ABSTRACT
BACKGROUND: Helping Babies Breathe (HBB) is a neonatal resuscitation curriculum that teaches life-saving interventions utilized in the first minutes after birth, reducing morbidity and mortality. Traditionally, it requires in-person facilitators for didactic and hands-on training. OBJECTIVES: The aim of this study was to offer HBB to nurses and nursing students in Guatemala, with the lead facilitator presenting concepts via telehealth and in-person facilitators providing hands-on demonstration. METHODS: Learners completed pre- and post-tests that included the standard HBB knowledge check, as well as an assessment of the course teaching model. Learners also completed the standard Objective Structured Clinical Evaluations (OSCEs). RESULTS: Eighteen learners were included in the analysis. All but one learner (94%) passed the course, and the average percent improvement from the pre- to post-test was 12%. All learners achieved passing scores on the OSCEs. Learners responded positively to questions regarding the technology, connection with the instructor, and ability to ask questions. Ninety-four percent of the learners agreed with the statement "this lecture was as good via telehealth as in person." A cost analysis demonstrated approximately USD 3,979.00 in savings using telehealth compared to a standard in-person course. CONCLUSIONS: The telehealth model was successful in delivering course material to the learners and was well received. This model represents a cost-effective way to improve access to HBB. This study may not be generalizable to other populations, and the ability to use telehealth requires reliable internet connectivity, which may not be available in all settings. Further study and expansion of this pilot are needed to assess success in other settings.
Subject(s)
Internship and Residency/standards , Primary Health Care , Quality Improvement , Humans , United StatesABSTRACT
BACKGROUND: We have previously demonstrated that CD133 and CD39 are expressed by hematopoietic stem cells (HSC), which are mobilized after liver injury and target sites of injury, limit vascular inflammation, and boost hepatic regeneration. Plasma microparticles (MP) expressing CD39 can block endothelial activation. Here, we tested whether CD133 MP might be shed in a CD39-dependent manner in a model of liver injury and could potentially serve as biomarkers of liver failure in the clinic. METHODS: Wild-type and Cd39-null mice were subjected to acetaminophen-induced liver injury. Mice were sacrificed and plasma MP were isolated by ultracentrifugation. HSC and CD133 MP levels were analyzed by fluorescence-activated cell sorting. Patients were enrolled with acute (n=5) and acute on chronic (n=5) liver injury with matched controls (n=7). Blood was collected at admission and plasma CD133 and CD39 MP subsets were analyzed by fluorescence-activated cell sorting. RESULTS: HSC and CD133 MP levels were significantly increased only in the plasma of wild-type mice with acetaminophen hepatotoxicity (P<0.05). No increases in CD133 MP were noted in Cd39-null mice. Plasma MP increases were observed in patients with liver injury. These MP were characterized by significantly higher levels of CD39 (P<0.05). CONCLUSIONS: HSC and plasma CD133 MP levels increase in a CD39-dependent manner during experimental acute liver injury. Increased levels of CD39 MP are differentially noted in patients with liver injury. Further research is needed to determine whether MP fluxes are secondary to pathophysiologic insults to the liver or might reflect compensatory responses.
