Treatment Of Local Anesthetic Toxicity Research Articles

Tetracaine hydrochloride induces macrophage pyroptosis through caspase‑1/11‑GSDMD signaling pathways.

Tetracaine hydrochloride (TTC) is a long-lasting local anesthetic commonly used for topical anesthesia. Inappropriate dosage or allergic reactions to TTC can lead to local anesthetic toxicity. TTC exerts cytotoxic effects on certain cell types by inducing apoptosis and necrosis; however, the effects of TTC on macrophages are currently unclear. In the present study, the RAW 264.7 and BV2 cell lines, and murine peritoneal macrophages, were used to evaluate the cytotoxicity of TTC. The present study demonstrated that TTC caused a decrease in cell viability according to a Cell Counting Kit-8 assay, increased lactate dehydrogenase and IL-1β secretion according to ELISA, and induced morphological changes characteristic of pyroptosis according to western blotting. Moreover, TTC-induced macrophage pyroptosis was mediated by gasdermin (GSDM)D, and the cleavage of GSDMD was modulated by both caspase-1 and caspase-11. These results were experimentally validated using caspase-1 and caspase-11 inhibitors. Furthermore, it was observed that TTC and lipopolysaccharide (LPS) exerted similar effects on macrophages. However, the mechanism of induction of pyroptosis by TTC was different from that of LPS. The present study demonstrated that TTC alone could induce macrophage pyroptosis mediated by canonical and non-canonical inflammatory caspases. Therapies targeting pyroptosis may potentially provide a promising future strategy for the prevention and treatment of local anesthetic toxicity induced by TTC.

Ropivacaine-induced seizures evoked pain sensitization in rats: Participation of 5-HT/5-HT3R

Due to the increasing use of local anesthetic techniques in various healthcare settings, local anesthetic toxicity still occurs. Seizures are the most common symptom of local anesthetic toxicity. The relationship between local anesthetic-induced seizures and the sensation of pain has not been established till now. Here, we assessed the development of pain hypersensitivity after ropivacaine-induced seizures (RIS) and the influence of RIS on incision-induced postsurgical pain and formalin-induced acute inflammatory pain. In addition, the involvement of spinal 5-HT/5-HT3R in RIS-induced pain sensitization was investigated. According to a sequential exploratory experimental strategy, we first calculated the 50% seizure dosage of ropivacaine to be 42.66 mg/kg (95% confidence interval: 40.19–45.28 mg/kg). We showed that RIS induced significant bilateral mechanical pain hypersensitivity that lasted around 5 days, accompanied by an increase in spinal 5-HT. Moreover, RIS considerably protracted postsurgical pain and enhanced formalin-induced spontaneous flinching in the second phase. Depletion of spinal 5-HT with intrathecal injection of 5,7-dihydroxytryptamine (5,7-DHT) reduced RIS-induced pain hypersensitivity and prevented the prolonging of postsurgical pain following RIS. Likewise, blocking spinal 5-HT3R by intrathecal administration of ondansetron reversed RIS-induced pain hypersensitivity and attenuated the pronociception of RIS in the formalin test. Our findings revealed that acute RIS led to pain hypersensitivity and had pronociceptive effects on incision-induced postsurgical pain and formalin-induced acute inflammatory pain. Moreover, our data implied that RIS-induced pain sensitization depends on spinal 5-HT/5-HT3R signaling. Thus, targeting the descending serotonergic facilitation system should be an important element of the precise treatment for local anesthetic toxicity.

The Bupivacaine Story: A Tribute to George A. Albright, MD (1931-2020).

In 1979, George A. Albright, MD (1931-2020) published a controversial editorial in Anesthesiology that raised the question of bupivacaine cardiotoxicity. In it, he presented several cases of rapid cardiovascular collapse after administration of the highly lipophilic local anesthetic and called for further investigation. Although the scientific community initially resisted Dr Albright's idea, his editorial would ultimately lead to several important advancements in anesthesiology. In 1983, the US Food and Drug Administration issued a black box warning that recommended against the use of 0.75% bupivacaine in obstetric anesthesia. This warning would remain in place until 1999. In addition, Dr Albright's article led to the following changes: laboratory research that proved the cardiotoxicity of bupivacaine; the development of safer, stereoselective agents like ropivacaine; and the acceptance of lipid emulsion as a treatment for local anesthetic toxicity. In this article, C. Philip Larson, Jr, MDCM, Editor-in-Chief of Anesthesiology at the time of publication of Albright's manuscript, provides a unique perspective on the bupivacaine story.

