Training to be a cleft surgeon in the UK

UK cleft services are centralised and involve working in a multidisciplinary team, offering patients a high quality of care and surgeons a potentially enormously rewarding career. Trainees wishing to specialise in cleft surgery should endeavour to gain targetted experience in cleft lip and palate from early in their surgical career as this will stand them in good stead for the cleft training fellowship applications towards the end of higher surgical training.

Diffusion tensor cardiovascular magnetic resonance detects altered myocardial microstructure in patients with acute st-elevation myocardial infarction

Background Diffusion Tensor Cardiovascular Magnetic Resonance (DT-CMR) can quantify metrics of tissue integrity (mean diffusivity [MD] and fractional anisotropy [FA]) and changes in laminar microstructures (sheetlets), which reorientate from more wall-parallel in diastole (DIA) towards wall-perpendicular in systole (SYS) as the myocardium thickens, quantified by E2 angle [E2A]. Microstructural changes after STEMI may provide new insights into adverse LV remodelling and risk stratification. Methods In vivo DT-CMR was performed 3–5 days after PPCI for first presentation STEMI (N=19, mean age 57±9, 79% male). DT-CMR was acquired in 2 short-axes (SYS & DIA) using a STEAM-EPI sequence. 12 segment analysis of MD, FA, E2A and E2A mobility (ΔE2A = E2ASYS − E2ADIA) was performed. Infarct (INF) segments were defined as >25% LGE, adjacent (ADJ, located contiguous to INF) and remote (REM, all other segments). Wilcoxon signed rank tests were used with threshold P<0.017 (Bonferroni corrected). Results See Table. MD in both SYS and DIA was significantly higher in INF and ADJ regions compared to REM. FA in both SYS and DIA was lower in the INF and ADJ compared to REM. E2ADIA was higher in INF, indicating a more wall-perpendicular orientation of sheetlets, compared to ADJ and REM zones. E2ASYS in INF was significantly reduced, indicating a more wall-parallel orientation of sheetlets, compared to ADJ and REM regions, resulting in significantly reduced sheetlet mobility (ΔE2A). Conclusions Microstructural changes can be detected after acute STEMI by in vivo DT-CMR. Zonal changes in MD and FA may suggest loss of barriers to water diffusion and altered cardiomyocyte organisation, respectively. We provide the first report of reduced sheetlet mobility after acute STEMI in INF. Ongoing work is evaluating the mechanisms and prognostic importance of altered sheetlet mobility after STEMI. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation Clinical Research Training Fellowship

Effect of delays in concordant antibiotic treatment on mortality in patients with hospital-acquired Acinetobacter spp. bacteremia in Thailand: a 13-year retrospective cohort

