Practice Guidelines for Monitoring Neuromuscular Blockade-Elements to Change to Increase the Quality of Anesthesiological Procedures and How to Improve the Acceleromyographic Method.

Neuromuscular blocking agents are a crucial pharmacological element of general anesthesia. Decades of observations and scientific studies have resulted in the identification of many risks associated with the uncontrolled use of neuromuscular blocking agents during general anesthesia or an incomplete reversal of neuromuscular blockade in the postoperative period. Residual relaxation and acute postoperative respiratory depression are the most serious consequences. Cyclic recommendations have been developed by anesthesiology societies from many European countries as well as from the United States and New Zealand. The newest recommendations from the American Society of Anesthesiologists and the European Society of Anesthesiology were published in 2023. These publications contain very detailed recommendations for monitoring the dosage of skeletal muscle relaxants in the different stages of anesthesia-induction, maintenance and recovery, and the postoperative period. Additionally, there are recommendations for various special situations (for example, rapid sequence induction) and patient populations (for example, those with organ failure, obesity, etc.). The guidelines also refer to pharmacological drugs for reversing the neuromuscular transmission blockade. Despite the development of several editions of recommendations for monitoring neuromuscular blockade, observational and survey data indicate that their practical implementation is very limited. The aim of this review was to present the professional, technical, and technological factors that limit the implementation of these recommendations in order to improve the implementation of the guidelines and increase the quality of anesthesiological procedures and perioperative safety.

Are There Any Advantages of the Low Opioid Anaesthesia and Non-Opioid Postoperative Analgesia Protocol: A Clinical Observational Study.

Purpose: The methods of perioperative analgesia and pain control have changed. The principle of opioid-based analgesia has been modified to multimodal analgesia, followed by LOA (low opioid anaesthesia) and OFA (opioid-free anaesthesia). The aim was to describe the effects of LOA on nausea, vomiting, and pain control during general anaesthesia and postoperative period after laparoscopic cholecystectomy. Patients and Methods: The protocol included the study group-40 patients received low-opioid anaesthesia (LOA), and the control group-40 patients received general anaesthesia with opioid analgesia (OA). The scheme of LOA was based on ketamine, lidocaine, magnesium sulfate, paracetamol, and metamizole. The OA was based on standard opioid (fentanyl) administration in induction and maintenance phase due to clinical observation. Postoperative analgesia included 1g of paracetamol and 1g of metamizol intravenously, with a 6-hour interval between doses. Results: Significant differences in the pain score in the periods of 2-6, 6-12, and 12-24 hours after anaesthesia between the groups were noticed (p < 0.001). Moreover, a significant difference in the frequency of nausea (p = 0.005) and vomiting (p = 0.04) between groups were presented. Nausea occurred in 54.05% of OA group, while in the LOA group, it occurred in a 23.08%. Vomiting occurred in 32.43% of control group, while in the study group, it occurred in 12.82% of patients. Conclusion: The LOA protocol was more beneficial in reducing nausea and vomiting than the opioid-based method of anaesthesia. The LOA protocol of general anaesthesia during laparoscopic cholecystectomy and non-opioid postoperative analgesia have better outcomes in pain control, as well as nausea and vomiting, and improve postoperative patient comfort. The LOA protocol during anaesthesia and non-opioid postoperative analgesia should be considered in routine practice.

Opioid Therapy and Implications for Oxidative Balance: A Clinical Study of Total Oxidative Capacity (TOC) and Total Antioxidative Capacity (TAC).

BACKGROUND: Opioids are used in pharmacotherapy for chronic pain. The phenomenon of their influence on the oxidative-antioxidant balance is poorly understood. Additionally, little is known about the oxidative status in patients receiving chronic opioid noncancer pain therapy. METHODS: The primary goal was to explore oxidative status using the total oxidative capacity (TOC) and total antioxidative capacity (TAC) in patients with chronic lower back pain (LBP) treated with opioids. The secondary task was to present the risk factors connected with the duration of therapy or anthropometric parameters. Plasma TOC and TAC were analyzed in the study group (n = 28), i.e., patients with chronic LBP treated with opioids, and in the control group (n = 11), i.e., healthy volunteers. RESULTS: The TAC was significantly lower in the study group compared to the control group (p < 0.05), while the TOC did not differ significantly. A statistically lower TOC for buprenorphine compared to oxycodone (p = 0.019) and tramadol (p = 0.036) was observed. The TOC did not differ between tramadol and oxycodone. The highest TAC was described for oxycodone, while the TAC for buprenorphine and tramadol was significantly lower in comparison with oxycodone (p = 0.007 and p = 0.016). The TOC/TAC ratio was higher in patients with nicotinism in both groups. CONCLUSIONS: Patients receiving chronic opioid therapy presented a lower antioxidative capacity. There were differences in opioid-induced oxidative imbalance, which is very important clinically. Nicotinism increases the oxidative-antioxidative imbalance. The least oxidative capacity was associated with buprenorphine, while oxycodone showed the greatest antioxidant activity. The most favorable TOC/TAC ratio was observed for buprenorphine. It is suggested that buprenorphine or oxycodone has the best profile, and there is no correlation with the duration of opioid therapy or the opioid dose. However, all opioid substances can potentially enhance the oxidative-antioxidative status.

Plasma Brain-Derived Neurotrophic Factor and Opioid Therapy: Results of Pilot Cross-Sectional Study.

Objective: The neurotoxic effect of opioid has not been thoroughly described. No studies have been conducted to explain the effect of opioids in chronic non-cancer pain therapy on the neurotrophic factors level. Due to the ability to cross the blood-brain barrier, it seems the determination of serum Brain-derived neurotrophic factor (BDNF) concentration is a reliable presentation of the concentration in the central nervous system. The aim of the study was to explore the changes of plasma BDNF concentration during long-term opioid therapy.Methods: The study group included 28 patients with chronic low back pain treated with opioid therapy buprenorphine (n=10), tramadol (n=8), oxycodone (n=6), morphine (n=3), fentanyl (n=1). The control group included 11 patients. Measurements of plasma BDNF concentrations were performed, and information about opioid therapy were recorded (age, sex, opioid substance type, daily dose and the duration of opioid therapy). Data were analyzed using nonparametric tests.Results: The median BDNF level in the study group was significantly lower (2.73 ng/mL) than that in the control group (5.04 ng/mL, P<0.05). BDNF levels did not differ among groups based on the type of opioid substance used, but the lowest median value was observed for tramadol (2.62 ng/mL), and the highest median value was observed for buprenorphine (2.73 ng/mL). The widest minimum-maximum ranges of BDNF for oxycodone were noted, minimum 1.23 ng/mL and maximum 4.57 ng/mL, respectively. BDNF concentrations were correlated with age in the tramadol group and with the duration of opioid therapy in the buprenorphine group.Conclusion: Chronic opioid therapy for noncancer pain induces specific changes in the BDNF concentration. Tramadol and buprenorphine exerted an important effect on BDNF levels in the examined patients. The BDNF level depends on duration of opioid therapy with buprenorphine, and age in tramadol therapy.