Do Podiatric Physicians and Surgeons Know How to Resuscitate a Patient From Local Anesthetic Toxicity?

All podiatric physicians and medical professionals should be familiar with signs and treatment of local anesthetic toxicity. However, upon review of several journals, we found it to be concerning that there was no literature regarding the resuscitation from local anesthetic systemic toxicity. On a daily basis, podiatric surgeons and physicians administer local anesthetic and should be aware of the checklists and steps to resuscitate a patient who may have toxicity.

In our opinion, it is strongly recommended that physicians are certified in basic life support (BLS) and advanced cardiac life support (ACLS), take a good physical examination, and have lipid emulsion therapy readily available in every podiatric clinical setting. In this journal review article, we have provided checklists/steps to follow in case a patient has signs and symptoms of local anesthetic systemic toxicity.

Insights on How LAST Occurs and Its Effects on Patients

Upon review of several journals, we found there to be no information regarding resuscitation from local anesthetic systemic toxicity (LAST). We found this to be concerning in case of a podiatric physician and/or podiatric surgeon needing to know how to resuscitate a patient quickly. According to the American College of Podiatric Physicians and Surgeons, approximately 83% of podiatric procedures performed in-office/hospitals/ambulatory surgical centers (ASCs) require local anesthetic and the remaining 17% of podiatric procedures require general anesthesia. The American Society of Regional Anesthesia (ASRA) offers a checklist that is helpful to us and is useful during times of stress when a patient unexpectedly shows signs of severe local anesthetic toxicity. An overdose of intravascular injection of local anesthetics is associated with cardiac toxicity, according to the Anesthesia Patient Safety Foundation (APSF).¹

Primary systemic toxicity usually occurs in the central nervous system (CNS), which will initially experience tremors/convulsions. The cardiac toxicity is characterized by atrioventricular conduction delay, hypotension, ultimately with cardiovascular failure. There have been major developments in understanding treatments for LAST, including early administration of lipid emulsion therapy.

The typical adverse effects due to local anesthetic systemic toxicity most often involves the central nervous system, cardiovascular system (CVS), and hematologic system.¹ Indicators of LAST usually show around 1 to 5 minutes after anesthetic injection. There may be delayed manifestations of LAST, which may appear 60 minutes after injection. Table 1 shows signs and symptoms associated with the systems being affected.² Table 1 notes the initial presentation of CVS symptoms only is about 24%, CNS symptoms only is 43%, and CNS + CVS together is 33%. 

The onset of local anesthetic toxicity is very rapid and potentially fatal, and is most commonly associated with administrative or therapeutic error. There are several types of factors that are associated with administration and the type of drug being used. To achieve the anticipated duration and range of anesthesia, one should give the local anesthetic at the lowest dose that can achieve these two goals. The serum concentration is induced by the dose, method of administration and the site. Local anesthetics may be injected, inhaled, administrated endotracheal tube, or applied topically to skin. The two critical factors for the administration for local anesthetic that should be known is the patient’s weight and the concentration of the local anesthetic that is being administered. Table 2 is a reference for the maximum recommended dosages with and without epinephrine for local anesthetic administration.²

Most adverse effects usually occur within 1 minute of administration of the local anesthetic. However, there can be a delayed onset of greater than 1 hour after the administration of the local anesthetic, demonstrating toxicity. In some situations there can be a delayed onset greater than 1 hour. Another variable that can increase the chances of LAST depends on which local anesthetic one uses. The more lipophilic the local anesthetic, the increased chances of toxicity. According to the choices of drugs in Table 3, for example, bupivacaine is more lipid soluble than mepivacaine. The dosage of administration is substantially less due to it being more potent, which can result in an amplified occurrence of local toxicity. Lastly, according to the American Society of Regional Anesthesia and Pain Medicine, epinephrine is typically added to low doses of local anesthetic solution to reduce the systemic absorption and maximum local anesthetic plasma concentrations.³

Preventing and Treating LAST

Most anesthetics are administered through peripheral nerve blocks, spinal/neuroaxial anesthesia, and combined spinal epidurals (CSE). Peripheral nerve blocks are the most common route of the administration of local anesthetics in a podiatric clinical setting. Podiatric physicians should be equipped and prepared for LAST treatment. Advanced cardiac life support and the administration of 20% lipid emulsion are the mainstay treatment remedies for LAST. One study states that 20% intralipid formula consists of 20% soybean oil, 1.2% egg yolk phospholipids, 2.25% glycerin, water, and sodium hydroxide.⁴ The shelf life for lipid emulsion is 24 months. We recommend physicians have 20% intralipid formula readily available for emergency use in podiatric clinical setting. We noted that one medical supply vendor, at time of writing this piece, was selling a case of 12 of 20% Lipid Emulsion, 500mL each, for the price of $222.17, which is less expensive than paying attorney fees for a malpractice claim.

