Rapid Assessment, Planning, Investigations and Discharge: Piloting the introduction of a senior doctor at triage model in an Australian paediatric emergency department.

OBJECTIVE: We implemented a senior doctor at triage (SDT) pilot programme at The Royal Children's Hospital, Melbourne. We examined the impact on ED length of stay, seen on time and fail to wait (FTW) rates. METHODS: A SDT model was piloted on Monday and Tuesday afternoons (pilot period) for 10 weeks, and compared with equivalent shifts for the preceding 10 weeks (pre-pilot period). We determined the differences between the proportions of patients seen on time, length of stay in the ED of less than 4 h and FTW rate, as well as the medians of time to clinician and length of stay in ED. RESULTS: A total of 2736 patients presented in the pilot period, and 2889 in the pre-pilot. The percentage of patients who were seen on time improved from 52.3% to 68.7% (absolute difference 16.4%, 95% confidence interval [CI] 13.6-19.2%, P < 0.001), the percentage of patients who had an ED length of stay of <4 h improved from 58.2% to 72.0% (absolute difference 13.8%, 95% CI 11.1-16.5%, P < 0.001) and the FTW rate reduced from 12.5% to 7.1% (absolute difference 5.4%, 95% CI 3.8-7.0%, P < 0.001) when the SDT model was operational. CONCLUSION: Implementation of a SDT model in a tertiary paediatric ED resulted in an increased proportion of patients being seen on time, having shorter length of stays in the ED and reduced the number of patients who FTW. Further studies are required to determine whether these improvements are sustained over time.

HHIPL1, a Gene at the 14q32 Coronary Artery Disease Locus, Positively Regulates Hedgehog Signaling and Promotes Atherosclerosis.

BACKGROUND: Genome-wide association studies have identified chromosome 14q32 as a locus for coronary artery disease. The disease-associated variants fall in a hitherto uncharacterized gene called HHIPL1 (hedgehog interacting protein-like 1), which encodes a sequence homolog of an antagonist of hedgehog signaling. The function of HHIPL1 and its role in atherosclerosis are unknown. METHODS: HHIPL1 cellular localization, interaction with sonic hedgehog (SHH), and influence on hedgehog signaling were tested. HHIPL1 expression was measured in coronary artery disease-relevant human cells, and protein localization was assessed in wild-type and Apoe-/- (apolipoprotein E deficient) mice. Human aortic smooth muscle cell phenotypes and hedgehog signaling were investigated after gene knockdown. Hhipl1-/- mice were generated and aortic smooth muscle cells collected for phenotypic analysis and assessment of hedgehog signaling activity. Hhipl1-/- mice were bred onto both the Apoe-/- and Ldlr-/- (low-density lipoprotein receptor deficient) knockout strains, and the extent of atherosclerosis was quantified after 12 weeks of high-fat diet. Cellular composition and collagen content of aortic plaques were assessed by immunohistochemistry. RESULTS: In vitro analyses revealed that HHIPL1 is a secreted protein that interacts with SHH and increases hedgehog signaling activity. HHIPL1 expression was detected in human smooth muscle cells and in smooth muscle within atherosclerotic plaques of Apoe-/- mice. The expression of Hhipl1 increased with disease progression in aortic roots of Apoe-/- mice. Proliferation and migration were reduced in Hhipl1 knockout mouse and HHIPL1 knockdown aortic smooth muscle cells, and hedgehog signaling was decreased in HHIPL1-deficient cells. Hhipl1 knockout caused a reduction of >50% in atherosclerosis burden on both Apoe-/- and Ldlr-/- knockout backgrounds, and lesions were characterized by reduced smooth muscle cell content. CONCLUSIONS: HHIPL1 is a secreted proatherogenic protein that enhances hedgehog signaling and regulates smooth muscle cell proliferation and migration. Inhibition of HHIPL1 protein function might offer a novel therapeutic strategy for coronary artery disease.

Management of retrieval service patients within a paediatric emergency department.

OBJECTIVE: The Victorian Paediatric Emergency Transport Service (PETS) transports critically unwell children to tertiary paediatric hospitals. Children not directly admitted to ICU go to a tertiary ED. These patients might require prolonged and high-level care. In light of the National Emergency Access Target, we describe this cohort, clinical care needs and process measures. METHODS: A retrospective chart review of patients retrieved by PETS to the Royal Children's Hospital (Melbourne, Australia) ED in 2012. Demographics, illness parameters and process measures were extracted. The ED length of stay (LOS) and time to ward suitability (time at which physiological parameters stabilised and high acuity treatments ceased) were related to patient and illness characteristics. Data are presented descriptively and analysed using spss. RESULTS: In 2012, 120 patients were transported to the ED. Conditions included lower respiratory (44), neurological (28), upper respiratory (16) and trauma (14). The median ED LOS was 4.8 h (interquartile range 2.9, 7.7). On arrival, 73 (60.8%) were ward-suitable, but 51 (43%) had LOS less than 4 h. Twenty-five (20.8%) patients stayed longer than 8 h. Administrative delay (principally bed block) is responsible for the bulk of the LOS; however, 25 (20.8%) had markedly abnormal vital signs after 4 h of ED care, mainly patients with lower respiratory tract disease. CONCLUSION: Most patients retrieved to the ED ultimately go to a ward rather than ICU and most have an ED stay in excess of National Emergency Access Target. Several retrieval associated care issues, such as timely and appropriate ward disposition, can be addressed by administrative changes.