Management of local anesthetic toxicity and importance of lipid infusion

Local anesthetics (LA) are one of the groups that block the transmission of sensory, motor and autonomic nerve impulses commonly used in clinical anesthesia. All local anesthetic molecules in clinical use consist of three parts: a lipophilic (aromatic) end, a hydrophilic (amine) end, and a chain that provides the connection between the ends. Physicochemical properties determine the clinical efficacy of local anaesthetics The part that determines the lipid solubility of local anesthetics is the aromatic ring. A higher dose of local anesthetics is required for cardiovascular system (CVS) toxicity. Hypertension, tachycardia and ventricular arrhythmia are the first of the diseases of CVS. Hypotension, arrhythmia, bradycardia and cardiac arrest develop as local anesthetics increase in blood. The symptoms of central nervous system (CNS) toxicity associated with LA are related to the plasma levels of drugs. Initially, there are drowsiness, dizziness, sedation, disorientation, tinnitus, nystagmus, metallic taste, nausea and vomiting. Then, restlessness, irritability, tremors and muscle twitches occur. After this, the tonic-clonic seizure and loss of consciousness develops, finally, apnea, cardiovascular collapse and coma. In the treatment of local anesthetic toxicity, it is recommended to provide airway, avoid the propofol if seizure occurs and treat with benzodiazepine. If cardiac arrest develops, it is recommended to switch to advanced life support, to reduce the given dose of adrenaline, to administer lipid emulsion (20%) and to respond to treatment if cardiopulmonary bypass is not provided.

Lipid Emulsion in Treatment of Local Anesthetic Toxicity.

Epidural, spinal, regional, local, and intravenous administration of local anesthetics (LAs) is a cornerstone of anesthetic practice. LA toxicity is a grave consequence that is of great significance to anesthesia providers. Outcomes of LA toxicity range from inconvenient symptoms such as tinnitus, twitching, and hypotension to seizures; cardiovascular or respiratory collapse; and death. Lipid emulsion has emerged as a potential "magic bullet" in treating LA toxicity. This literature review provides background information and proposed mechanisms of action for LAs and lipid emulsion as well as animal experiments and a case report that speak to the effectiveness of lipid emulsion in the face of LA toxicity.

Board #214 - Program Innovation The Use of Trigger Films to Improve the Differential Diagnosis and Management of Critical Events in the Operating Room (Submission #11612)

Objectives Critical events (such as hemorrhage, bronchospasm, and ventricular fibrillation) that occur in the operating room or in critical care environments are the subjects of most anesthesia and critical care simulation scenarios. Because of the time constraints and available personnel, it is not feasible for every learner or practitioner to experience the event in a simulated environment. In addition, there is literature that identifies deficiencies in recognition and management of rare critical events.1 For example, large amounts of time can pass without a practitioner experiencing a critical event. However, if and when a critical event was to occur, the learner or clinician is expected to act decisively and appropriately. Viewing and analyzing trigger films can provide the visual and auditory education that today’s learners expect in a format that allows them to experience several critical events in a timely manner. These films have the potential to help students and practitioners become increasingly familiar with critical events that they may not experience until it occurs during patient care. Description Trigger films are short video clips (30 seconds to two minutes) that portray situations a learner or clinician may experience. Our focus is to demonstrate how these films can help with the identification and management of critical events. We will begin with films that show limited clinical data compelling the learner to assess several different causes of the crisis, which can then be discussed. Each trigger film builds on the previous one providing more clinical data until a diagnosis can be made. This model promotes active learning and encourages in-depth evaluation and discussion about the holistic view of a critical event. Then once the diagnosis has been determined, both effective and non-effective management options for the crisis can be viewed allowing the learner to see the differences in management options, and thus potentially improve their knowledge. The use of this active learning technique differs from existing teaching strategies because these films are interactive, can be presented in any location in a limited time frame, and requires only one instructor. There is evidence that demonstrates how students can improve their identification and management of anesthetic crises after they have participated in trigger film education.2 Conclusion Trigger films that focus on critical events and professional issues in the clinical area have several future applications. One such application could be future research. This research could evaluate how both learners and clinicians perform during a critical event in a simulated environment. Trigger films could also be used during critical care simulations to introduce a scenario, as well as demonstrate effective and less effective ways of managing different crisis situations. These films could be integrated into an educational curriculum. An example of how they could be used clinically would be to demonstrate an interscalene block. The film could start by demonstrating the appropriate anatomy, needle placement, and ultrasound technique. Then another film could focus on the identification and treatment of local anesthetic toxicity. Finally, these films could be the stimulus to create gaming simulations where the learner becomes a part of the simulation scenario. For an example of the films we have please visit this website: http://vimeo.com/channels/kpsanfilms.

