along with investigational approaches to immune-inflammatory modulation. Relevant approaches include prehabilitation, pathways for enhanced recovery after surgery, opioid-sparing multimodal analgesia, regional anesthesia, individualized anesthetic selection, and selected pharmacological adjuncts. Preoperative assessment of sarcopenia, serum albumin, and the neutrophil-to-lymphocyte ratio may complement the assessment of physiological vulnerability but does not specifically quantify inflammaging. Future studies should evaluate biomarker-guided risk stratification and determine whether anesthetic interventions have different effects according to biological aging and inflammaging status.
Background: Virtual reality (VR) reduces pain and anxiety, but influencing factors remain ambiguous. This study evaluated the effect of interactivity within a VR experience on heat pain threshold (HPT), pressure pain threshold (PPT), and immediate and recalled pain and anxiety.Methods: The Stanford Chariot Program conducted this prospective, randomized, crossover clinical trial at Stanford Children’s Hospital Stanford, Stanford Hospital, and Stanford Medical School. Healthy adult participants meeting inclusion criteria were randomized by hand dominance and condition sequence and underwent standardized pain threshold tests with a heat thermode or pressure algometer during active and passive VR conditions. The primary outcome was the impact of active VR on HPT. Secondary outcomes evaluated its effects on PPT, immediate and recalled pain, and immediate and recalled anxiety.Results: 163 total participants were included, 81 who underwent HPT testing and 82 who underwent PPT testing. Active VR increased pain thresholds for both HPT (P = 0.0001) and PPT (P ≤ 0.0001). There was no difference in initial pain scores between VR conditions for HPT (P = 0.63), though there was for PPT (P = 0.006). There was no difference in recalled pain scores for HPT (P = 0.13) or PPT (P = 0.39). Active VR reduced initial and recalled anxiety scores for HPT (P = 0.012, P = 0.002; respectively) and initial anxiety scores for PPT (P = 0.04). Recalled anxiety scores for PPT did not differ (P = 0.32).Conclusions: Active VR improved pain tolerance and anxiety more than passive VR.
