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IMPORTANCE: Optimal hemostatic resuscitation in pediatric trauma is not well defined. OBJECTIVE: To assess the association of prehospital blood transfusion (PHT) with outcomes in injured children. DESIGN, SETTING, AND PARTICIPANTS: This retrospective cohort study of the Pennsylvania Trauma Systems Foundation database included children aged 0 to 17 years old who received a PHT or emergency department blood transfusion (EDT) from January 2009 and December 2019. Interfacility transfers and isolated burn mechanism were excluded. Analysis took place between November 2022 and January 2023. EXPOSURE: Receipt of a blood product transfusion in the prehospital setting compared with the emergency department. MAIN OUTCOMES AND MEASURES: The primary outcome was 24-hour mortality. A 3:1 propensity score match was developed balancing for age, injury mechanism, shock index, and prehospital Glasgow Comma Scale score. A mixed-effects logistic regression was performed in the matched cohort further accounting for patient sex, Injury Severity Score, insurance status, and potential center-level heterogeneity. Secondary outcomes included in-hospital mortality and complications. RESULTS: Of 559 children included, 70 (13%) received prehospital transfusions. In the unmatched cohort, the PHT and EDT groups had comparable age (median [IQR], 47 [9-16] vs 14 [9-17] years), sex (46 [66%] vs 337 [69%] were male), and insurance status (42 [60%] vs 245 [50%]). The PHT group had higher rates of shock (39 [55%] vs 204 [42%]) and blunt trauma mechanism (57 [81%] vs 277 [57%]) and lower median (IQR) Injury Severity Score (14 [5-29] vs 25 [16-36]). Propensity matching resulted in a weighted cohort of 207 children, including 68 of 70 recipients of PHT, and produced well-balanced groups. Both 24-hour (11 [16%] vs 38 [27%]) and in-hospital mortality (14 [21%] vs 44 [32%]) were lower in the PHT cohort compared with the EDT cohort, respectively; there was no difference in in-hospital complications. Mixed-effects logistic regression in the postmatched group adjusting for the confounders listed above found PHT was associated with a significant reduction in 24-hour (adjusted odds ratio, 0.46; 95% CI, 0.23-0.91) and in-hospital mortality (adjusted odds ratio, 0.51; 95% CI, 0.27-0.97) compared with EDT. The number needed to transfuse in the prehospital setting to save 1 child’s life was 5 (95% CI, 3-10). CONCLUSIONS AND RELEVANCE: In this study, prehospital transfusion was associated with lower rates of mortality compared with transfusion on arrival to the emergency department, suggesting bleeding pediatric patients may benefit from early hemostatic resuscitation. Further prospective studies are warranted. Although the logistics of prehospital blood product programs are complex, strategies to shift hemostatic resuscitation toward the immediate postinjury period should be pursued.

Pediatric critical administration threshold (CAT) can be defined as >20 mL/kg of blood products within 1 hour. Exceeding this volume is associated with increased in-hospital mortality and need for urgent surgery, and should prompt activation of massive transfusion protocols.

The role of age and sex in mediating traumatic coagulopathy is unclear. Comparison of TEG profiles in injured children revealed sex dimorphisms in coagulation appear after puberty, driven by lower fibrinolysis for older females and relative hypocoagulable state for older males.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in the preterm infant. The dismal results of current treatment for NEC highlight the urgent need for greater understanding of the pathogenesis of this disease, and the importance of discovering novel, molecular-specific therapies for it. Current dogma indicates that NEC development reflects an abnormal response by the premature infant to the microbial flora that colonizes the gastrointestinal tract, although the mechanisms that mediate these abnormal bacterial-enterocyte interactions and the reasons for the particularly increased susceptibility of the premature infant to the development of NEC remain incompletely explained. Recent evidence has shed light on an emerging role for the Toll-like receptors (TLRs) of the innate immune system as central players in the pathways that signal in response to enteric bacteria resulting in the development of NEC. We now review recent advances in the field of NEC and identify several exciting potential avenues for novel treatments by focusing on abnormal TLR4 signaling in the premature intestine in the pathogenesis of NEC. In so doing, we seek to offer new hope to the patients and their families who are affected by this devastating disorder.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in the preterm infant. The dismal results of current treatment for NEC highlight the urgent need for greater understanding of the pathogenesis of this disease, and the importance of discovering novel, molecular-specific therapies for it. Current dogma indicates that NEC development reflects an abnormal response by the premature infant to the microbial flora that colonizes the gastrointestinal tract, although the mechanisms that mediate these abnormal bacterial-enterocyte interactions and the reasons for the particularly increased susceptibility of the premature infant to the development of NEC remain incompletely explained. Recent evidence has shed light on an emerging role for the Toll-like receptors (TLRs) of the innate immune system as central players in the pathways that signal in response to enteric bacteria resulting in the development of NEC. We now review recent advances in the field of NEC and identify several exciting potential avenues for novel treatments by focusing on abnormal TLR4 signaling in the premature intestine in the pathogenesis of NEC. In so doing, we seek to offer new hope to the patients and their families who are affected by this devastating disorder.

Necrotizing enterocolitis (NEC) is the leading cause of death and long-term disability from gastrointestinal disease in preterm infants, and is characterized by acute and chronic intestinal inflammation that may lead to systemic sepsis and multi-system organ failure. NEC typically develops in the preterm infant after the administration of tube feeds, although it may occasionally be seen in full-term babies. Despite extensive clinical experience in the management of patients with NEC, the underlying cellular and molecular mechanisms leading to its development remain incompletely understood. Several animal models have therefore been developed in a variety of species in order to study the pathogenesis of NEC and to develop more effective treatment strategies. This review seeks to examine the pros and cons of animal models that have been developed in the study of NEC over the past 30 years. It will highlight the various strengths and weaknesses of experimental approaches that have been used, and discuss potential directions for the development of such models for the future.