The effect of acute hyperglycaemia on brachial artery flow mediated dilatation in normal volunteers.

BACKGROUND: Endothelial function is known to be abnormal in patients with diabetes and acute hyperglycaemia may play an aetiological role. AIMS: The aim of this randomised controlled study was to determine if acute systemic hyperglycaemia impairs endothelial function in normal subjects. METHODS: Endothelial function was assessed by the change in brachial artery diameter in response to forearm ischaemia using B-mode ultrasound in ten healthy subjects (eight male) aged 19-35 years. Brachial artery blood flow velocity and diameter were measured before and after five minutes of forearm ischaemia. Measurements were performed in the supine position after an overnight fast, before and after 60 minute infusions of 0.9% saline or 10% dextrose. Measurements were made on two separate occasions at least 24 hours apart, and subjects were randomised to saline first or dextrose first. The largest diameter measured after ischaemia was divided by the resting arterial diameter to calculate percent dilatation of the artery from baseline, and is reported as flow-mediated dilatation (FMD). RESULTS: Dextrose infusion resulted in a significant rise in mean (SD) serum glucose 5.2 (0.1) to 9.2 (0.3) mmol/L and insulin concentration 6.3 (1.4) to 20.6 (3.7) mU/L p<0.002. Brachial artery blood flow velocity and diameter increased significantly from baseline after ischaemia (p<0.002). Mean FMD (SEM) before and after infusion were not, however, significantly different (p=0.4) (pre-saline 7.3 [1.0]%, post saline 5.2 [1.5]% and predextrose 8.1 [2.0]%, post dextrose 5.9 [1.7]%). CONCLUSIONS: These data suggest that acute hyperglycaemia does not impair FMD in normal subjects.

Diabetic ketoacidosis in adults at Auckland Hospital, 1988-1996.

BACKGROUND: Diabetic ketoacidosis (DKA) is associated with significant morbidity and mortality. Recent evidence suggests that patients with both type 1 and type 2 diabetes can develop DKA. AIM: To review the experience in managing patients admitted to Auckland Hospital with DKA over an eight year period. METHODS: A retrospective chart review was undertaken to identify patients with a discharge code of DKA admitted to Auckland Hospital between May 1988 and October 1996. RESULTS: One hundred and twenty-five patients were identified who met the defined criteria for DKA. The in-patient mortality for the group was 2.4%. Thirteen patients (10.4%) probably had type 2 diabetes. Thirty-eight (30.4%) patients were admitted to the Department of Critical Care Medicine (DCCM)--these patients had a significantly lower systolic blood pressure and arterial pH, together with a significantly higher admission blood glucose and longer duration of insulin infusion than those not admitted to DCCM. Following their index admission 25% of patients were readmitted to hospital with DKA during the study period. Errors in insulin self-administration that contributed to admission to hospital with DKA were identified in 61% of the patients with known diabetes. CONCLUSIONS: Patients with DKA in this study spent about a week in hospital and a significant proportion were admitted to the DCCM. In spite of this the overall mortality was low. Many of these patients were readmitted to hospital with DKA. A small number of patients with DKA may have type 2 diabetes and may not need long term insulin therapy. More effort on patient education regarding insulin use with illness, may prevent admission to hospital with DKA.