An assessment of the awareness of local anesthetic systemic toxicity among multi-specialty postgraduate residents.

Local anesthetics (LAs) are extensively used in clinical practice by both anesthesiologists and non-anesthesiologists and are often associated with systemic toxicity. We hypothesize that this awareness is inadequate among medical specialists and entails a risk of misdiagnosis and underreporting of such events. We therefore conducted a cross-sectional questionnaire-based study to assess the level of understanding of LA use and effective management of systemic toxicity among 200 postgraduate residents of various specialties (with the exception of anesthesiology) in a tertiary care hospital in India from October to December 2013. Among those residents who had used LAs (193/200), 27 and 25% of responders correctly identified the toxic doses of lidocaine and of lidocaine + adrenaline, respectively. Of the responders, 70% always performed a negative aspiration of blood before injecting the drug, 27% sometimes aspirated and the remaining 3% never aspirated. The majority of the responders (93%) were unaware of the toxic dose of bupivacaine. Only 70% of responders believed that LAs could be toxic [95 % confidence interval (CI) 65.5-74.5%], and 81% of these correctly identified the signs and symptoms of cardiotoxicity. Only 2% of responders knew that lipid emulsion is a part of its treatment (95 % CI 0.6-3.4%). Based on these results, there is a definite need to increase the awareness of detection and treatment of local anesthetic toxicity among all medical practitioners who regularly use LAs.

Clinical experience of propofol in treatment of local anesthetic toxicity induced by sacral block

Objective To study the effect of propofol in treatment of local anesthetic toxicity induced by sacral block.Methods We retrospectively analyzed 22 cases(P)who had experienced local anesthetic toxicity induced by sacral block and received a treatment of propofol in our department from January 2002 to November 2010.Other 18 patients(D)who received diazepam therapy from September 1997 to May 2002 were taken as the control.Those data of HR,SpO2 and MAP which were measured immediately prior to,3,5,10 and 20 min after drug administration were analyzed.Results The symptoms of local anesthetic toxicity induced by sacral block were treated effectively in both groups.However,the time of toxic symptoms withdrawl (15±6)s and awakening(6±4)min were significantly shorter in group P(P＜0.01).Conclusions Local anesthetic toxicity induced by sacral block can be effectively treated,and toxic symptom quickly can be corrected by intravenous injection of propofol.Thus,it may become a promising treatment. Key words: Propofol; Sacral block; Toxic reaction; Local anesthetic

Management and Treatment of Local Anaesthetic Toxicity

Local anaesthetics have been used within surgical practice since the late 1800s, when the ophthalmologist Carl Koller discovered the tissue numbing properties of cocaine (Odedra & Lyons 2010). Since that time, the ongoing development of anaesthetic drugs has provided many different local anaesthetics (LA) to clinical practice. The techniques for using these drugs in surgical practice have also developed, shaping the modern practices we know today. Increasing numbers of surgical procedures are now carried out under LA that once necessitated general anaesthetic, for example carotid endarterectomy as first described by Eastcott et al (1954). This type of procedure can now be safely carried out under LA but does require a large volume of the drug (up to 25 mls, see Table 1 for variations) to infiltrate a very vascular surgical field, and the LA may need supplementing during surgery (AIIman & Wilson 2006). The practice of routinely injecting large volumes of LA agents into surgical wounds to aid post-operative pain control also increases the risk of inadvertent intravascular injection that couldlead to LA toxicity (Parker et al 2009).

