Cellulitis in the Emergency Department: A prospective cohort study with patient-centred follow-up.

OBJECTIVE: There is substantial practice variation in the management of cellulitis with limited prospective studies describing the course of cellulitis after diagnosis. We aimed to describe the demographics, clinical features (erythema, warmth, swelling and pain), patient-reported disease trajectory and medium-term follow-up for ED patients with cellulitis. METHODS: Prospective observational cohort study of adults diagnosed with cellulitis in two EDs in Southeast Queensland, Australia. Patients with (peri)orbital cellulitis and abscess were excluded. Data were obtained from a baseline questionnaire, electronic medical records and follow-up questionnaires at 3, 7 and 14 days. Clinician adjudication of day 14 cellulitis cure was compared to patient assessment. Descriptive analyses were conducted. RESULTS: Three-hundred patients (mean age 50 years, SD 19.9) with cellulitis were enrolled, predominantly affecting the lower limb (75%). Cellulitis features showed greatest improvement between enrolment and day 3. Clinical improvement continued gradually at days 7 and 14 with persistent skin erythema (41%) and swelling (37%) at day 14. Skin warmth was the feature most likely to be resolved at each time point. There was a discrepancy in clinician and patient assessment of cellulitis cure at day 14 (85.8% vs. 52.8% cured). CONCLUSIONS: A clinical response of cellulitis features can be expected at day 3 with ongoing slower improvement over time. Over one third of patients had erythema or swelling at day 14. Patients are less likely than clinicians to deem their cellulitis cured at day 14. Future research should include parallel patient and clinician evaluation of cellulitis to help develop clearer definitions of treatment failure and cure.

Wearing hats and blending boundaries: harmonising professional identities for clinician simulation educators.

Many clinicians working in healthcare simulation struggle with competing dual identities of clinician and educator, whilst those who harmonise these identities are observed to be highly effective teachers and clinicians. Professional identity formation (PIF) theories offer a conceptual framework for considering this dilemma. However, many clinician simulation educators lack practical guidance for translating these theories and are unable to develop or align their dual identities.An unusual experience involving the first author's suspension of disbelief as a simulation facilitator sparked a novel reflection on his dual identity as a clinician and as a simulation educator. He re-framed his clinician and simulation 'hats' as cooperative and fluid rather than competing and compartmentalised. He recognised that these dual identities could flow between clinical and simulation environments through leaky 'blended boundaries' rather than being restricted by environmental demarcations.This personal story is shared and reflected upon to offer a practical 'hats and boundaries' model. Experimenting with the model in both clinical and simulation workplaces presents opportunities for PIF and alignment of dual identities. The model may help other clinician simulation educators navigate the complexities of merging their dual identities.

Reversible changes in pancreatic islet structure and function produced by elevated blood glucose.

Diabetes is characterized by hyperglycaemia due to impaired insulin secretion and aberrant glucagon secretion resulting from changes in pancreatic islet cell function and/or mass. The extent to which hyperglycaemia per se underlies these alterations remains poorly understood. Here we show that ß-cell-specific expression of a human activating KATP channel mutation in adult mice leads to rapid diabetes and marked alterations in islet morphology, ultrastructure and gene expression. Chronic hyperglycaemia is associated with a dramatic reduction in insulin-positive cells and an increase in glucagon-positive cells in islets, without alterations in cell turnover. Furthermore, some ß-cells begin expressing glucagon, whilst retaining many ß-cell characteristics. Hyperglycaemia, rather than KATP channel activation, underlies these changes, as they are prevented by insulin therapy and fully reversed by sulphonylureas. Our data suggest that many changes in islet structure and function associated with diabetes are attributable to hyperglycaemia alone and are reversed when blood glucose is normalized.