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1.
Pediatr Qual Saf ; 9(3): e738, 2024.
Article in English | MEDLINE | ID: mdl-38868756

ABSTRACT

Introduction: Asthma exacerbations are common presentations to pediatric emergency departments. Standard treatment for moderate-to-severe exacerbations includes administration of oral corticosteroids concurrently with bronchodilators. Early administration of corticosteroids has been shown to decrease emergency department length of stay (LOS) and hospitalizations. Our SMART aim was to reduce the time from arrival to oral corticosteroids (dexamethasone) administration in pediatric patients ≥2 years of age with an initial Pediatric Asthma Severity Score >6 from 60 to 30 minutes within 6 months. Methods: We used the model for improvement with collaboration between ED physicians, nursing, pharmacy, and respiratory therapists. Interventions included nursing education, dosage rounding in the electronic medical record, supplying triage with 1-mg tablets and a pill crusher, updates to an asthma nursing order set and pertinent chief complaints triggering nurses to document a Pediatric Asthma Severity Score in the electronic medical record and use the order set. Our primary outcome measure was the time from arrival to dexamethasone administration. Secondary outcome measures included ED LOS for discharged patients and admission rate. We used statistical process control to analyze changes in measures over time. Results: From October 2021 to March 2022, the average time for dexamethasone administration decreased from 59 to 38 minutes. ED LOS for discharged asthma exacerbation patients rose with overall ED LOS for all patients during the study period. There was no change in the admission rate. Conclusions: Using quality improvement methodology, we successfully decreased the time from ED arrival to administration of dexamethasone in asthma exacerbation patients from 59 to 38 minutes over 10 months.

2.
J Emerg Med ; 54(5): 651-655, 2018 05.
Article in English | MEDLINE | ID: mdl-29602529

ABSTRACT

BACKGROUND: Syphilis is a sexually transmitted infection that was nearly eradicated in 2001 but is now making a resurgence. It has a wide range of clinical manifestations depending on disease stage. Neurosyphilis is an infrequently seen infectious disease with central nervous system involvement that can occur in either early- or late-stage syphilis. The diagnosis of neurosyphilis is challenging, primarily because Treponema pallidum, the infecting organism, cannot be cultured in vitro. This article describes a patient with neurosyphilis and reviews the epidemiology and clinical manifestations, diagnostics, and treatment of neurosyphilis. CASE REPORT: In compliance with the request of the Privacy Board of our institution, the numerical age of this patient has been omitted. A sexually active teenage girl who was treated for primary syphilis 2 years earlier presented to a tertiary children's hospital with paresthesia and weakness of her right leg, left arm, and neck. Magnetic resonance imaging revealed cervical intramedullary cord edema consistent with transverse myelitis. Serum studies showed positive syphilis enzyme immunoassay, T. pallidum particle agglutination assay, and fluorescent treponemal antibody absorption. A serum rapid plasma reagin test was negative. A lumbar puncture was performed with normal cell count and protein. A cerebrospinal fluid Venereal Disease Research Laboratory test was negative. She was diagnosed with neurosyphilis and treated with intravenous steroids and penicillin G, with near complete resolution of symptoms. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The Centers for Disease Control and prevention has noted a steady rise of the incidence of syphilis since 2002. Emergency physicians should be familiar with the spectrum of the clinical manifestations of syphilis, challenges in diagnostics, and appropriate treatment course.


Subject(s)
Myelitis, Transverse/etiology , Neurosyphilis/complications , Neurosyphilis/diagnosis , Adolescent , Adolescent Behavior/psychology , Female , Humans , Muscle Weakness/etiology , Paresthesia/etiology , Sexually Transmitted Diseases/complications , Treponema pallidum/pathogenicity
3.
Clin Pediatr (Phila) ; 52(8): 707-9, 2013 Aug.
Article in English | MEDLINE | ID: mdl-23539688

ABSTRACT

We present a 10-month-old baby girl who developed a neck abscess from the penetration of neck skin by 2 goose feathers that leaked from a down comforter. We review the risks of down and feather bedding and discuss consumer recommendations for parents and pediatricians.


Subject(s)
Abscess/etiology , Bedding and Linens/adverse effects , Feathers , Parents/education , Skin Diseases/etiology , Abscess/physiopathology , Abscess/therapy , Animals , Anti-Bacterial Agents/therapeutic use , Consumer Product Safety , Drainage/methods , Female , Geese , Guidelines as Topic , Humans , Infant , Neck , Risk Assessment , Skin Diseases/physiopathology , Skin Diseases/therapy
4.
Mol Endocrinol ; 21(12): 3071-86, 2007 Dec.
Article in English | MEDLINE | ID: mdl-17823303

ABSTRACT

GnRH and activin independently and synergistically activate transcription of the FSH beta-subunit gene, the subunit that provides specificity and is the limiting factor in the synthesis of the mature hormone. This synergistic interaction, as determined by two-way ANOVA, is specific for FSHbeta and may, therefore, contribute to differential expression of the two gonadotropin hormones, which is critical for the reproductive cycle. We find that the cross-talk between the GnRH and activin signaling pathways occurs at the level of p38 MAPK, because the synergy is dependent on p38 MAPK activity, which is activated by GnRH, and activin cotreatment augments p38 activation by GnRH. Both the Smad and activator protein-1 binding sites on the FSHbeta promoter are necessary and sufficient for synergy. After cotreatment, Smad 3 proteins are more highly phosphorylated on the activin-receptor signaling-dependent residues on the C terminus than with activin treatment alone, and c-Fos is more highly expressed than with GnRH treatment alone. Inhibition of p38 by either of two different inhibitors or a dominant-negative p38 kinase abrogates synergy on FSHbeta expression, reduces c-Fos induction by GnRH, and prevents the further increase in c-Fos levels that occurs with cotreatment. Additionally, p38 is necessary for maximal Smad 3 C-terminal phosphorylation by activin treatment alone and for the further increase caused by cotreatment. Thus, p38 is the pivotal signaling molecule that integrates GnRH and activin interaction on the FSHbeta promoter through higher induction of c-Fos and elevated Smad phosphorylation.


Subject(s)
Activins/pharmacology , Follicle Stimulating Hormone, beta Subunit/metabolism , Gonadotropin-Releasing Hormone/pharmacology , Proto-Oncogene Proteins c-fos/metabolism , Smad Proteins/metabolism , p38 Mitogen-Activated Protein Kinases/metabolism , Activins/metabolism , Animals , Binding Sites , Cell Line , Follicle Stimulating Hormone, beta Subunit/genetics , Gene Expression Regulation/drug effects , Mice , Molecular Sequence Data , Phosphorylation/drug effects , Promoter Regions, Genetic/genetics , Protein Binding , Protein Isoforms/metabolism , Signal Transduction/drug effects , Smad Proteins/genetics , Transcription Factor AP-1/metabolism
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