From Local to Global

IN clinical practice, lipid emulsion is used commonly as a component of parenteral nutrition. Lipid emulsion also is used as therapy for severe cardiotoxicity secondary to accidental overdose of local anesthetics, an effect that has been confirmed in animals1–3and humans.4,5Because patients with local anesthetic-induced cardiac arrest are considered to be less responsive for standard resuscitation methods, this finding is striking, and currently infusion of lipid emulsion is considered the primary treatment for local anesthetic toxicity. In this issue of Anesthesiology, Rahman et al. 6report a new and potentially clinically relevant benefit of lipid emulsion therapy.Classic preconditioning7produces in the heart a state profoundly protected from ischemia–reperfusion injury; however, the prerequisite for knowing when the ischemic injury will occur has limited the clinical translation and relevance of preconditioning. Recently, a potentially more clinically relevant form of cardiac protection, termed postconditioning, has been described.8Postconditioning involves the application of protective interventions (e.g. , brief ischemia–reperfusion, volatile anesthetics, opioids, and other classic cardioprotective agents) after ischemia but before reperfusion.Rahman et al. extend the list of postconditioning agents to include Intralipid (Sigma, St. Louis, MO). They show that lipid emulsion infusion just before reperfusion (i.e. , postconditioning) protects from myocardial ischemia–reperfusion injury.9Subsequent mechanistic studies define a role for glycogen synthase kinase-3β and the mitochondrial permeability transition pore (mPTP) in this response. Mitochondria, a source of cellular adenosine triphosphate, are increasingly implicated in cell survival and death signaling in the heart. In particular, the mPTP has been suggested as the final effector in cardiac myocyte protection.10The mPTP opening in response to stress leads to an increase in mitochondrial membrane permeability to small molecules, resulting in cellular apoptosis and necrosis. Thus, regulating the mPTP opening has been considered to be a promising target for cardiac protection, and others have suggested the involvement of mPTP in postconditioning.11,12Postconditioning is mediated via a complex molecular signaling cascade involving the reperfusion injury salvage kinase and the survivor activating factor enhancement pathways.13Rahman et al. implicate common survival pathways, such as PI3K-Akt and ERK, in lipid emulsion-induced protection. In addition, they link these upstream survival kinases to downstream regulation of glycogen synthase kinase-3β. Recent work has shown that increased phosphorylation of glycogen synthase kinase-3β reduces the affinity of the adenine nucleotide translocase for cyclophilin D, suggesting that assembly of the complex is targeted by protective signals to limit mPTP opening.14Thus, there appears to be a direct link between survival kinase regulation and mPTP end effector function.These intriguing findings by Rahman et al. leave us with some important questions to be addressed in future investigation. First, how does lipid emulsion activate survival kinases—via a direct effect or secondary to receptor stimulation? General protective interventions appear to signal through G-protein–coupled receptor pathways,15including preconditioning and postconditioning via opioids, volatile anesthetics, and other cardioprotective agents. It would be important to determine whether lipid emulsion is sensitive to G-protein–coupled receptor inhibition. Second, does intra-lipid modulate membrane lipid composition to modulate cardiac protection? Signaling components involved in cardioprotection are localized in membrane microdomains (i.e. , lipid rafts and caveolae) that are enriched in cholesterol and sphingolipids.16,17A recent publication suggests there may be some link between lipid emulsion and caveolin18; however, a direct effect of lipid emulsion on caveolins was not tested in this study. Other studies show that perturbing caveolae can alter survival kinase signaling critical to protection from cardiac and neuronal ischemia–reperfusion injury.19–24It would be interesting to know whether Intralipid, being a lipid emulsion, affects membrane microdomains such as lipid rafts and caveolae to produce protection. Third, does the protective effect of lipid emulsion identified in this study play some role in the effects of propofol (where 10% lipid emulsion is the vehicle) that have been noted in ischemia–reperfusion injury? The potential protective effects of propofol are controversial,25,26and the lipid emulsion effects need to be considered separately from the potential direct effects of propofol. Studies using fospropofol (a water-soluble formulation of a phosphate ester prodrug of propofol) may be useful in resolving this issue.In summary, the current study by Rahman et al. focuses on a potentially important role for lipid emulsion in cardiac protection. Additional studies are needed to focus on mechanisms and potential clinical trials in humans. If similar protective effects are demonstrated in patients, lipid emulsion may play a novel and important role as a therapeutic intervention for patients with ischemic heart disease.* Department of Anesthesiology, University of California, San Diego, La Jolla, California. † Department of Anesthesiology, University of California, San Diego, and Veterans Affairs San Diego Healthcare System, San Diego, California. hepatel@ucsd.edu

