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Background: High-quality cardiopulmonary resuscitation (CPR) can restore spontaneous circulation (ROSC) and neurological function and save lives. We conducted an umbrella review, including previously published systematic reviews (SRs), that compared mechanical and manual CPR; after that, we performed a new SR of the original studies that were not included after the last published SR to provide a panoramic view of the existing evidence on the effectiveness of CPR methods. Methods: PubMed, EMBASE, and Medline were searched, including English in-hospital (IHCA) and out-of-hospital cardiac arrest (OHCA) SRs, and comparing mechanical versus manual CPR. A Measurement Tool to Assess Systematic Reviews (AMSTAR-2) and GRADE were used to assess the quality of included SRs/studies. We included both IHCA and OHCA, which compared mechanical and manual CPR. We analyzed at least one of the outcomes of interest, including ROSC, survival to hospital admission, survival to hospital discharge, 30-day survival, and survival to hospital discharge with good neurological function. Furthermore, subgroup analyses were performed for age, gender, initial rhythm, arrest location, and type of CPR devices. Results: We identified 249 potentially relevant records, of which 238 were excluded. Eleven SRs were analyzed in the Umbrella review (January 2014–March 2022). Furthermore, for a new, additional SR, we identified eight eligible studies (not included in any prior SR) for an in-depth analysis between April 1, 2021, and February 15, 2024. The higher chances of using mechanical CPR for male patients were significantly observed in three studies. Two studies showed that younger patients received more mechanical treatment than older patients. However, studies did not comment on the outcomes based on the patient's gender or age. Most SRs and studies were of low to moderate quality. The pooled findings did not show the superiority of mechanical compared to manual CPR except in a few selected subgroups. Conclusions: Given the significant heterogeneity and methodological limitations of the included studies and SRs, our findings do not provide definitive evidence to support the superiority of mechanical CPR over manual CPR. However, mechanical CPR can serve better where high-quality manual CPR cannot be performed in selected situations. [ABSTRACT FROM AUTHOR]

This is an interim analysis of the Beta-blocker (Propranolol) use in traumatic brain injury (TBI) based on the high-sensitive troponin status (BBTBBT) study. The BBTBBT is an ongoing double-blind placebo-controlled randomized clinical trial with a target sample size of 771 patients with TBI. We sought, after attaining 50% of the sample size, to explore the impact of early administration of beta-blockers (BBs) on the adrenergic surge, pro-inflammatory cytokines, and the TBI biomarkers linked to the status of high-sensitivity troponin T (HsTnT). Patients were stratified based on the severity of TBI using the Glasgow coma scale (GCS) and HsTnT status (positive vs negative) before randomization. Patients with positive HsTnT (non-randomized) received propranolol (Group-1; n = 110), and those with negative test were randomized to receive propranolol (Group-2; n = 129) or placebo (Group-3; n = 111). Propranolol was administered within 24 h of injury for 6 days, guided by the heart rate (> 60 bpm), systolic blood pressure (≥ 100 mmHg), or mean arterial pressure (> 70 mmHg). Luminex and ELISA-based immunoassays were used to quantify the serum levels of pro-inflammatory cytokines (Interleukin (IL)-1β, IL-6, IL-8, and IL-18), TBI biomarkers [S100B, Neuron-Specific Enolase (NSE), and epinephrine]. Three hundred and fifty patients with comparable age (mean 34.8 ± 9.9 years) and gender were enrolled in the interim analysis. Group 1 had significantly higher baseline levels of IL-6, IL-1B, S100B, lactate, and base deficit than the randomized groups (p = 0.001). Group 1 showed a significant temporal reduction in serum IL-6, IL-1β, epinephrine, and NSE levels from baseline to 48 h post-injury (p = 0.001). Patients with severe head injuries had higher baseline levels of IL-6, IL-1B, S100B, and HsTnT than mild and moderate TBI (p = 0.01). HsTnT levels significantly correlated with the Injury Severity Score (ISS) (r = 0.275, p = 0.001), GCS (r = − 0.125, p = 0.02), and serum S100B (r = 0.205, p = 0.001). Early Propranolol administration showed a significant reduction in cytokine levels and TBI biomarkers from baseline to 48 h post-injury, particularly among patients with positive HsTnT, indicating the potential role in modulating inflammation post-TBI. Trial registration: ClinicalTrials.gov NCT04508244. It was registered first on 11/08/2020. Recruitment started on 29 December 2020 and is ongoing. The study was partly presented at the 23rd European Congress of Trauma and Emergency Surgery (ECTES), April 28–30, 2024, in Estoril, Lisbon, Portugal. [ABSTRACT FROM AUTHOR]

