Safely Shifting MRIs for Seizure Evaluation to the Outpatient Setting.

BACKGROUND AND OBJECTIVES: When a patient is admitted for seizure-like activity, in addition to obtaining a thorough history and physical exam, the evaluation may include a neurology consultation, EEG, and brain MRI. The cost of an inpatient MRI is significant and only 2% of MRIs yield clinically significant findings. At our institution, there was a 20% increase in patients undergoing inpatient MRI from 2018 to 2020. Our aim: Decrease the percentage of patient encounters receiving inpatient brain MRIs for seizure evaluation from 50% to 40% in 6 months by safely shifting MRIs to the outpatient setting. METHODS: Initially, provider variability in ordering practices of MRIs was analyzed. Stakeholders were gathered and a local guideline was developed to standardize MRI utilization. A process map was created and highlighted barriers to obtaining an outpatient MRI. A new standard process was developed that streamlined and automated processes, and reduced delays and reliance on patients' families. RESULTS: Since implementation of the new clinical guideline, the percentage of inpatient MRIs ordered for patient encounters presenting with seizures and seizure-like episodes decreased from a mean of 50% to 26%. Significant reductions occurred for patients with complex febrile seizures, provoked but afebrile seizures, and unprovoked seizures. The MRI guideline recommendations were followed in 93% of encounters in the final 12 months. None of the patients who underwent outpatient MRI required readmission for acute findings. CONCLUSIONS: In this project, the percentage of inpatient MRIs was safely decreased with the implementation of a clinical guideline and standardized process.

Further refinement of the differentially methylated distant lung-specific FOXF1 enhancer in a neonate with alveolar capillary dysplasia.

Heterozygous SNVs or CNV deletions involving the FOXF1 gene, or its distant enhancer, are causative for 80-90% of cases of alveolar capillary dysplasia with misalignment of pulmonary veins. Recently, we proposed bimodal structure and parental functional dimorphism of the lung-specific FOXF1 enhancer, with Unit 1 having higher activity on the paternal chr16 and Unit 2 on the maternal chr16. Here, we describe a novel unusually sized pathogenic de novo copy-number variant deletion involving a portion of the FOXF1 enhancer on maternal chr16 that implies narrowing Unit 2 to an essential ~ 9-kb segment. Using a restrictase-based assay, we found that this enhancer segment is weakly methylated at ApT adenine, with about twice the frequency of methylation on the maternal versus paternal chr16. Our data provide further insight into the FOXF1 enhancer structure and function.