Treatment of local-anesthetic toxicity with lipid emulsion therapy

The use of lipid emulsion to treat local-anesthetic toxicity is discussed. Systemic toxicity from local anesthetics is a rare but potentially fatal complication of regional anesthesia. There is increasing evidence that lipid emulsion may be an effective treatment to reverse the cardiac and neurologic effects of local-anesthetic toxicity. A literature search identified seven case reports of local-anesthetic toxicity in which lipid emulsion was used. Lipid emulsion was found to be successful in the treatment of local-anesthetic toxicity associated with various regional anesthetic techniques and multiple local anesthetics. The majority of patients in the case reports reviewed were unresponsive to initial management of local-anesthetic toxicity with standard resuscitative measures, but all recovered completely after receiving lipid emulsion therapy. The initial dose of lipid emulsion administered varied among the case reports, as well as whether a lipid emulsion infusion was started and at what point during resuscitation. Based on the case reports reviewed, an initial bolus dose of 1.5 mL/kg followed by an infusion of 10 mL/min as soon as local-anesthetic toxicity is suspected seems most beneficial. The pharmacokinetics of lipid emulsion therapy in the treatment of local-anesthetic toxicity has not been fully elucidated but likely involves increasing metabolism, distribution, or partitioning of the local anesthetic away from receptors into lipid within tissues. Lipid emulsion has been reported useful in the treatment of systemic toxicity caused by local anesthetics. The mechanism of effect is unclear, and evidence for the benefit of lipid therapy in humans is from case reports only.

Instillagel, lipid rescue and the Medicines and Healthcare products Regulatory Agency

Lipid rescue for the treatment of local anaesthetic toxicity is becoming increasingly recognised. The first published case reports of its use in humans appeared in 2006, and by December 2007, more than 80% of hospitals surveyed had adopted lipid rescue [1]. Instillagel® (Farco-Pharma, Koln, Germany) is a 2% lidocaine gel, commonly used to aid catheterisation. It comes in both 6-ml (120 mg) and 11-ml (220 mg) prefilled syringes. The maximum advised lidocaine dosage for injection is 200 mg, or 500 mg for adrenaline-containing solutions [2]. Regarding topical application, the product information states that for doses of up to 800 mg (equates to 40 ml) instilled in the urethra, blood concentration remains in the low range and below toxic levels [3]. Traumatic catheterisation can increase absorption. The manufacturer states that Instillagel should not be used in patients with damaged or bleeding mucous membranes because of the risk of systemic absorption [3]. During difficult urethral catheterisation, trauma may occur and several doses of Instillagel may have been used, running the risk of systemic toxicity. Anecdotal evidence suggests this has resulted in cardiac arrest. The product guidelines for overdose recommend ‘arresting the convulsions and ensuring adequate ventilation with oxygen’ [3]. However, lipid rescue, which is recommended by the UK Resuscitation Council in suspected local anaesthetic toxicity and induced cardiac arrest, is not mentioned [4]. One distributor for Instillagel recommends suxamethonium for local anaesthetic-induced convulsions [5]. We asked the UK Instillagel distributor, CliniMed (CliniMed Ltd., High Wycombe, Bucks., UK) why lipid rescue was not mentioned. They contacted their manufacturers, Farco-Pharma, and they informed us that any amendments to the summary of product characteristics were made following advice from the Medicines and Healthcare products Regulatory Agency (MHRA). We then contacted the MHRA, which told us that lipid rescue was an interesting new treatment strategy but one that should still be regarded as experimental. They felt that the use of lipid emulsions in this way is ‘off-label’, and the MHRA would not expect distributors to include lipid therapy in the summary of product characteristics. We would suggest that many practitioners are not fully aware of the risks associated with Instillagel, seeing it more as a lubricant than as a local anaesthetic. The MHRA does not feel that manufacturers of any local anaesthetic containing products need to update their product characteristic advice to include lipid rescue in treatment of overdose. We believe that this should now be amended. No external funding and no competing interests declared.