The American Society of Regional Anesthesia (ASRA) has developed a procedure checklist to be followed for the stabilization of a patient undergoing local anesthetic systemic toxicity (Figure 1).⁵

There are multiple theories describing how local anesthetic systemic toxicity affect the body, but one major effect is the mitochondrial oxidative-phosphorylation pathway. Essentially the local anesthetic toxicity disables cells from regenerating adenosine triphosphate (ATP) for energy. Without the energy production of ATP for major organs such as the heart, lungs, and brain, normal conduction is disrupted, and then we see the symptoms of LAST-induced arrest. This is when one would administer the 20% lipid emulsion, which has a mechanism of action by a protein-type lipid mechanism that acts like a sink that draws in local anesthetic and binds it up. Local anesthetics such as bupivacaine are very lipophilic, meaning they are able to dissolve or combine with lipids and/or fats. When a patient experiences toxicity, the lipid emulsion begins to make a lipid compartment in the bloodstream called a “lipid sink” or lipid reservoir.⁴ The local anesthetics are then drawn away from areas with high plasma concentrations/ high perfusion tissues such as the heart, lungs, and brain to the lipid reservoir compartment. Once the local anesthetic enters the lipid reservoir, it is then reallocated to liver for detoxification and muscle for storage.⁶ The lipid compartment works rapidly and has been indicated to improve the cardiac output and blood pressure.

The Anesthesia Patient Safety Foundation (APSF) and the AHA suggest the use of cardiac arrest drugs such as high-dose epinephrine can be counterproductive in treatment of LAST.⁵ Therefore, the AHA and APSF recommend using the lowest dose of epinephrine in local anesthetic solution, because epinephrine could be used later in higher doses if one were to have a LAST reaction.⁷ After successfully resuscitating and stabilizing the patient from local anesthetic toxicity, admit the patient to the intensive care setting for 24 hours of monitoring and have them re-evaluated. As needed, consult cardiology, nephrology, and neurology and other medical specialties to check so there are no residual cardiac, renal, or neurological dysfunctions, etc.  

The best prevention and treatment for local anesthetic toxicity on the market currently today is the immediate availability of 20% lipid for immediate resuscitation of local anesthetic toxicity. These resources are efficient and readily available to every podiatric physician. We strongly recommend podiatric physicians to be BCLS- and ACLS-certified. BCLS- and ACLS-trained podiatric physicians along with readily available 20% lipid emulsion and the low dose administration of the least potent local anesthetics all combine to provide a reasonable margin of safety for the patient.

In Conclusion

We urge podiatric physicians to perform a good physical diagnosis and patient selection for surgical procedures involving local anesthetics. The podiatric physician is intimately aware that aside for providing care for the lower extremity, attention must always be provided systemically to the patient as a whole. Podiatric physicians and surgeons should be aware of local anesthetic toxicity and the treatment modality for the local anesthetic toxicity. 

Beverly Cirella, BS, is a fourth year podiatric medical student at Barry University School of Podiatric Medicine, Class of 2023.

Robert Miller, DO, is a member of the ACLS Faculty, Wheeling Hospital/WVU Medicine in Wheeling, WV.

Stanley R. Dennison Jr., MD, MBA, is a Clinical Assistant Professor in the Anesthesia Assistant Program, Nova Southeastern University. He is the Medical Director of South Tampa Surgery Center.

References
1. Weinberg G, Rupnik B, Aggarwal N, Fettiplace M, Gitman M. Local anesthetic system toxicity (LAST) revisited: a paradigm in evolution. Anesthesia Patient Safety Foundation. 2020;35(1):1–7.
2. El-Boghdadly K, Pawa A, Chin KJ. Local anesthetic systemic toxicity: current perspectives. Local Reg Anesth. 2018; 11:35–44. https://doi.org/10.2147/LRA.S154512
3. Neal JM, Barrington MJ, Fettiplace MR, et al. The Third American Society of Regional Anesthesia and Pain Medicine Practice Advisory on Local Anesthetic Systemic Toxicity: Executive Summary 2017. Reg Anesth Pain Med. 2018;43(2):113–123.
4. Rothschild L, Bern S, Oswald S, Weinberg G. Intravenous lipid emulsion in clinical toxicology. Scand J Trauma Resusc Emerg Med. 2010; 18:51. https://doi.org/10.1186/1757-7241-18-51
5. Neal JM, Weinberg GL. A checklist for treating local anesthetic systemic toxicity. Anesthesia Patient Safety Foundation. 2012;27(1):13–27. doi:https://www.apsf.org/article/a-checklist-for-treating-local-anesthetic-systemic-toxicity/.
6. Sepulveda EA, Pak A. Lipid emulsion therapy. [Updated 2021 Jul 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549897/
7. Sekimoto K, Tobe M, Saito S. Local anesthetic toxicity: acute and chronic management. Acute Med Surg. 2017; 4(2):152–160. https://doi.org/10.1002/ams2.265