Background: A quantitative understanding of the impact of delays to concordant antibiotic treatment on patient mortality is important for designing hospital antibiotic policies. Acinetobacter spp are among the most prevalent pathogens causing multidrug-resistant hospital-acquired infections in developing countries. We aimed to determine the causal effect of delays in concordant antibiotic treatment on 30-day survival of patients with hospital-acquired Acinetobacter spp bacteremia in a resource-limited setting. Methods: We included patients with Acinetobacter spp–related hospital-acquired bacteremia (HAB) in a hospital in Thailand over a 13-year period. We classified patients into 4 groups: those with no delays to concordant antibiotic treatment; those with a 1-day delay; those with 2-day delays; and those with >2 days of delay. We adopted an analytical approach that aimed to emulate a randomized controlled trial and compared the expected potential outcomes of patients between the exposure groups using a marginal structural model with inverse-probability weightings to adjust for confounders and immortal time bias. Results: Between January 2003 and December 2015, 1,203 patients had HAB with Acinetobacter spp., of which 682 patients (56.7%) had ≥1 days of delay in concordant antibiotic treatment. These delays were associated with an absolute increase in 30-day mortality of 6.6% (95% CI 0.2%-13.0%), from 33.8% to 40.4%. Among the 1,203 patients, 521 had no delays to concordant antibiotic treatment (i.e. concordant therapy on the day of blood collection), 224 patients had a 1-day delay, 119 had a 2-day delay, and 339 had a delay of ≥3 days. The crude 30-day mortality was substantially lower in patients with ≥3 days of delay in concordant treatment compared to those with 1 to 2-days of delays. After adjusting for measured confounders and immortal time bias, the expected probability of dying in the hospital within 30-days of blood collection if patient had no delays in concordant therapy was 39.7% (95% CI: 32.3-47.2%), for a 1-day delay it was 42.7% (95% CI: 29.8-55.7%), for a 2-day delay it was 51.0% (95% CI: 38.9-63.2%), and for a ≥3 days was 40.9% (36.0-45.7%).Conclusions: Delays to concordant antibiotic therapy are linked to increased mortality among patients with HAB due to Acinetobacter spp. Accounting for confounders and immortal time bias is necessary when attempting to estimate causal effects of delayed concordant treatment and, in this case, it helped resolve paradoxical results in crude data.Funding: The Mahidol Oxford Tropical Medicine Research Unit (MORU) is funded by the Wellcome Trust [grant number 106698/Z14/Z]. CL is funded by a Wellcome Trust Research Training Fellowship [grant number 206736/Z/17/Z]. MY is supported by a Singapore National Medical Research Council Research Fellowship [grant number NMRC/Fellowship/0051/2017]. BSC is funded by the UK Medical Research Council and Department for International Development [grant number MR/K006924/1]. DL is funded by a Wellcome Trust Intermediate Training Fellowship [grant number 101103]. The funder has no role in the design and conduct of the study, data collection, or in the analysis and interpretation of the data.Disclosures: None

Effect of delays in concordant antibiotic treatment on mortality in patients with hospital-acquired Acinetobacter spp. bacteremia: a 13-year retrospective cohort

BackgroundTherapeutic options for multidrug-resistant Acinetobacter spp. are limited, and resistance to last resort antibiotics in hospitals is increasing globally. Quantifying the impact of delays in concordant antibiotic treatment on patient mortality is important for designing hospital antibiotic policies.MethodsWe included patients with Acinetobacter spp. hospital-acquired bacteremia (HAB) in a hospital in Thailand over a 13-year period. For each day of stay following the first positive blood culture we considered antibiotic treatment to be concordant if the isolated organism was susceptible to at least one antibiotic given. We used marginal structural models with inverse-probability weightings to determine the association between delays in concordant treatment and 30-day mortality.ResultsBetween January 2003 and December 2015, 1,203 patients had HAB with Acinetobacter spp., of which 682 patients (56.7%) had one or more days of delay in concordant treatment. These delays were associated with an absolute increase in 30-day mortality of 6.6% (95% CI 0.2%-13.0%), from 33.8% to 40.4%. Crude 30-day mortality was substantially lower in patients with three or more days of delays in concordant treatment compared to those with one to two days of delays. Accounting for confounders and immortal time bias resolved this paradox, and showed similar 30-day mortality for one, two and three or more days of delays.ConclusionsDelays in concordant antibiotic treatment were associated with a 6.6% absolute increase in mortality among patients with hospital-acquired Acinetobacter spp. bacteremia. If this association is causal, switching fifteen patients from discordant to concordant initial treatment would be expected to prevent one death.FundingThe Mahidol Oxford Tropical Medicine Research Unit (MORU) is funded by the Wellcome Trust [grant number 106698/Z14/Z]. CL is funded by a Wellcome Trust Research Training Fellowship [grant number 206736/Z/17/Z]. MY is supported by a Singapore National Medical Research Council Research Fellowship [grant number NMRC/Fellowship/0051/2017]. BSC is funded by the UK Medical Research Council and Department for International Development [grant number MR/K006924/1]. DL is funded by a Wellcome Trust Intermediate Training Fellowship [grant number 101103]. The funder has no role in the design and conduct of the study, data collection, or in the analysis and interpretation of the data.