Intensive insulin therapy to non-cardiac ICU patients: a prospective study.

OBJECTIVE: Intensive insulin therapy reduced mortality in patients admitted to an intensive care unit following mainly cardiac surgery. The aim of this prospective study was to evaluate, if intensive insulin therapy could reduce mortality in medical and non-cardiac surgical patients admitted to a multidisciplinary intensive care unit. PATIENTS AND METHODS: For 6 months all adult patients, admitted to the intensive care unit, were included. Insulin was administered, if blood glucose 12 mmol L-1. For the next 6 months blood glucose level was reduced with intensive insulin therapy (aim 4.4 < BG < 6.1 mmol L-1); 271 patients were included. Patient characteristics data, APACHE II score, morbidity and mortality were recorded. RESULTS: At admission the two groups were comparable. The overall relative mortality was reduced 20% in the intensive insulin treated group (n.s.). In the intensive insulin treated group mortality was 13.1% in the medical patients and 11.2% in the surgical patients compared to 15.8% and 14.4%, respectively, in the conventional treated group (n.s.). The frequency of secondary infections was 21.5% in the intensive insulin treated group and 16.0% in the conventional treated group (n.s.). The proportion of hypoglycaemia increased from 4% to 14% (P < 0.05). CONCLUSIONS: Following intensive insulin therapy there was a trend towards reduced mortality in medical and non-cardiac surgical patients but less pronounced as in cardiac surgical patients. Intensive insulin therapy increased the frequency of hypoglycaemia. Around 4400 patients would have to be included in any future randomized study to reach significance.

Pulmonary endothelial dysfunction after cardiopulmonary bypass in neonatal pigs.

BACKGROUND: In neonatal pigs cardiopulmonary bypass (CPB) is associated with endothelial dysfunction in isolated large pulmonary arteries. It is, however, of great importance if this functional change extends to the small pulmonary resistance arteries, which are the key regulators of pulmonary flow and pressure. The aim of this study was to assess changes in pulmonary microvascular function after CPB using a clinically relevant pediatric procedure. METHODS: From three groups of neonatal pigs (CPB-, sham- and control group) pulmonary resistance arteries and systemic resistance arteries (from skeletal muscle) were isolated and mounted as ring preparations in wire myographs. Vessel diameters were less than 500 microm. Concentration-response curves were constructed for norepinephrine (NA), vasopressin (Vp), and the thromboxane A2-analog U46619, while the endothelium-dependent and -independent vasodilator functions were assessed as responses to acetylcholine and nitric oxide (NO). RESULTS: Maximum pulmonary vasodilator response to acetylcholine was attenuated after CPB compared with sham-operated and control animals (P=0.04). NO-induced relaxation, and contractile responses to NA, Vp, and U46619 were not influenced by CPB. In systemic arteries no changes in contractile or relaxant responses were seen after CPB. CONCLUSION: CPB seems to induce pulmonary endothelial dysfunction in pulmonary but not peripheral resistance arteries in neonatal piglets.