Background: We aimed to analyze in-hospital timing and risk factors for mortality in a level 1 trauma center. Methods: This is a retrospective analysis of all trauma-related mortality between 2013 and 2018. Patients were divided and analyzed based on the time of mortality (early (≤48 h) vs late (>48 h)), and within different age groups. Multivariate regression analysis was performed to predict in-hospital mortality. Results: 8624 trauma admissions and 677 trauma-related deaths occurred (47.7% at the scene and 52.3% in-hospital). Among in-hospital mortality, the majority were males, with a mean age of 35.8 ± 17.2 years. Most deaths occurred within 3–7 days (35%), followed by 33% after 1 week, 20% on the first day, and 12% on the second day of admission. Patients with early mortality were more likely to have a lower Glasgow coma scale, a higher shock index, a higher chest and abdominal abbreviated injury score, and frequently required exploratory laparotomy and massive blood transfusion (P <.005). The injury severity scores and proportions of head injuries were higher in the late mortality group than in the early group. The severity of injuries, blood transfusion, in-hospital complications, and length of intensive care unit stay were comparable among the age groups, whereas mortality was higher in the age group of 19 to 44. The higher proportions of early and late in-hospital deaths were evident in the age group of 24 to 29. In multivariate analysis, the shock index (OR 2.26; 95%CI 1.04-4.925; P =.04) was an independent predictor of early death, whereas head injury was a predictor of late death (OR 4.54; 95%CI 1.92-11.11; P =.001). Conclusion: One-third of trauma-related mortalities occur early after injury. The initial shock index appears to be a reliable hemodynamic indicator for predicting early mortality. Therefore, timely hemostatic resuscitation and appropriate interventions for bleeding control may prevent early mortality. [ABSTRACT FROM AUTHOR]

Trauma is a serious public health issue, and remains a major cause of mortality and disability worldwide. The notion that genetic factors contribute to an individual's response to traumatic injury has advanced significantly. Genetic variations in severely injured patients have been linked to mortality, morbidity, and psychological outcomes. We conducted a comprehensive review of beta-adrenergic receptor polymorphisms and their impact on the pathogenetics of traumatic injuries, which could pave the way for a transformational frontier of personalized medicine in neurotrauma. It remains unclear why some individuals are vulnerable to worse outcomes, whereas others are resilient. Although genetic factors may be significant, the intricate interplay between environmental and genetic factors may be responsible for variations in the presentation and outcome after injury. Recent advancements in genetic analysis and molecular physiology have helped to shed light on the causes of such variability. Although exposure to trauma can initiate a cascade of stress-related responses, these responses alone are insufficient to explain etiopathogenesis. Therefore, gaining insights into how trauma and genetic predispositions to adrenergic variations interact at the molecular level to affect an individual's susceptibility and recuperation could provide an essential understanding of the molecular pathogenesis of traumatic injuries. Therefore, it is imperative to identify potential genetic and physiological markers to guide early management and prognosis of trauma. Such knowledge could pave the way for the discovery of novel biomarkers that can identify a transdiagnostic subgroup that is at high risk and requires early intervention. This could lead to the adoption of personalized medical approaches in neurotrauma care. [ABSTRACT FROM AUTHOR]