Components of an Updated Disaster Medicine Curriculum Included in Emergency Medicine Residency and Emergency Medical Services Fellowship in the United States.

INTRODUCTION: Disaster medicine (DM) is a unique field that has undergone significant development as disaster events become increasingly complicated to respond to. However, DM is not recognized by the American Board of Medical Specialties (ABMS) or Accreditation Committee of Graduate Medical Education (ACGME), and therefore lacks board certification. Furthermore, prior studies have shown that there is unique body of DM knowledge not being addressed in emergency medicine (EM) residency or Emergency Medical Services (EMS) fellowship, resulting in fundamental DM topics not being covered amongst graduate medical education (GME) programs most prepared to produce DM physicians. A recently published DM core curriculum addresses this knowledge gap and seeks to promote standardization of DM training. STUDY OBJECTIVE: The objective of this study is to analyze EM residency and EMS fellowship curricula for the inclusion of DM major curriculum topics and subtopics, using the most recently published DM core curriculum as a control. METHODS: Both EM residency and EMS fellowship curricula were analyzed for inclusion of DM curriculum topics and subtopics, using the DM curriculum recommendations published by Wexler, et al as a control. A major curriculum topic was deemed covered if at least one related subtopic was described in the curricula. The included and excluded DM topics and subtopics were analyzed using descriptive statistics. RESULTS: While all the DM major curriculum topics were covered by either EM residency or EMS fellowship, EMS fellowship covered more major curriculum topics (14/15; 93%) than EM residency (12/15; 80%) and EMS fellowship covered more DM curriculum subtopics (58/153; 38%) than EM residency (24/153; 16%). Combined, EM residency and EMS fellowship covered 65 out of 153 (42%) of the DM curriculum subtopics. CONCLUSION: Although this study finds that all the DM major curriculum topics will be covered in EM residency followed by EMS fellowship, over one-half of the subtopics are not covered by either program (16% and 38%, respectively) or both programs combined (42%). Increasingly relevant subtopics, such as climate change, droughts, and flooding, are amongst those not covered by either curriculum. Even amongst the DM topics included in GME curricula, an emphasis on themes such as mass treatment, preparedness, and mitigation is likely under-represented. Accreditation from ACGME for DM fellowship would further promote uniform implementation of the updated core curriculum and ensure optimal training of disaster-ready physicians.

Intranasal insulin attenuates hypoxia-ischemia-induced short-term sensorimotor behavioral disturbances, neuronal apoptosis, and brain damage in neonatal rats.

There is a significant need for additional therapy to improve outcomes for newborns with acute Hypoxic-ischemic (HI) encephalopathy (HIE). New evidence suggests that insulin could be neuroprotective. This study aimed to investigate whether intranasal insulin attenuates HI-induced brain damage and neurobehavioral dysfunction in neonatal rats. Postnatal day 10 (P10), Sprague-Dawley rat pups were randomly divided into Sham + Vehicle, Sham + Insulin, HI + Vehicle, and HI + Insulin groups with equal male-to-female ratios. Pups either had HI by permanent ligation of the right common carotid artery followed by 90 min of hypoxia (8% O2) or sham surgery followed by room air exposure. Immediately after HI or Sham, pups were given fluorescence-tagged insulin (Alex-546-insulin)/vehicle, human insulin (25 µg), or vehicle in each nare under anesthesia. Shortly after administration, widespread Alex-546-insulin-binding cells were detected in the brain, primarily co-localized with neuronal nuclei-positive neurons on double-immunostaining. In the hippocampus, phospho-Akt was activated in a subset of Alex-546-insulin double-labeled cells, suggesting activation of the Akt/PI3K pathway in these neurons. Intranasal insulin (InInsulin) reduced HI-induced sensorimotor behavioral disturbances at P11. InInsulin prevented HI-induced increased Fluoro-Jade C+ degenerated neurons, cleaved caspase 3+ neurons, and volume loss in the ipsilateral brain at P11. There was no sex-specific response to HI or insulin. The findings confirm that intranasal insulin provides neuroprotection against HI brain injury in P10 rats associated with activation of intracellular cell survival signaling. If further pre-clinical research shows long-term benefits, intranasal insulin has the potential to be a promising non-invasive therapy to improve outcomes for newborns with HIE.