Intralipid reverses coma associated with zopiclone and venlafaxine overdose

Intralipid reverses coma associated with zopiclone and venlafaxine overdose

Intravenous lipid emulsion for treatment of local anesthetic toxicity

Clinical questionIs intravenous lipid emulsion a safe and effective therapy for the reversal and treatment of local anesthetic toxicity?ResultsSystematic reviews, human case reports, and experimental animal studies have demonstrated the efficacy of intravenous lipid emulsion therapy in successfully reversing cardiac arrhythmias, cardiac arrest, and cardiac collapse seen with severe systemic local anesthetic toxicity. There are fewer data to support treatment of neurologic toxicities associated with local anesthetics.ImplementationIntravenous lipid emulsion 20% should be available whenever patients receive large doses of local anesthetics in operating rooms and emergency departments. Various dosing protocols have been published in the medical literature. Although the dosing protocols are based on low-level evidence, a lack of major adverse events makes lipid emulsion an appropriate therapy for treating cardiotoxic symptoms induced by local anesthetics.

Dose of lipid emulsion in obstetric anaesthesia in the UK

We read with interest the article on the availability of lipid emulsion in obstetric anaesthesia in the UK and would like to congratulate the authors [1]. Our hospital had drafted its own protocol for use of Intralipid before the AAGBI guidelines [2] were published. We feel the need to highlight the fact that the above article says that most labour wards included in the survey used regimens that were based on two versions suggested by Weinberg et al. [3, 4]. On referring to the original articles, most of the references included by the authors and the AAGBI guidelines on the use of Intralipid for treatment of local anaesthetic toxicity, we found that all recommend the dose of Intralipid as 1.5 ml.kg−1 of 20% solution which amounts to 21 g for a 70-kg patient. Williamson and Haines mention a dose of 1.5 mg.kg−1 of Intralipid 20% which amounts to 105 mg for a 70-kg patient. There is a huge dose difference in the two mentioned dose regimens and it needs to be clarified that the dose recommended in all the references is ml.kg−1 of 20% Intralipid solution rather than mg.kg−1.

Intravenous lipid emulsion for local anesthetic toxicity: A review of the literature

The use of intravenous lipid emulsion (IVLE) has been proposed as a new potential treatment for local anesthetic toxicity. Local anesthetics work through reversible binding at sodium channels, and signs and symptoms of toxicity include central nervous system and cardiovascular effects. Cardiovascular collapse is a potential result of local anesthetic toxicity, and is generally resistant to resuscitation efforts with standard measures. Various animal studies have been published investigating the use of IVLE in local anesthetic toxicity. IVLE has been shown to increase the lethal dose of bupivacaine required, resuscitate animals that underwent local anesthetic-induced cardiovascular collapse, and more quickly reduce the amount of local anesthetic in the myocardium (compared to administration of control solution). Four human case reports utilizing IVLE for presumed local anesthetic toxicity, with varying presentations, are reviewed. IVLE has shown to be an interesting prospect for local anesthetic toxicity. Human case reports have shown successful resuscitation with use of IVLE, using varying dosing regimens. More studies are needed to determine the optimal dosing regimen, as well as to determine the potential adverse effects of IVLE when used in this setting.

Intravenous Lipid Infusion in the Successful Resuscitation of Local Anesthetic-Induced Cardiovascular Collapse After Supraclavicular Brachial Plexus Block

We describe a case of successful resuscitation with an i.v. lipid infusion of local anesthetic-induced cardiovascular toxicity after supraclavicular brachial plexus block with mepivacaine and bupivacaine. Lipid therapy was initiated after 10 min of unsuccessful resuscitation and resulted in restoration of cardiovascular activity and hemodynamic stability. This case illustrates the utility of i.v. lipid therapy in the treatment of local anesthetic toxicity.

Lipid Emulsion for the Treatment of Local Anesthetic Toxicity: Patient Safety Implications

Lipid Emulsion for the Treatment of Local Anesthetic Toxicity: Patient Safety Implications

Successful Resuscitation After Ropivacaine and Lidocaine-Induced Ventricular Arrhythmia Following Posterior Lumbar Plexus Block in a Child

We report the case of a 13-yr-old girl scheduled for knee surgery under general anesthesia and posterior lumbar plexus block. A ventricular arrhythmia developed 15 min after local anesthetic injection. A 20% lipid emulsion was successful in converting the ventricular arrhythmia to a sinus rhythm. This is consistent with previous reports suggesting that lipid emulsion is an effective emergency treatment of local anesthetic toxicity. We recommend the immediate availability of lipid emulsion along with other emergency therapeutics in operating rooms where local anesthetics are used.

Lipid Reversal of Central Nervous System Symptoms of Bupivacaine Toxicity

Lipid Reversal of Central Nervous System Symptoms of Bupivacaine Toxicity