Compliance with a COPD bundle of care in an Australian emergency department: A cohort study.

INTRODUCTION: Bundles of care are gaining popularity for treating acute severe illness. OBJECTIVE: To describe compliance with bundle of care elements (individually and as a "bundle") for patients treated for chronic obstructive pulmonary disease (COPD) exacerbations in the emergency department (ED). METHODS: Retrospective observational study of patients presenting in the 2014 calendar year with an ED diagnosis of COPD. The primary outcomes of interest were compliance with key bundle of care elements (individually and as a "bundle"). Analysis is descriptive. RESULTS: 381 patients were studied. Median age was 71 (IQR 64-80), 60% were male and 77% arrived by ambulance. Median duration of symptoms was 3 days (IQR 2-6 days). Compliance with the bundle elements was 90% for administration of controlled oxygen therapy (if oxygen given), 87% for administration of inhaled bronchodilators, 79% for administration of systemic corticosteroids, 75% of administration of antibiotics if evidence of infection, 77% for taking of a blood gas in non-mild disease, 98% for taking of a chest X-ray, and 74% for administration of NIV if pH <7.3. Compliance with all appropriate elements of the defined bundle of care was 49%. There was no difference in mean length of stay for admitted patients (P = .44), in-hospital mortality (P = 1.00) or re-admission within 30 days (P = .72) by bundle compliance. CONCLUSION: Compliance with individual assessment and treatment recommendations was generally high; however, compliance with the overall recommended bundle was only 49%. This indicates that there is an opportunity to improve care in these patients.

A Case of Beare-Stevenson Syndrome with Unusual Manifestations.

BACKGROUND: Beare-Stevenson syndrome (BSS) is an extremely rare genetic disorder, with fewer than 25 cases reported worldwide. This autosomal dominant syndrome has been linked to two mutations in the fibroblast growth factor receptor 2 gene (FGFR2), Tyr375Cys and Ser372Cys, both causing amino acid changes. CASE REPORT: BSS is characterized by a range of morphological features, some more classically associated than others, of which craniosynostosis has been almost uniformly present. Other common features include cutis gyrata, acanthosis nigricans, ear and eye defects, skin/mucosal tissue tags, prominent umbilical stump, and anogenital anomalies. This account reports what we believe to be the 25th case of BSS, and exhibits a constellation of the characteristic features similar to those previously described, including the presence of cutis gyrata, proptosis, a bifid scrotum, and hypospadias. However, craniosynostosis was not detected prenatally by ultrasound or at birth. Prenatal ultrasound may detect some dysmorphic features of BSS. Many of these features have also been associated with other genetic disorders with overlapping phenotypes. Our case presented with the unusual features of a natal tooth and absence of craniosynostosis at birth. At birth, a diagnosis of BSS was suspected based on clinical features despite the absence of craniosynostosis. This was later confirmed with the use of molecular analysis, revealing a Tyr375Cys mutation of exon 9 of the FGFR2 gene. CONCLUSIONS: We suggest that a normal antenatal ultrasound scan and the absence of craniosynostosis at birth should not preclude further workup for BSS if this possibility is clinically suspected.

Antiinflammatory treatment ameliorates HPA stress axis dysfunction in a mouse model of stress sensitivity.

Dysregulated stress responsivity is a hallmark of neuropsychiatric disease. The regulation of stress activation and recovery involves tight coordination between neuronal and glial networks. At a certain threshold of sensitivity, stress exposure can evoke a neuroimmune response. Astrocytes are potential mediators of these effects because they are able to respond to neuroimmune effector molecules and regulate neuronal activity. Mice deficient in corticotropin-releasing factor receptor-2 display increased stress sensitivity and are therefore a useful model in which to examine the intersection of neuroimmune activation and stress pathway dysregulation. We hypothesized that a component of elevated stress reactivity may involve an engagement of neuroimmune effectors, including astrocytes. Therefore, we hypothesized that this phenotype may be rescued by concomitant nonsteroidal antiinflammatory drug (NSAID) treatment. To examine this, mice exposed to chronic stress were treated with NSAID in their drinking water, and changes in hypothalamic-pituitary-adrenal stress axis function were examined. As a correlate of altered astrocyte function, levels of glial fibrillary acidic protein were measured. Supportive of our hypothesis, NSAID treatment rescued the hypothalamic-pituitary-adrenal stress axis dysfunction in stress-sensitive corticotropin-releasing factor receptor-2(-/-) mice and also reversed the stress-induced increase in glial fibrillary acidic protein in stress-regulating brain regions including the paraventricular nucleus of the hypothalamus, ventral hippocampus, and prefrontal cortex. These findings support the local involvement of astrocytes in the exacerbation of stress pathway dysregulation. The specificity of these effects in a stress-sensitive genotype highlights the importance of utilizing a model of stress dysregulation in the examination of factors that may translate to neuropsychiatric disease.