Balancing patient needs with environmental impacts for best practices in general anesthesia: Narrative review and clinical perspective.

Discussions of the environmental impacts of general anesthetics have focused on greenhouse gas (GHG) emissions from inhaled agents, with those of total intravenous anesthesia (TIVA) recently coming to the forefront. Clinical experts are calling for the expansion of research toward life cycle assessment (LCA) to comprehensively study the impact of general anesthetics. We provide an overview of proposed environmental risks, including direct GHG emissions from inhaled anesthetics and non-GHG impacts and indirect GHG emissions from propofol. A practical description of LCA methodology is also provided, as well as how it applies to the study of general anesthesia. We describe available LCA studies comparing the environmental impacts of a lower carbon footprint inhaled anesthetic, sevoflurane, to TIVA/propofol and discuss their life cycle steps: manufacturing, transport, clinical use, and disposal. Significant hotspots of GHG emission were identified as the manufacturing and disposal of sevoflurane and use (attributed to the manufacture of the required syringes and syringe pumps) for propofol. However, the focus of these studies was solely on GHG emissions, excluding other environmental impacts of wasted propofol, such as water/soil toxicity. Other LCA gaps included a lack of comprehensive GHG emission estimates related to the manufacturing of TIVA plastic components, high-temperature incineration of propofol, and gas capture technologies for inhaled anesthetics. Considering that scarce LCA evidence does not allow for a definite conclusion to be drawn regarding the overall environmental impacts of sevoflurane and TIVA, we conclude that current anesthetic practice involving these agents should focus on patient needs and established best practices as more LCA research is accumulated.

Validation of Waste Anaesthetic Gas Exposure Limits When Using a Closed Vaporizer Filling System: A Laboratory-Based Study.

INTRODUCTION: It is desirable to minimise exposure of personnel to halogenated inhaled anaesthetics in the operating room to avoid deleterious short-term and long-term health effects. The objective of this study was to determine whether, while filling anaesthetic vaporizers with sevoflurane using AbbVie's closed vaporizer filling system (Quik-Fil™), concentrations of sevoflurane in ambient air remained at or below recommended levels when measured at different operator heights. METHODS: Nine filling runs were conducted, with measurement heights of 95, 130, 140, 150, 160, and 185 cm. Within each 15-min run, five vaporizers were sequentially filled from bottles of sevoflurane with the closed valving system. Ambient-air sevoflurane concentration in the breathing zone was continuously measured once per second by using a MIRAN SapphIRe 205BXL portable ambient air analyser. RESULTS: The use of the closed filling system maintained a level of waste anaesthetic gas exposure that was well below (mean, 0.10 ppm; maximum, 0.16 ppm) the recommended short-term value of 20 ppm average for 15 min provided by the Swedish Work Environment Authority and also fell below the US limit of a time-weighted average of 2 ppm provided by the National Institute for Occupational Safety and Health. Exposure to sevoflurane appeared to be independent of the height at which the measurement was made. CONCLUSIONS: The presence of sevoflurane in the work environment while using the closed filling system maintains a level of waste anaesthetic gas exposure well below the recommended levels at all tested operator heights.

Evaluation of Lipid Profile and Residual Cardiovascular Risk in Patients Prior to Initiation of Niaspan Therapy.

Background: Despite significant impact of statins, there are a number of patients with residual risk of cardio vascular disease who have optimally controlled low-density lipoprotein cholesterol (LDL-C). Niaspan (extended-release nicotinic acid or niacin-ER) is indicated for its use as monotherapy for the treatment of very high triglyceride (TG) levels and for the raising of high-density lipoprotein cholesterol (HDL-C) representing those residual risk populations. The patient characteristics and lipid profile, prior to initiation of therapy, in the real-world clinical setting has not been well documented. Objectives: This study evaluated lipid levels among patients initiating Niaspan in real-world clinical practice. Methods: Patients with a first prescription of Niaspan were identified using electronic medical record data from GE. Lipid values were categorized into optimal and nonoptimal TG or HDL-C levels. Results: There were 89 091 new users. Most patients had nonoptimal TG, HDL-C, TG/HDL-C ratio, LDL-C, and non-HDL-C levels. Among those with nonoptimal TG and HDL, the ratio of TG to HDL-C was higher among younger age groups (mean ratio 12.0 in males; 10.58 in females aged 18 to <40 years). TG was significantly correlated with non-HDL-C (0.41, P < .001) but not with LDL-C. Among those with LDL-C <100 mg/dL, 64.3% had nonoptimal TG/HDL-C ratio and approximately 70% had non-HDL-C ≥130 mg/dL. More than a third of the patients had diagnosis of coronary heart disease or coronary heart disease risk equivalent. Conclusion: Majority of Niaspan users had nonoptimal TG and/or HDL-C. The correlation of nonoptimal TG levels with non-HDL-C levels further support that Niaspan was targeted to population with residual risk for cardiovascular disease.

Investigations of the immunoglobulin subtype transformation of anti-heparin-platelet factor 4 antibodies during treatment with a low-molecular-weight heparin (clivarin) in orthopedic patients.

CONTEXT: It is now widely accepted that the pathophysiology of heparin-induced thrombocytopenia (HIT) syndrome is mediated by the generation of a wide array of functional and molecularly heterogeneous anti-heparin-platelet factor 4 (AHPF4) antibodies that may mediate platelet and/or endothelial cell activation/destruction. OBJECTIVE: We investigated the differential prevalence and functionality of AHPF4 immunoglobulin subtypes (IgA, IgG, and IgM) in plasmas obtained from orthopedic patients immobilized with Plaster-Cast and treated with clivarin (a low-molecular-weight heparin) in comparison to a placebo for the prophylaxis of deep-vein thrombosis. DESIGN AND METHODS: Clivarin was administered subcutaneously at a fixed daily dosage of 1750 U without any adjustment or loading dosage. Citrated plasmas were obtained at baseline, at 10 to 14 days, and at postbrace procedure (5-12 weeks). An enzyme-linked immunosorbent assay (ELISA) was used to quantitate the AHPF4 antibody titers. The functionality of the ELISA-positive samples was determined by a 14C-serotonin release assay (SRA). RESULTS: In the ELISA test, 16 of 1073 samples (1.5%; 6 in clivarin and 10 in placebo groups) were positive for AHPF4 antibodies (mean optical density [OD] = 0.46 +/- 0.02). None of the ELISA-positive samples for AHPF4 antibodies could mediate platelet activation responses as determined by the SRA (0%-3% serotonin release, P >.10, n = 16). Through differential immunoglobulin subtype analysis of the samples positive for (cumulative) AHPF4 antibodies, we determined that their relative prevalence in plasma were as follows: IgM (mean OD = 0.71 +/- 0.13) > IgG (0.31 +/- 0.08) > IgA (0.14 +/- 0.02). Although there was no significant difference in the total antibody titers between clivarin and placebo groups, the antibody subtyping data showed conversion trends (ie, IgA [clivarin to placebo], IgG [placebo to clivarin], and IgM [clivarin to placebo]). CONCLUSION: These observations indicate that even at reduced dosages, clivarin can shift the immunogenic up-regulation toward the IgG subpopulation; however, the IgG subtype is of a nonfunctional type of AHPF4 antibody and thus may not cause any HIT-related pathogenic responses.