RESUMEN
The origins of the high-energy cosmic neutrino flux remain largely unknown. Recently, one high-energy neutrino was associated with a tidal disruption event (TDE). Here we present AT2019fdr, an exceptionally luminous TDE candidate, coincident with another high-energy neutrino. Our observations, including a bright dust echo and soft late-time x-ray emission, further support a TDE origin of this flare. The probability of finding two such bright events by chance is just 0.034%. We evaluate several models for neutrino production and show that AT2019fdr is capable of producing the observed high-energy neutrino, reinforcing the case for TDEs as neutrino sources.
RESUMEN
BACKGROUND: Major brain injury and uncontrolled blood loss remain the primary causes of early trauma-related mortality. One-quarter to one-third of trauma patients exhibit trauma-induced coagulopathy (TIC). Thromboelastometry (ROTEM) and thrombelastography (TEG) are valuable alternatives to standard coagulation testing, providing a more comprehensive overview of the coagulation process. PURPOSE: Evaluating thromboelastographic profile, the incidence of fibrinolysis (defined as Ly30 > 3%) in severe trauma patients, and factors influencing pathological coagulation pattern. METHODS: Prospective observational 2 years cohort study on severe trauma patients assisted by Helicopter Emergency Medical System (HEMS) and Level 1 Trauma Center, in a tertiary referral University Hospital. RESULTS: Eighty three patients were enrolled, mean NISS (new injury severity score) 36 (± 13). Mean R value decreased from 7.25 (± 2.6) to 6.19 (± 2.5) min (p < 0.03); 48 (60%) patients had a reduction in R from T0 to T1. In NISS 25-40 and NISS > 40 groups, changes in R value increased their significance (p = 0.04 and p < 0.03, respectively). Pathological TEG was found in 71 (88.8%) patients at T0 and 74 (92.5%) at T1. Hypercoagulation was present in 57 (71.3%) patients at T0, and in 66(82.5%) at T1. 9 (11.3%) patients had hyperfibrinolysis at T0, 7 (8.8%) patients at T1. Prevalence of StO2 < 75% at T0 was greater in patients whose TEG worsened (7 patients, 46.7%) against whose TEG remained stable or improved (8 patients, 17.4%) from T0 to T1 (p = 0.02). 48 (57.8%) patients received < 1000 mL of fluids, while 35 (42.2%) received ≥ 1000 mL. The first group had fewer patients with hypercoagulation (20, 41.6%) than the second (6, 17.6%) at T1 (p < 0.03). No differences were found for same TEG pattern at T0, nor other TEG pattern. CONCLUSION: Our population is representative of a non-hemorrhagic severe injury subgroup. Almost all of our trauma population had coagulation abnormalities immediately after the trauma; pro-coagulant changes were the most represented regardless of the severity of injury. NISS appears to affect only R parameter on TEG. Hyperfibrinolysis has been found in a low percentage of patients. Hypoperfusion parameters do not help to identify patients with ongoing coagulation impairment. Small volume resuscitation and mild hypotermia does not affect coagulation, at least in the early post-traumatic phase.
