Barriers and facilitators associated with establishment of emergency department-initiated buprenorphine for opioid use disorder in rural Maine.

PURPOSE: The opioid epidemic in the United States continues to grow, particularly impacting rural communities served by critical access hospitals (CAHs) in Maine. Buprenorphine is an effective medication for the treatment of opioid use disorder (OUD) that can be successfully initiated in the emergency department (ED). However, many EDs have not implemented programs to initiate buprenorphine. This study sought to identify barriers and facilitators to successful implementation of buprenorphine programs inCAH EDs. METHODS: Semistructured interviews were conducted with ED directors of Maine CAHs regarding barriers and facilitators to developing programs for ED-initiated buprenorphine. Seventeen Maine CAH EDs exist and 11 of their directors agreed to participate and completed interviews, which were audio-recorded, transcribed, and analyzed using a thematic approach. RESULTS: Four themes and 11 subthemes were identified, including (1) compelled to act-directors' personal experiences with patients facilitated the development of buprenorphine programs in their EDs; (2) leadership and mentorship-peer mentorship from other CAH ED directors facilitated, and senior hospital administrators facilitated, or created a barrier in some cases; (3) stigma-fear that EDs would be overcrowded by drug-seeking patients was a common barrier; and (4) follow-up-finding appropriate outpatient follow-up for OUD patients created the greatest logistical barrier. DISCUSSION: ED directors' clinical experience with OUD patients, supportive hospital leadership, and peer mentorship facilitated ED-initiated buprenorphine programs in rural Maine CAH EDs. Overcoming stigma, developing community outreach, and appropriate follow-up were the greatest barriers. Future research should focus on enhancing peer mentorship, administrative support, community outreach, and staff education.

High contents of hypotaurine and thiotaurine in hydrothermal-vent gastropods without thiotrophic endosymbionts.

Invertebrates at hydrothermal vents and cold seeps must cope with high levels of toxic H2S. In addition, these and all marine invertebrates must balance internal osmotic pressure with that of the ocean. Cells usually do so with organic osmolytes, primarily free amino acids (e.g., taurine, glycine) and methylamines (e.g., betaine). At vents and seeps, clams, mussels, and vestimentiferans with thiotrophic endosymbionts have high levels of hypotaurine and thiotaurine (a product of hypotaurine and HS-). These serve as osmolytes but their primary function may be to transport and/or detoxify sulfide; indeed, thiotaurine has been proposed to be a marker of thiotrophic symbiosis. To test this, we analyzed Depressigyra globulus snails and Lepetodrilus fucensis limpets from Juan de Fuca Ridge vents (1,530 m). Neither has endosymbionts, though the latter has thiotrophic ectosymbionts. Some specimens were rapidly frozen, while other live ones were kept in laboratory chambers, some with and others without sulfide. Non-vent gastropods from a variety of depths (2-3,000 m) were also collected. Tissues were analyzed for major osmolytes and taurine derivatives. The dominant osmolytes of non-vent snails were betaine in all species, and either taurine in shallow-living species or scyllo-inositol, glycerophosphorylcholine, and other amino acids in deep-sea species. In contrast, the dominant osmolytes were hypotaurine and betaine in D. globulus, and hypotaurine in L. fucensis. Both species had thiotaurine (as well as hypotaurine) at levels much greater than previously reported for vent and seep animals without endosymbionts. The ratio of thio- to thio- plus hypotaurine, a possible indicator of sulfide exposure, decreased in both species when kept in laboratory chambers with low or no sulfide, but stayed at high levels in snails kept with 3-5 mM sulfide. Thus, in some vent animals without endosymbionts, sulfide may be detoxified via conversion of hypotaurine to thiotaurine. The latter may be a marker of high sulfide exposure but not of thiotrophic endosymbionts.