[Recommendations of the new S1 guidelines on airway management]. / Empfehlungen zur neuen S1-Leitlinie Atemwegsmanagement.

The German guidelines for airway management aim to optimize the care of patients undergoing anesthesia or intensive care. The preanesthesia evaluation is an important component for detection of anatomical and physiological indications for difficult mask ventilation and intubation. If predictors for a difficult or impossible mask ventilation and/or endotracheal intubation are present the airway should be secured while maintaining spontaneous breathing. In an unexpectedly difficult intubation, attempts to secure the airway should be limited to two with each method used. A video laryngoscope is recommended after an unsuccessful direct laryngoscopy. Therefore, a video laryngoscope should be available at every anesthesiology workspace throughout the hospital. Securing the airway should primarily be performed with a video laryngoscope in critically ill patients and patients at risk of pulmonary aspiration. Experienced personnel should perform or supervise airway management in the intensive care unit.

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.

[Anesthesia in obesity surgery : Recommendations from the practice for the practice]. / Anästhesie in der Adipositaschirurgie : Empfehlungen aus der Praxis für die Praxis.

BACKGROUND: Due to unsuccessful conservative treatment concepts and the steady increase in the prevalence of obesity, obesity surgery has gained importance worldwide. In Germany alone, around 20,000 surgical operations for obesity are performed each year. In addition to patient history and physical examination a close interdisciplinary cooperation taking into account the currently applicable standards and guidelines of the professional societies are prerequisites for best patient care and to evaluate and mitigate patient risks. AIM: The aim of this work was to compile and consent experiences of experts in the implementation of applicable standards and guidelines for anesthesia in obesity surgery for daily clinical practice. METHOD: Anesthesiologists from five bariatric centers, comprising about 10% of the obesity surgery caseload of Germany per year, have collated their clinical experiences to agree on a consensus for procedures. The procedures for preoperative patient evaluation, drug premedication and PONV prophylaxis, induction of anesthesia and drug dosage recommendations for anesthetics were consented based on the authors' practice. RESULTS AND CONCLUSION: The procedures described herein were developed as part of a joint work process. The authors describe a practically applicable approach to the anesthesiological care of obesity surgery patients and recommend using a pragmatic formula for dosing the medication calculated on the basis of total body weight (TBW).

History-based preoperative evaluation of antibiotic-related allergies and design of an easy to use questionnaire.

BACKGROUND: An unconfirmed history of antibiotic allergies may negatively influence prescribing patterns for preoperative antibiotic prophylaxis and increase rates of postoperative wound infections through unnecessary use of alternative antibiotics. METHODS: After a literature search, we developed a questionnaire for the structured collection of antibiotic allergy history in the anesthesia consultation center and tested it over 2 years at a tertiary care hospital under everyday conditions as part of a quality assurance project. All data were evaluated completely anonymously in the context of standard care. RESULTS: After refining the questionnaire, we analyzed 4866 recorded optimized questionnaires, of which 51 were incomplete. An antibiotic allergy was denied 4312 times and affirmed 503 times, which corresponds to 10% in our sample. The most frequent single substances or groups in the 503 respondents with a positive history of antibiotic allergy were penicillin in 271 (54%), amoxicillin in 65 (13%), an unknown single agent in 50 (10%) and multiple substances in 25 (5%). The reported event occurred more than 10 years ago in 192 (38%) of the respondents, less than 10 years ago in 116 (23%), and 195 (39%) could not provide information. The time from exposure to symptom onset was less than 1h in 96 (19%), between 1 and 24 h in 75 (15%), more than 24 h in 106 (21%), and the remainder could not provide information. Allergy-specific treatment was recalled by 75 (15%) respondents, 287 (57%) reported not having received specific treatment, and the remainder could not recall. A specific allergy test was reported by 55 (11%) respondents, 337 (67%) said no allergy test had been made, and the rest could not recall. A substance-specific allergy passport was issued in 80 (16%) respondents. According to expert assessment, symptoms compatible with an IgE-mediated reaction were present in 96 (19%) of the respondents. An IgE-mediated reaction was considered possible in 70 (14%) and could be excluded by history in 337 (67%) of respondents. Out of 503 respondents with a positive history 51 (10%) could not remember the allergic substance but 7 (14%) of the 51 reported symptoms compatible with severe anaphylaxis or anaphylactic shock and 6 of the 51(12%) reported symptoms possibly related to an IgE-mediated reaction. DISCUSSION: Our survey revealed approximately 10% of respondents reporting an antibiotic allergy, which is in the upper range of data published in international literature and corresponds most closely to American data. Thus, the topic is also relevant to German anesthesia consultation centers, given the high rate of respondents who could have been "delabeled" based on the comprehensive assessment of their history. More expert allergy testing is needed in patients who report symptoms related or probably related to an IgE-mediated reaction. In our opinion, a special issue exists in those patients who did not remember the exact antibiotic but reported symptoms compatible with severe anaphylaxis putting them at high risk of unintended re-exposure.

