Search

BackgroundIn March of 2020, the World Health Organization declared coronavirus disease 2019 (COVID-19)-a disease caused by a novel coronavirus-a pandemic, and it continued to spread rapidly in the community. Our institution implemented an emergency medicine telehealth system that sought to expedite care of stable patients, decrease provider exposure to COVID-19, decrease overall usage rate of personal protective equipment, and provide a platform so that infected or quarantined physicians could continue to work. This effort was among the first to use telehealth to practice emergency medicine in the setting of a pandemic in the United States.DiscussionOutside the main emergency departments at each of 2 sites of our academic institution, disaster tents were erected with patient care equipment and medications, as well as technology to allow for telehealth visits. The triage system was modified to appropriately select low-risk patients with symptoms suggestive of COVID-19 who could be seen in these disaster tents. Despite some issues that needed to be addressed, such as provider discomfort, limited medication availability, and connectivity problems, the model was successful overall.ConclusionsOther emergency departments might find this proof of concept article useful. Telehealth will likely be used more broadly in the future, including emergency care. It is imperative that the health care system continues to adapt to respond appropriately to challenges such as pandemics.

Background: A host defense function for Alkaline phosphatases (ALPs) is suggested by the contribution of intestinal ALP to detoxifying bacterial lipopolysaccharide (endotoxin) in animal models in vivo and the elevation of ALP activity following treatment of human cells with inflammatory stimuli in vitro. However the activity of ALP in human plasma (primarily tissue-nonspecific ALP; TNAP) on lipopolysaccharide and other microbial products has not been assessed, nor has its expression been studied in preterm newborns, a vulnerable population at high risk of sepsis. In this context, the aim of our study was to characterize the activity of TNAP on Toll-like receptor (TLR) agonists and assess the concentrations of plasma ALP during late-onset sepsis in preterm newborns. Methods: Recombinant human TNAP was incubated with microbial products and phosphate release was measured by malachite green assay. Plasma ALP activity was measured serially in a cohort of preterm (N = 129) infants at high risk of late-onset sepsis (LOS). Results: TNAP dephosphorylates poly-inosine:cytosine (Toll-like receptor (TLR) 3 agonist) and LPS from Klebsiella pneumoniae and Salmonella minnesota (TLR4 agonists). Plasma ALP significantly increased postnatally over the first 4 weeks of life in preterm and term newborns. Bacteremic LOS in preterm infants (gestational age ≤ 30 weeks) was associated with significantly elevated plasma ALP at 4 weeks postnatal age. Conclusions: TNAP, the main circulating isozyme of ALP, de-phosphorylates TLR agonists, demonstrates a post-natal age dependent increase in preterm and term plasma across the first 4 weeks of life, and is elevated in association with preterm LOS.