Background: Sodium–glucose co-transporter-2 (SGLT-2) inhibitors are widely prescribed for type 2 diabetes mellitus (T2DM) because of their cardiovascular and renoprotective benefits. However, their use is associated with euglycemic diabetic ketoacidosis (EDKA), a rare but potentially life-threatening complication characterized by severe ketoacidosis despite relatively normal blood glucose levels. Failure to discontinue SGLT-2 inhibitors before surgery, as recommended in current guidelines, together with perioperative fasting and surgical stress, increases the risk of EDKA. Diagnostic complexity is compounded when concurrent postoperative surgical complications provide an alternative explanation for persistent metabolic acidosis. Methods: A 71-year-old man with T2DM receiving uninterrupted empagliflozin underwent direct lateral interbody fusion under general anesthesia. On postoperative day 2, he developed severe high anion-gap metabolic acidosis (pH 7.204, HCO₃⁻ 10.1 mEq/L) with near-normal blood glucose levels (178 mg/dL). Pneumoperitoneum identified on imaging was attributed to Hemovac drain-related peritoneal injury, and emergent laparoscopic exploration was performed under a working diagnosis of surgical sepsis. Although surgical source control was successfully achieved, severe metabolic acidosis persisted postoperatively (pH 7.275). Euglycemic diabetic ketoacidosis is an uncommon diabetic complication associated with several perioperative risk factors, including prolonged fasting and surgical stress. Subsequent serum ketone analysis demonstrated markedly elevated beta-hydroxybutyrate levels (4.8 mmol/L), confirming co-existing EDKA. Results: Following empagliflozin discontinuation, targeted treatment with concurrent insulin–dextrose infusion resulted in complete resolution of acid-base imbalance within five days. Conclusions: A concurrent surgical complication appeared to mask EDKA and contributed to a delay in its recognition. In patients receiving SGLT-2 inhibitors, metabolic acidosis that persists after an apparent surgical cause has been addressed should prompt measurement of serum ketones, irrespective of the blood glucose concentration. Structured perioperative protocols for SGLT-2 inhibitor management and postoperative ketone surveillance may help to prevent similar events.

Background: Systemic inflammation significantly impacts graft survival and clinical outcomes following living donor liver transplantation (LDLT). The systemic immune-inflammation index (SII), which integrates peripheral neutrophil, platelet, and lymphocyte counts, has shown prognostic value in various clinical settings, but its role in LDLT has not been thoroughly investigated. Methods: This retrospective cohort study included 378 consecutive adult patients with end-stage liver disease (ESLD) who underwent primary LDLT between March 2016 and February 2025. The SII was calculated as (neutrophil × platelet)/lymphocyte. Spearman correlation analysis was used to assess the relationships between the preoperative SII, neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) and clinical outcomes, including the preoperative Model for End-Stage Liver Disease (MELD) score, duration of mechanical ventilation, and lengths of stay in the intensive care unit (ICU) and hospital. Receiver operating characteristic (ROC) curve analysis determined the optimal cut-off values for predicting 30-day mortality, and the areas under the curve (AUROCs) were compared using the DeLong test. Multivariable logistic regression was used to identify independent predictors of 30-day mortality. Results: Among 378 analyzable patients, the 30-day mortality rate was 7.9% (30/378). Both the SII and the NLR were significantly higher in non-survivors than in survivors (SII: median 368.8 vs. 169.1, p < 0.001; NLR: 6.0 vs. 2.4, p < 0.001), whereas the PLR did not differ significantly. On ROC analysis for 30-day mortality, the NLR and the SII showed comparable discrimination (NLR AUROC = 0.729, 95% CI: 0.63–0.82; SII AUROC = 0.705, 95% CI: 0.60–0.80; DeLong p = 0.43), both exceeding the PLR (AUROC = 0.541). The optimal SII cut-off was 275 × 10⁹ cells/L (sensitivity 70.0%; specificity 69.5%). Patients with an SII ≥ 275 × 10⁹ cells/L had significantly lower 30-day survival than those below the cut-off (83.5% vs. 96.4%; log-rank p < 0.001). On multivariable logistic regression adjusting for age and MELD score as continuous variables, an SII ≥ 275 × 10⁹ cells/L remained an independent predictor of 30-day mortality (aOR = 3.78; 95% CI: 1.60–8.93; p = 0.002); the MELD score was also independently predictive (aOR = 1.04 per point; 95% CI: 1.01–1.08; p = 0.018). The association persisted when the SII was modelled continuously (aOR = 1.60 per unit log SII; 95% CI: 1.08–2.38; p = 0.020). At the 275 cut-off, sensitivity for 30-day death was 70.0% and the positive predictive value 16.5%. Conclusions: The preoperative SII and NLR are simple, inexpensive, CBC-derived inflammatory indices significantly associated with 30-day mortality after LDLT for ESLD. An elevated preoperative SII independently predicts early post-transplant mortality and may aid perioperative risk stratification, although it does not outperform the NLR.