Perioperative Tight Glucose Control Reduces Postoperative Adverse Events in Nondiabetic Cardiac Surgery Patients.

CONTEXT: Tight glucose control (TGC) reduces morbidity and mortality in patients undergoing elective cardiac surgery, but only limited data about its optimal timing are available to date. OBJECTIVE: The purpose of this article was to compare the effects of perioperative vs postoperative initiation of TGC on postoperative adverse events in cardiac surgery patients. DESIGN: This was a single center, single-blind, parallel-group, randomized controlled trial. SETTINGS: The setting was an academic tertiary hospital. PARTICIPANTS: Participants were 2383 hemodynamically stable patients undergoing major cardiac surgery with expected postoperative intensive care unit treatment for at least 2 consecutive days. INTERVENTION: Intensive insulin therapy was initiated perioperatively or postoperatively with a target glucose range of 4.4 to 6.1 mmol/L. MAIN OUTCOME MEASURES: Adverse events from any cause during postoperative hospital stay were compared. RESULTS: In the whole cohort, perioperatively initiated TGC markedly reduced the number of postoperative complications (23.2% vs 34.1%, 95% confidence interval [CI], 0.60-0.78) despite only minimal improvement in glucose control (blood glucose, 6.6 ± 0.7 vs 6.7 ± 0.8 mmol/L, P < .001; time in target range, 39.3% ± 13.7% vs 37.3% ± 13.8%, P < .001). The positive effects of TGC on postoperative complications were driven by nondiabetic subjects (21.3% vs 33.7%, 95% CI, 0.54-0.74; blood glucose 6.5 ± 0.6 vs 6.6 ± 0.8 mmol/L, not significant; time in target range, 40.8% ± 13.6% vs 39.7% ± 13.8%, not significant), whereas no significant effect was seen in diabetic patients (29.4% vs 35.1%, 95% CI, 0.66-1.06) despite significantly better glucose control in the perioperative group (blood glucose, 6.9 ± 1.0 vs 7.1 ± 0.8 mmol/L, P < .001; time in target range, 34.3% ± 12.7% vs 30.8% ± 11.5%, P < .001). CONCLUSIONS: Perioperative initiation of intensive insulin therapy during cardiac surgery reduces postoperative morbidity in nondiabetic patients while having a minimal effect in diabetic subjects.

Bioenergetic gain of citrate anticoagulated continuous hemodiafiltration--a comparison between 2 citrate modalities and unfractionated heparin.

PURPOSE: To determine bioenergetic gain of 2 different citrate anticoagulated continuous hemodiafiltration (CVVHDF) modalities and a heparin modality. MATERIALS AND METHODS: We compared the bio-energetic gain of citrate, glucose and lactate between 29 patients receiving 2.2% acid-citrate-dextrose with calcium-containing lactate-buffered solutions (ACD/Ca(plus)/lactate), 34 on 4% trisodium citrate with calcium-free low-bicarbonate buffered fluids (TSC/Ca(min)/bicarbonate), and 18 on heparin with lactate buffering (Hep/lactate). RESULTS: While delivered CVVHDF dose was about 2000 mL/h, total bioenergetic gain was 262 kJ/h (IQR 230-284) with ACD/Ca(plus)/lactate, 20 kJ/h (8-25) with TSC/Ca(min)/bicarbonate (P < .01) and 60 kJ/h (52-76) with Hep/lactate. Median patient delivery of citrate was 31.2 mmol/h (25-34.7) in ACD/Ca(plus)/lactate versus 14.8 mmol/h (12.4-19.1) in TSC/Ca(min)/bicarbonate groups (P < .01). Median delivery of glucose was 36.8 mmol/h (29.9-43) in ACD/Ca(plus)/lactate, and of lactate 52.5 mmol/h (49.2-59.1) in ACD/Ca(plus)/lactate and 56.1 mmol/h (49.6-64.2) in Hep/lactate groups. The higher energy delivery with ACD/Ca(plus)/lactate was partially due to the higher blood flow used in this modality and the calcium-containing dialysate. CONCLUSIONS: The bioenergetic gain of CVVHDF comes from glucose (in ACD), lactate and citrate. The amount substantially differs between modalities despite a similar CVVHDF dose and is unacceptably high when using ACD with calcium-containing lactate-buffered solutions and a higher blood flow. When calculating nutritional needs, we should account for the energy delivered by CVVHDF.

Quantification of systemic delivery of substrates for intermediate metabolism during citrate anticoagulation of continuous renal replacement therapy.

BACKGROUND: There are limited data on systemic delivery of metabolic substrates during citrate anticoagulation. The direct citrate measurements are usually not available. METHODS: Patients on 2.2% acid-citrate-dextrose (ACD, n = 41) were compared to a control group on unfractionated heparin (n = 17). All were treated on 1.9-m(2) polysulfone filters. Samples were taken from the central venous catheter, ports pre- and post-filter and from effluent. RESULTS: The gain of citrate in CVVH (n = 18) was not different from CVVHDF (n = 23, p = 0.8). Mean gain of citrate was 25.4 ± 6.4 mmol/h. The systemic loads of lactate (p = 0.12) and glucose (p = 0.23) in CVVH were similar to CVVHDF. Mean inputs of lactate and glucose were 62.9 ± 21.1 and 26.6 ± 10.4 mmol/h, respectively. The mean difference between post- and prefilter unmeasured anions (d-UA) correlated with mean difference of citrate concentrations (p < 0.0001, r(2) = 0.66). The estimated caloric load of the citrate modalities was 5,536 ± 1,385 kJ/ 24 h. CONCLUSIONS: ACD might represent a significant load of metabolic substrates, particularly if used with lactate buffer. Systemic delivery of citrate can be predicted using d-UA in the extracorporeal circuit.