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We describe the work of a multidisciplinary inpatient diabetes care team in a 400 bed district general hospital over a four‐year period. Also included are some observations on a positive contribution to reduced length of stay for people with diabetes in hospital, and low incidences of prescription and management errors in the first National Diabetes Inpatient Audit in 2009.Specifically between 2005 and 2007 the average length of stay in days for all patients whose diagnosis included diabetes fell from 9.39 to 3.76 days despite the total number of patients increasing from 507 to 633 over the same quarter each year. The inpatient team provided almost 1000 visits to patients with diabetes in the first six months of each year 2008 and 2009, and at the first National Diabetes Inpatient Audit had only 5% prescription errors and 3% management errors (versus 19% and 14% respectively nationally) with 100% appropriate blood glucose testing.We suggest that a dedicated inpatient diabetes care team raises the quality of care for patients and enhances patient and professional education; we also suggest that audit standards should be developed for inpatient diabetes care and assessed in future national audits. Copyright © 2011 John Wiley & Sons.

Diabetes mellitus and, in particular, the hyperosmolarity associated with the hyperosmolar hyperglycaemic state (HHS) is associated with an increased risk of thrombotic events. This risk is acknowledged by the authors of the national HHS guideline who recommend prophylactic low molecular weight heparin (LMWH) for all patients with HHS for the full duration of their admission.We present a case of fatal pulmonary embolism in a 39year old man admitted with HHS who was treated according to local hospital trust and national guidance with prophylactic LMWH.In the absence of evidence from randomised studies comparing prophylactic and treatment dose anticoagulation in thrombosis prevention in HHS further research is needed to facilitate development of evidencebased guidelines.

Background: Sodium-glucose linked transporter 2 inhibitors (SGLT2s) are currently favoured for their tolerability, cardiovascular benefit and renal protective effects. However, due to their mechanism of action, they are only licensed for use in those with preserved renal function at baseline. Previous analyses with other drugs in the class showed potential benefits even when used in those with estimated glomerular filtration rate (eGFR) below licensed level. Methods: Data was extracted from the ABCD nationwide empagliflozin audit and then stratified into groups, as follows, based on baseline eGFR (mL/min/1.73m2): CKD1 (n=2900, eGFR≥90), CKD2 (n=2753, eGFR<90, eGFR≥60), CKD3a (n=210, eGFR<60, eGFR≥45) and CKD3b+ (n=17, eGFR<45). Data was analysed using paired t-tests and ANOVA in Stata 16. Results: 5880 datasets were included with mean (±SD) age 59.5yrs (±10.4), 61.1% male, 86% Caucasian (where known), BMI 33.1kg/m2 (±6.6), HbA1c 9.17% (±1.61) and median duration diabetes 7.3 years (2.2-12.1 IQR) and were broadly similar across groups apart from age: those with more impaired renal function being generally older (CKD1 55.4yrs±9.5 v CKD3b+ 69.6yrs±8.5) with a longer duration diabetes with median (IQR) in CKD1 6.6yrs (1.8-10.9) v CKD3b+ 14.5yrs (8.9-17.3). Reductions in HbA1c, weight and BMI occurred in all groups (P<0.005); reductions in HbA1c were of a smaller magnitude as eGFR declined (ANOVA P<0.01). Changes in systolic (SBP) and diastolic blood pressure (DBP) were significant in those in CKD1- CKD3a but not in CKD3b+ (SBP +2.6mmHg, 95% CI +14.9, -9.6). eGFR was observed to decrease in CKD1 and CKD2 (CKD1 eGFR -2.1mL/min/1.73m2, CI 95% -1.8, -2.3). Conclusion: The use of empagliflozin at eGFR<45mL/min/1.73m2 may still confer HbA1c improvement (although perhaps of lower magnitude) and weight loss, though SBP and DBP reduction may be limited. More evidence is needed regarding its use at lower levels of eGFR. Disclosure T.S.J. Crabtree: None. K. Adamson: None. A. Bickerton: None. S.M. Phillips: None. A. Evans: Other Relationship; Self; AstraZeneca. A.M. Robinson: None. M. Atkin: Speaker’s Bureau; Self; AstraZeneca, Napp Pharmaceuticals. D.S. Morris: None. D.M. Williams: None. J.W. Stephens: Speaker’s Bureau; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Napp Pharmaceuticals, Novo Nordisk A/S. D.K. Sennik: Speaker’s Bureau; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Novo Nordisk Inc., Sanofi. A. Rohilla: None. M.L. Cull: None. R.P. Raghavan: Research Support; Self; Allergan plc. Speaker’s Bureau; Self; Abbott, AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Lilly Diabetes, Napp Pharmaceuticals, Takeda UK. Other Relationship; Self; Napp Pharmaceuticals. M. Yadagiri: None. I.W. Gallen: None. R.E. Ryder: Consultant; Self; GI Dynamics Inc. Other Relationship; Self; Novo Nordisk A/S.

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