Background/Objective: Pediatric trauma frequently prompts computed tomography (CT) in emergency departments; however, the cumulative radiation burden and its distribution across initial clinical risk strata remain incompletely characterized. We aimed to describe CT utilization and cumulative effective dose in a tertiary care pediatric trauma cohort and examine how radiation exposure accrues across pragmatic presentation-based risk groups. Methods: We conducted a retrospective cohort audit of pediatric trauma presentations at our institution. Risk stratification was based on the triage category and readily available initial physiological parameters. CT utilization and radiation burden were assessed at the patient level using the cumulative effective dose (mSv) derived from scanner dose metrics and region-specific conversion coefficients. Secondary analyses examined the dose distribution according to ED disposition and consultation pathways. Sensitivity analyses were performed using green triage only as an “ultra-low-risk” definition. Results: Among the 935 children, 545 (58.3%) underwent at least one CT examination. Although higher-risk categories had higher CT use and higher per-patient dose, a substantial share of the cohort’s cumulative radiation burden accrued in children initially classified as low-risk and/or ultimately discharged. Combined-region CT protocols contributed disproportionately to the higher dose categories. The findings were consistent in sensitivity analyses using a stricter ultra-low-risk definition. Conclusions: In this single-center audit, CT utilization and cumulative radiation burden were high, and non-trivial radiation exposure accrued among children initially classified as low-risk. These findings support targeted radiation stewardship interventions, including pathway optimization and the implementation of validated decision tools, where feasible, particularly for discharge-eligible and low-risk presentations.

Background: We evaluated the diagnostic discrimination of serum endothelin-1 (ET-1), copeptin, and chemerin in adults evaluated for acute pulmonary embolism (PE). Methods: This prospective, single-center diagnostic study included 65 adults with CTPA-confirmed PE and 64 CTPA-negative controls recruited from the same emergency-department source population of patients evaluated for suspected PE. Controls were consecutively enrolled among dyspneic patients in whom CTPA excluded PE; no individual matching was used. Biomarkers were compared with D-dimer and the Wells score. Results: ET-1 was higher in the PE group (median, 12.96 vs. 6.41 pg/mL; p < 0.001) and showed moderate discrimination (AUROC, 0.731; 95% CI, 0.644–0.818), but was inferior to D-dimer (AUROC, 0.905; 95% CI, 0.852–0.958). Adding ET-1 to D-dimer changed the AUROC from 0.905 to 0.923 (DeLong p = 0.128), and adding ET-1 to Wells plus D-dimer changed it from 0.966 to 0.971 (DeLong p = 0.224). An age-adjusted D-dimer threshold preserved sensitivity (96.9%) and increased specificity from 48.4% to 56.3% relative to 0.50 mg/L FEU. Conclusions: ET-1 was associated with acute PE in this selected sample but did not materially improve discrimination beyond established comparators. Because the near-ceiling Wells–D-dimer model and selected sampling frame limit inference, external validation in an unselected diagnostic cohort is required.

Early diagnosis of acute myocardial infarction (AMI) remains challenging in patients with initially non-elevated high-sensitivity cardiac troponin I (hs-cTnI). We assessed the diagnostic contribution of copeptin, with endothelin-1 and chemerin as exploratory comparators. This prospective, single-center case–control study included 160 adults with suspected acute coronary syndrome: 40 controls, 40 with unstable angina, 40 with non-ST-elevation myocardial infarction (NSTEMI), and 40 with ST-elevation myocardial infarction (STEMI). Samples were obtained at presentation, and diagnoses were adjudicated blinded to investigational biomarkers. Twelve of the 80 AMI cases had initially non-elevated hs-cTnI (7 STEMI; 5 NSTEMI). Copeptin was positive in 8/12 and the three-marker panel in 9/12. Among the five initially troponin-negative NSTEMI cases, all positive on repeat hs-cTnI testing, copeptin was positive in 4/5 (80.0%; 95% confidence interval, 28.4–99.5%). The hs-cTnI OR copeptin strategy increased sensitivity from 85.0% to 95.0%, while specificity among controls decreased from 95.0% to 62.5%. Adding the biomarkers to a clinical model containing hs-cTnI changed the apparent area under the curve from 0.961 to 0.965, without significantly improving model fit (likelihood-ratio p = 0.718). These findings may support evaluating adjunctive copeptin within contemporary accelerated troponin pathways.

Background/Objectives: Early mortality risk stratification after CT-confirmed cervical spine fractures remains clinically challenging in patients with major trauma. Imaging establishes a structural diagnosis, but it does not fully capture early physiological deterioration. This study aimed to develop and internally validate a prognostic model for in-hospital mortality and evaluate whether a MAP-derived Shock Index provides incremental prognostic information beyond routinely available clinical variables and the Injury Severity Score (ISS). Methods: This retrospective single-center cohort study included 131 adults with CT-confirmed cervical spine fractures and ISS ≥ 15 who were admitted to a tertiary trauma center between 2013 and 2023. The MAP-derived Shock Index was calculated as heart rate divided by estimated systolic blood pressure, where estimated systolic blood pressure was defined a priori as 1.5 × MAP. Four prespecified logistic regression models were evaluated: a base clinical model, base plus MAP-derived Shock Index, base plus ISS, and base plus MAP-derived Shock Index plus ISS. Discrimination, Brier score, calibration, bootstrap internal validation, and decision curve analyses were performed. Results: The in-hospital mortality rate was 22.9% (30/131). The base plus MAP-derived Shock Index model achieved an apparent AUC of 0.93 and an optimism-corrected AUC of 0.91. The MAP-derived Shock Index provided incremental prognostic information beyond the ISS; as an individual predictor, its AUC was 0.82 compared with 0.74 for the ISS. With each 0.1-unit increase, the MAP-derived Shock Index was associated with higher odds of in-hospital mortality. Decision curve analysis suggested a higher apparent net benefit across clinically relevant thresholds. Conclusions: In this internally validated retrospective cohort, the MAP-derived Shock Index complemented clinical and ISS-based assessments for early in-hospital mortality risk stratification after CT-confirmed cervical spine fracture. The index is not the conventional SBP-based Shock Index, and the model requires external multicenter validation before clinical use.