Anesthesiology最新文献

Background: Electroencephalogram burst suppression can be associated with postoperative delirium; however, the results of relevant studies are discrepant. This systematic review and meta-analysis aimed to assess the association between intraoperative burst suppression and postoperative delirium in adult surgical patients.

Methods: PubMed, MEDLINE, Embase, Google Scholar, and the Cochrane Central Register of Controlled Trials were systematically searched and updated in May 2023. We included cohort studies, case-control studies, and randomized-controlled studies reporting on postoperative delirium incidence with documented intraoperative burst suppression in adults receiving general anesthesia for any surgery. The primary outcome was the pooled odds ratio (OR) for postoperative delirium in cases with intraoperative burst suppression compared to those without burst suppression, calculated using a random-effects model. Two independent investigators extracted the data. The protocol was prospectively registered in PROSPERO (registration number: CRD42022326479); the results were reported according to PRISMA guidelines.

Results: Fourteen studies (6435 patients) were included in the analysis. The overall incidence of postoperative delirium was 21.1% (1358/6435). Patients with intraoperative burst suppression had a higher incidence of postoperative delirium than those without burst suppression (pooled OR, 1.492; 95% confidence interval (CI) [1.022-2.178]; I2 =44%; 95% CI [0%-75%]; τ2 = 0.110). The intraoperative duration of burst suppression was significantly longer in patients who developed postoperative delirium (standardized mean difference [SMD] 0.462 [95% CI, 0.293-0.632]; I2 = 63%; 95% CI [16%-84%]; τ2 = 0.027). The burst suppression ratio was significantly higher in the delirium group (SMD 0.150; 95% CI [0.055-0.245]; I2 = 0%; 95% CI [0%-85%]; τ2 = 0.00).

Conclusion: Our meta-analysis suggests an association between intraoperative burst suppression and postoperative delirium; however, the quality of evidence was very low. The limited number of studies and substantial heterogeneity across them emphasize the need for further high-quality studies to establish a more robust conclusion.

Background: Drug shortages are a frequent challenge in current clinical practice. Certain drugs, (e.g., protamine) lack alternatives and inadequate supplies can limit access to services. Conventional protamine dosing uses heparin ratio-based calculations for heparin reversal following CPB and may result in excess protamine utilization, and potential harm due to its intrinsic anticoagulation. We hypothesized that a fixed 250-mg protamine dose would be comparable, as measured by the activated clotting time, to a 1:1 (1 mg for every 100 U) protamine to heparin ratio-based strategy for heparin reversal and that protamine would be conserved.

Methods: In a single-center, double-blinded trial, consenting elective adult cardiac surgical patients without pre-existing coagulopathy or ongoing anticoagulation, and a calculated initial heparin dose of ≥ 27500 U were randomized to receive, following CPB, protamine as a fixed dose (250 mg) or a ratio-based dose (1 mg:100 U heparin). The primary outcome was the activated clotting time following initial protamine administration, assessed by Student's t-test. Secondary outcomes included total protamine, the need for additional protamine, and the cumulative 24-h chest tube output.

Results: There were 62 and 63 patients in the fixed- and ratio-based dose groups, respectively. The mean post-protamine ACT was not different between groups (-2.0 s, 95% CI -7.2 to 3.3 s, P = 0.47). Less total protamine per case was administered in the fixed-dose group (2.1 50-mg vials, 95% CI -2.4 to -1.8, P < 0.0001). There was no difference in the cumulative 24-h chest tube output (difference = -77 ml, 95% CI 220 to 65 ml, P = 0.28).

Conclusions: A 1: 1 heparin ratio-based protamine dosing strategy compared to a fixed 250-mg dose resulted in the administration of a larger total dose of protamine no difference in either the initial ACT or the amount postoperative chest-tube bleeding.

Background: The incidence of central venous catheter-related thrombosis and the long-term effects of thrombosis on catheterized veins in neonates is unknown. We therefore determined the incidence of central venous thrombosis, identified associated risk factors, and evaluated outcomes at 6 months.

Methods: We enrolled neonates aged less than 28 days scheduled for major intestinal or cardiac surgery whom we expected to require central venous catheters for at least 48 hours. Catheter size, insertion method, and puncture site were determined by the attending anesthesiologist. The duration of catheterization was also determined by clinical need. Central venous thrombi were diagnosed by color Doppler ultrasound imaging within 48 hours after catheter removal; results were not shared with clinicians. Ultrasound examinations were repeated 1, 3, and 6 months after discharge.

Results: We enrolled 188 neonates over 2 years. The median duration of catheter insertion was 12 days. 128 (68%) of the neonates had central venous thrombi at the catheter site, all of which were asymptomatic. Among patients with thrombi, 29 (23%) had complete vessel occlusion and 5 (4%) had venous stenosis at 6 months after discharge. Thrombi therefore spontaneously resolved by 6 months in 73% of the neonates. CVC/vein diameter ratio, duration of catheterization, and catheter dysfunction were independent risk factors for vessel thrombus. Complete vessel occlusion was most common in patients whose thrombus occupied more than 58% of the vessel at the initial assessment.

Conclusions: Covert central venous thrombosis is frequent in neonates who have central venous catheters, and complications are most common in patients who have large intravascular thrombi. Neonates with large intravascular thrombi should be followed, and considered for anticoagulation.

Background: Few studies have assessed the dose ratio of calcium gluconate to calcium chloride or defined the time course of change in serum ionized calcium concentration after intravenous injection.

Methods: In a bioequivalence (dose ratio) trial, parturients undergoing cesarean delivery were randomly assigned to receive calcium chloride 0.5 grams or calcium gluconate 1.5 or 2 grams by 10-minute intravenous infusion. Venous serum ionized calcium concentration was measured prior to calcium infusion and approximately 5, 10, 15, 30, and 60 minutes after infusion start. We combined these data with serum ionized calcium concentration measurements in parturients who received 1 gram calcium chloride or saline placebo in two recent clinical trials to define the pharmacokinetics of intravenous calcium over the first hour during and after drug administration.

Results: The bioequivalence study enrolled 34 participants, from whom we collected 181 serum ionized calcium concentration measurements. The dose ratio of calcium gluconate to calcium chloride was 3.11 (95% CI: 2.77-3.48). Population pharmacokinetics of calcium were determined using 311 serum ionized calcium concentration measurements from 70 parturients. The pharmacokinetics of intravenous calcium were described by a two-compartment model with systemic clearance of 0.18 (95% CI: 0.07-0.27) L/min, distributional clearance of 1.25 (95%CI: 1.03-1.56) L/min, central volume of 10.9 (95% CI: 9.3-12.6) L, and peripheral volume of 16.5 (95% CI: 12.5-24.7) L. After adjusting for the dose ratio, calcium gluconate and calcium chloride had identical time courses. A one-gram infusion of calcium chloride results in a peak increase in serum ionized calcium concentration of 0.39 (0.38-0.42 mmol/L), which decreases by half 29 (23-40) minutes after initiation of the 10-minute infusion.

Conclusions: We confirmed a 3:1 dose ratio of calcium gluconate to calcium chloride and estimated the pharmacokinetics over the first hour following intravenous delivery. These data inform clinical care and may guide future trials assessing calcium efficacy to reduce bleeding in obstetric patients.

Clinicaltrials.gov registration: NCT05973747 (bioequivalence), NCT05027048, and NCT03867383 (trials included in pharmacokinetic assessment).