Mitochondria and Pharmacologic Cardiac Conditioning-At the Heart of Ischemic Injury.

Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via complex signaling networks. These networks have been an intriguing research field for decades, largely advancing our knowledge on cardiac signaling beyond the conditioning response. The centerpieces of this system are the mitochondria, a dynamic organelle, almost acting as a cell within the cell. Mitochondria comprise a plethora of functions at the crossroads of cell death or survival. These include the maintenance of aerobic ATP production and redox signaling, closely entwined with mitochondrial calcium handling and mitochondrial permeability transition. Moreover, mitochondria host pathways of programmed cell death impact the inflammatory response and contain their own mechanisms of fusion and fission (division). These act as quality control mechanisms in cellular ageing, release of pro-apoptotic factors and mitophagy. Furthermore, recently identified mechanisms of mitochondrial regeneration can increase the capacity for oxidative phosphorylation, decrease oxidative stress and might help to beneficially impact myocardial remodeling, as well as invigorate the heart against subsequent ischemic insults. The current review highlights different pathways and unresolved questions surrounding mitochondria in myocardial I/R injury and pharmacological cardiac conditioning.

The Role of Cyclooxygenase-1 and -2 in Sevoflurane-Induced Postconditioning Against Myocardial Infarction.

Cyclooxygenase (COX)-2 mediates ischemic pre- and postconditioning as well as anesthetic-induced preconditioning. However, the role of COX-1 and -2 in anesthetic-induced postconditioning has not been investigated. We evaluated the role of COX-1 and -2 in sevoflurane-induced postconditioning in vivo. Pentobarbital-anaesthetized male C57BL/6 mice were subjected to 45 minutes of coronary artery occlusion and 3 hours of reperfusion. Animals received either no intervention, the vehicle dimethyl sulfoxide (DMSO, 10 µL/g intraperitoneally), acetylsalicylic acid (ASA, 5 µg/g intraperitoneally), the selective COX-1 inhibitor SC-560 (10 µg/g intraperitoneally), or the selective COX-2 inhibitor NS-398 (5 µg/g intraperitoneally). 1.0 MAC (minimum alveolar concentration) sevoflurane was administered for 18 minutes during early reperfusion either alone or in combination with ASA, SC-560, and NS-398. Infarct size was determined with triphenyltetrazolium chloride. Statistical analysis was performed using 1-way and 2-way analyses of variance with post hoc Duncan testing. The infarct size in the control group was 44% ± 9%. DMSO (42% ± 7%), ASA (36% ± 6%), and NS-398 (44% ± 18%) had no effect on infarct size. Sevoflurane (17% ± 4%; P < .05) and SC-560 (26% ± 10%; P < .05) significantly reduced the infarct size compared with control condition. Sevoflurane-induced postconditioning was not abolished by ASA (16% ± 5%) and SC-560 (22% ± 4%). NS-398 abolished sevoflurane-induced postconditioning (33% ± 14%). It was concluded that sevoflurane induces postconditioning in mice. Inhibition of COX-1 elicits a myocardial infarct size reduction and does not abolish sevoflurane-induced postconditioning. Blockade of COX-2 abolishes sevoflurane-induced postconditioning. These results indicate that sevoflurane-induced postconditioning is mediated by COX-2.

