BACKGROUND: Unmanned aerial vehicles (UAVs) have been shown to shorten delivery times of medical products in health care, providing a potential answer to the question of prehospital resuscitation where blood and blood products are not readily available. While the capabilities and efficiencies of delivery via UAVs are already well established, the postdelivery viability and hemostatic function of whole blood has not been examined. METHODS: Whole blood units were sampled for a preflight control and loaded onto a fixed wing UAV. The UAVs flew in predetermined flight paths to either deliver via parachute drop or direct recovery after UAV capture by arresting gear. Postflight and preflight samples were assayed for coagulation function with thromboelastography, blood chemistry, and free hemoglobin to observe hemolysis. RESULTS: No significant differences in any metric were observed between the blood samples assayed preflight versus those flown and parachute dropped or those flown and recovered from the UAV. CONCLUSION: The use of UAVs for delivery of whole blood offers significant benefits for prehospital care. Further innovations in UAV and transportation technologies will expand on an already strong foundation. LEVEL OF EVIDENCE: Therapeutic/Care Management; Level IV.

Acute kidney injury (AKI) is a complex and multifactorial syndrome characterized by the rapid decline of renal function following ischemic, septic, traumatic, hypoxic, or nephrotoxic insults. Despite advances in critical care, exacerbation of AKI is associated with substantial morbidity, mortality, progression to chronic kidney disease (CKD) and multiorgan dysfunction. Current therapies remain largely supportive and do not directly target the molecular pathways driving AKI, underscoring the need for mechanism-based diagnostics and precision-guided therapeutic strategies. Accumulating evidence supports that AKI is driven by mechanistic crosstalk among cellular injury pathways involving mitochondrial dysfunction, oxidative stress, endothelial damage, immune dysregulation, and regulated cell death. Flow cytometry has emerged as a powerful platform for high-dimensional single-cell and extracellular vesicle analysis, enabling comprehensive assessment of immune cell phenotypes, platelet activation, endothelial alterations, mitochondrial dysfunction, and circulating extracellular vesicles associated with AKI. Advances in artificial intelligence (AI), machine learning and emerging explainable AI (XAI) enhance the ability to identify clinically relevant patterns from complex datasets. This review aims to integrate AKI pathophysiology with flow cytometry-based biomarker discovery and AI-enabled analytical approaches. We discuss translational applications in AKI-relevant clinical settings, including trauma, hemorrhagic shock, sepsis, and radiation-combined injury, with particular emphasis on Prolonged Casualty Care and other austere environments, where rapid, mechanism-based diagnostics are critically needed.

Background: While anti-shock therapy provided early after hemorrhage may be beneficial, the problem of delivery of potential therapeutics to ischemic tissue has not been well-appreciated. Polydatin (PD) and 5-aminoimidazole-4-carboxamide 1-β-D-ribonucleoside (AICAR) alleviate mitochondrial dysfunction and acute renal injury (AKI) following resuscitation, but it is unclear whether PD or AICAR are still effective before resuscitation when drug delivery can be still impeded. Because a low volume of polyethylene glycol (PEG) improves tissue perfusion in rats following hemorrhagic shock, we hypothesized that either PD or AICAR, when administered in combination with PEG, will be more effective on restoring hemodynamic function and mitochondrial function than when either drug is administered without PEG. Methods: Rats were randomized into 6 treatment groups (n=8/group): saline, PEG, PD, PD+PEG, AICAR, and AICAR+PEG. Extremity trauma was induced in anesthetized rats followed by pressure-controlled hemorrhage (mean arterial pressure (MAP) = 55 mmHg) for 45 minutes, at which point treatment was administered without fluid resuscitation. MAP, renal blood flow (RBF) and oxygen delivery (DO2), glomerular filtration rate (GFR), and sodium and potassium reabsorption were measured. Two hours after treatment, rats were euthanized to measure renal mitochondrial function. Results: Hemorrhage caused hyperlactatemia and decreased RBF, DO2, GFR, and urine flow; PEG, PD+PEG, and AICAR+PEG similarly improved these parameters, but neither PD nor AICAR alone showed any hemodynamic effects. However, preserved renal mitochondrial respiratory activities were only observed in PD+PEG and AICAR+PEG but not in PD, AICAR, or PEG alone groups. In addition, PD+PEG but not PD alone inhibited the tubular mitochondrial activity during shock as indicated by decreased renal sodium and potassium reabsorption. Conclusion: During hemorrhagic shock, PD or AICAR demonstrated preservation of mitochondrial function only when co-administered with PEG to alleviate tissue ischemia. This finding suggests a potential pharmacologic strategy to improve tissue delivery of therapeutics when resuscitation is limited.