Treatment, Management, and Otolaryngology Consultation for Epistaxis in the Emergency Room: An Institutional Experience.

BACKGROUND: Epistaxis is a common reason for emergency department (ED) visits, accounting for approximately 1 of every 200 ED visits in the United States annually and up to one-third of all otolaryngology (ENT)-related ED encounters. OBJECTIVES: To detail reasons for ENT consultation for epistaxis in the ED, understand how consultation impacts patient care, assess follow-up patterns after emergency care, and study patient care after transfer or referral into the ED. METHODS: Retrospective chart review of 592 adult patients with epistaxis managed in a tertiary care ED setting between 2017 and 2018. Patients with known follow-up, ENT consult in the ED, or admission were included, while patients with trauma, recent head and neck surgery, or abnormal anatomy were excluded. RESULTS: The most common reasons for ENT consultation for epistaxis were for advanced management, referral to the ED from an outside facility or provider, and recent head and neck surgery. In total, 48.2% of patients treated for epistaxis in the ED received an ENT consultation. ENT consultation was associated with a higher likelihood of receiving absorbable or nonabsorbable packing (92.4% vs 36.1%). In total, 40.4% of patients referred into the ED from an outside facility or provider had no change in their management after receiving an ENT consult. Patients referred to the ED and White patients were significantly more likely to receive an ENT consult. Secondary analyses revealed that more White patients had an established outpatient ENT provider than patients of other races. On multivariate analysis, patients who received an ENT consult spent 75.2 min longer in the ED. CONCLUSION: The high percentage of patients referred or transferred to the ED for epistaxis management with no change in interventions after ENT consultation indicates a continued need to develop more precise clinical care pathways. Additionally, there may be gaps between White and non-White patients in access to ENT care.

SLC26A4-linked CEVA haplotype correlates with phenotype in patients with enlargement of the vestibular aqueduct.

BACKGROUND: Recessive mutations of coding regions and splice sites of the SLC26A4 gene cause hearing loss with enlargement of the vestibular aqueduct (EVA). Some patients also have a thyroid iodination defect that can lead to multinodular goiter as part of Pendred syndrome. A haplotype of variants upstream of SLC26A4, called CEVA, acts as a pathogenic recessive allele in trans to mutations affecting the coding regions or splice sites of SLC26A4. Our first hypothesis is that CEVA, acting as a pathogenic recessive allele, is correlated with a less severe phenotype than mutations affecting the coding regions and splice sites of SLC26A4. Our second hypothesis is that CEVA acts as a modifier of the phenotype in patients with EVA caused by mutations affecting the coding regions or splice sites of both alleles of SLC26A4 or EVA caused by other factors. METHODS: This was a prospective cohort study of 114 individuals and 202 ears with EVA. To test our first hypothesis, we compared the thyroid and auditory phenotypes of subjects with mutations affecting coding regions of both alleles of SLC26A4 with those of subjects carrying CEVA in trans to mutations affecting the coding regions. To test our second hypothesis, we compared the phenotypes associated with the presence versus absence of CEVA among subjects with no coding region mutations, as well as among subjects with mutations affecting coding regions of both alleles. RESULTS: Subjects carrying CEVA in trans to a mutation of SLC26A4 have a normal thyroid phenotype and less severe hearing loss in comparison to individuals with mutations affecting coding regions of both alleles of SLC26A4. In subjects with no mutant alleles of SLC26A4, hearing loss was more severe in subjects who carry the CEVA haplotype in comparison to non-carriers. There was no correlation of CEVA with the phenotype of subjects with mutations affecting coding regions of both alleles. CONCLUSIONS: CEVA, acting as a likely pathogenic recessive allele, is associated with a less severe phenotype than alleles with a mutation affecting the coding regions or splice sites of SLC26A4. CEVA may act as a genetic modifier in patients with EVA caused by other factors.