Endothelial nitric oxide synthase mediates the first and inducible nitric oxide synthase mediates the second window of desflurane-induced preconditioning.

OBJECTIVES: Nitric oxide synthases (NOSs) mediate the first window of anesthetic-induced preconditioning (APC). The authors tested the hypothesis that endothelial NOS (eNOS) mediates the first window and inducible NOS (iNOS) mediates the second window of APC. DESIGN: Randomized, prospective, blinded laboratory investigation. SETTING: Experimental laboratory. PARTICIPANTS: Mice. INTERVENTIONS: Mice were subjected to a 45-minute coronary artery occlusion (CAO) and a 180-minute reperfusion. C57BL/6 mice received desflurane, 1.0 minimum alveolar concentration, for 30 minutes or 12, 24, 48, or 96 hours before CAO. In eNOS(-/-) and iNOS(-/-) mice, desflurane was given 30 minutes and 48 hours before CAO. In the control groups, no desflurane was administered. Myocardial infarct size (IS) was determined after staining with Evans blue and triphenyltetrazolium chloride. MEASUREMENTS AND MAIN RESULTS: The second window of APC was detectable at 48 hours but not at 12, 24, and 96 hours after preconditioning. In the control groups, IS was not different among the wild-type (50 ± 10%), eNOS(-/-) (52 ± 14%), and iNOS(-/-) (46 ± 10%) mice. The IS decreased significantly (p < 0.05) when desflurane was administered 30 minutes (10 ± 6%) or 48 hours (16 ± 7%) before CAO in wild-type mice, 48 hours (21 ± 13%) before CAO in eNOS(-/-) mice, and 30 minutes (13 ± 6%) before CAO in iNOS(-/-) mice. Desflurane given 30 minutes before CAO in eNOS(-/-) mice (60 ± 10%) and 48 hours before CAO in iNOS(-/-) mice (48 ± 21%) did not decrease the IS significantly compared with controls. CONCLUSIONS: Endothelial NOS and iNOS work independently to mediate the first and second windows of APC, respectively. Endothelial NOS is not necessary to trigger the second window of APC.

Aromatase inhibition attenuates desflurane-induced preconditioning against acute myocardial infarction in male mouse heart in vivo.

The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. We hypothesized that endogenous estrogens play a role as mediators of desflurane-induced preconditioning against myocardial infarction. In this study, we tested the hypothesis that desflurane effects local estrogen synthesis by modulating enzyme aromatase expression and activity in the mouse heart. Aromatase metabolizes testosterone to 17ß- estradiol (E2) and thereby significantly contributes to local estrogen synthesis. We tested aromatase effects in acute myocardial infarction model in male mice. The animals were randomized and subjected to four groups which were pre-treated with the selective aromatase inhibitor anastrozole (A group) and DES alone (DES group) or in combination (A+DES group) for 15 minutes prior to surgical intervention whereas the control group received 0.9% NaCl (CON group). All animals were subjected to 45 minutes ischemia following 180 minutes reperfusion. Anastrozole blocked DES induced preconditioning and increased infarct size compared to DES alone (37.94 ± 15.5% vs. 17.1 ± 3.62%) without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. Protein localization studies revealed that aromatase was abundant in the murine cardiovascular system with the highest expression levels in endothelial and smooth muscle cells. Desflurane application at pharmacological concentrations efficiently upregulated aromatase expression in vivo and in vitro. We conclude that desflurane efficiently regulates aromatase expression and activity which might lead to increased local estrogen synthesis and thus preserve cellular integrity and reduce cardiac damage in an acute myocardial infarction model.

Activation of adenosine-monophosphate-activated protein kinase abolishes desflurane-induced preconditioning against myocardial infarction in vivo.

OBJECTIVES: Myocardial ischemia is accompanied by a rapid activation of adenosine-monophosphate-activated protein kinase (AMPK). However, it is unclear whether this represents a potentially beneficial or detrimental event in the course of ischemic injury. The role of AMPK activation in the cardioprotective setting of desflurane-induced preconditioning has not been investigated to date. Hence, the current study was undertaken to address the role of AMPK activation during desflurane-induced preconditioning in vivo. DESIGN: A prospective randomized vehicle-controlled study. SETTING: A university research laboratory. SUBJECTS: Male New Zealand white rabbits (n = 44). INTERVENTIONS: The animals were subjected to a 30-minute coronary artery occlusion (CAO) followed by 3 hours of reperfusion. Desflurane (1.0 minimum alveolar concentration) was administered for 30 minutes and discontinued 30 minutes prior to CAO. Different groups of animals received the AMPK activator, 5-aminoimidazole-4-carboxamide-1-b-riboside (AICAR), alone or in combination with desflurane. Infarct size was determined gravimetrically; AMPK activity and myocardial glycogen content were measured using specific assays. Phosphorylation of the AMPK substrate, acetyl-CoA carboxylase, was assessed by immunoblotting. Data are mean ± standard error of the mean. RESULTS: Desflurane significantly reduced the myocardial infarct size (36.7 ± 1.9%, p < 0.05) compared with the control group (61.6% ± 3.0%), concomitant with increased myocardial tissue levels of glycogen (2.09 ± 0.07 µg, p < 0.05). Activation of the AMPK by AICAR alone did not protect against ischemic injury (65% ± 3.3), but did abolish the cardioprotection elicited by desflurane (61.8% ± 4.2%) at the same time as increasing myocardial glycogen consumption (1.42 ± 0.15 µg/mL). CONCLUSIONS: The results obtained show that the pharmacologic activation of AMPK abolishes cardioprotection elicited by desflurane.

Propofol inhibits desflurane-induced preconditioning in rabbits.

OBJECTIVES: The authors tested the hypothesis that ischemic and desflurane-induced preconditioning are blocked by propofol. DESIGN: A prospective, randomized, vehicle-controlled study. SETTING: A university research laboratory. SUBJECTS: New Zealand white rabbits (n = 52). METHODS: Pentobarbital-anesthetized rabbits were subjected to 30 minutes of coronary artery occlusion followed by 3 hours of reperfusion. Rabbits received 0.0 (control) or 1.0 minimum alveolar concentration of desflurane (30 minutes' duration and a 30-minute memory period) or ischemic preconditioning (5 minutes of ischemia and a 30-minute memory period) in the absence or presence of propofol (10 mg/kg/h intravenously) or its vehicle (10% Intralipid emulsion; B Braun, Melsungen, Germany). The myocardial infarct size was measured with triphenyltetrazolium staining. Statistical analysis was performed with 1-way and 2-way analysis of variance when appropriate, followed by a post hoc Duncan test. Data are mean ± standard deviation. RESULTS: Myocardial infarct size was 56% ± 8% in control animals (n = 7). Desflurane significantly (p < 0.05) reduced the infarct size to 37% ± 6% (n = 7). Desflurane-induced preconditioning was blocked by propofol (65% ± 10%, n = 7) but not by its vehicle (45% ± 11%, n = 5). Propofol and its vehicle alone had no effect on the infarct size (62% ± 8% [n = 6] and 58% ± 3% [n=5], respectively). Ischemic preconditioning reduced infarct size in the absence or presence of propofol to 24% ± 7% (n = 7) and 29% ± 12% (n = 6). CONCLUSION: Desflurane-induced preconditioning markedly reduced infarct size and was blocked by propofol, whereas ischemic preconditioning was not blocked by propofol. The results suggest an important interference between propofol and anesthetic-induced preconditioning and might explain some contradictory findings in studies in humans.