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Local Anesthetic Toxicity Treatment & Management

  • Author: Raffi Kapitanyan, MD; Chief Editor: Asim Tarabar, MD  more...
Updated: Apr 30, 2016

Approach Considerations

In the patient with suspected local anesthetic toxicity, the initial step is stabilization of potential threats to life. If the signs and symptoms develop during administration of the local anesthetic, stop the injection immediately and prepare to treat the reaction. Ensure adequate oxygenation, whether by face mask or by intubation.

Attention to impending airway compromise, significant hypotension, dysrhythmias, and seizures takes precedence. Once other possible etiologies of the patient's new symptoms have been excluded, management of the specific symptoms can begin.

Benzodiazepines are the drugs of choice for seizure control. Propofol can be used to control seizures but has the risk of potentiating cardiovascular toxicity. Refractory seizures may require neuromuscular blockade (eg, with succinylcholine).

In severe reactions, monitor the cardiovascular system and support the patient with intravenous fluids and vasopressors as required. Small bolus doses of epinephrine are preferred. Vasopressin is not recommended.

Hypoxemia and metabolic acidosis may potentiate the cardiovascular toxicity of lidocaine and other local anesthetics. Early control of seizures and aggressive airway management to treat hypoxemia and acidosis may prevent cardiac arrest. Use of sodium bicarbonate may be considered to treat severe acidosis.

Cardiac arrest due to local anesthetic toxicity is a rare but well recognized complication that may occur in cases of large overdose, especially those involving inadvertent intravascular injection. These patients have a favorable prognosis if circulation can be restored before hypoxemic injury occurs. Aggressive resuscitation is therefore indicated in most cases. Cardiopulmonary bypass has been used effectively to treat cardiac arrest due to local anesthetic toxicity.[5]

Increasing evidence suggests that the intravenous (IV) infusion of lipid emulsions can reverse the cardiac and neurologic effects of local-anesthetic toxicity. Although no blinded studies have been conducted in humans, studies in animal models and multiple case reports in human patients have shown favorable results. Indeed, case reports support the early use of lipid emulsion at the first sign of arrhythmia, prolonged seizure activity, or rapid progression of toxic manifestations in patients with suspected local anesthetic toxicity.[1]

Infrequently, local anesthetics may provoke an allergic or hematologic reaction. Allergic reactions can be treated with diphenhydramine or, for more serious reactions, epinephrine or corticosteroids. Methemoglobinemia should initially be treated symptomatically. Subsequent treatment is guided by blood levels of methemoglobin; methylene blue and hyperbaric oxygen may be required in severe cases. See Methemoglobinemia for specific treatment.

Local ischemic or nerve toxicities may occur, particularly in the extremities with prolonged anesthesia or use of agents containing epinephrine. Suspected nerve damage should prompt neurologic consultation for urgent peripheral nerve studies. If vascular compromise, such as limb ischemia, is suspected, consult a vascular surgeon immediately. Therapy for extravasation (eg, warm compresses, phentolamine, nitroglycerin cream) should be initiated for localized vascular toxicity.

Patients with persistent or unresolved significant reactions require admission to a monitored bed for observation, further evaluation, and treatment. Patients who are stable and have minor or easily controlled adverse reactions can be discharged and monitored on an outpatient basis.

Finally, the prevention of local anesthetic toxicity should always be the primary consideration. Although all adverse reactions cannot be anticipated, complications can be minimized by strict adherence to the guidelines of anesthetic dosing, identification of patients at increased risk, and implementation of appropriate anesthetic application techniques to avoid unintentional intravascular injection.


Guidelines for the management of local anesthetic toxicity have been published by the following groups:

  • American Society of Regional Anesthesia and Pain Medicine (ASRA) [1]
  • Association of Anaesthetists of Great Britain and Ireland (AAGBI) [6]
  • Resuscitation Council of the UK [7]

Treatment of Central Nervous System Toxicity

Treatment of central nervous system (CNS) complications and toxicity remains controversial. Seizures have been treated successfully with benzodiazepines or barbiturates (eg, phenobarbital); case reports indicate that 1 mg/kg of intravenous propofol (Diprivan) and 2 mg/kg of intravenous thiopental (Pentothal) are successful in stopping local anesthetic-induced seizures and muscle twitching.

The American Society of Regional Anesthesia and Pain Control (ASRA) recommends benzodiazepines as first-line treatment of local anesthetic–induced seizures, because these drugs have limited potential for causing cardiac depression. If seizures persist despite benzodiazepines, the ASRA recommends considering the use of small doses of succinylcholine or a similar neuromuscular blocker, to minimize acidosis and hypoxemia.[1] Use of a neuromuscular blocker requires intubation.

If benzodiazepines are not available, the ASRA considers propofol or thiopental acceptable alternatives, but notes that these agents should be used at their lowest effective dose, because of their potential to worsen hypotension or cardiac depression.[1] In particular, propofol should be avoided in patients showing signs of cardiovascular instability, as it can cause significant bradycardia.


Treatment of Cardiovascular Toxicity

Prolonged PR, QRS, and QT intervals potentiating reentrant tachycardias with aberrant conduction may herald cardiovascular toxicity. Cardiac resuscitation of such patients may be difficult and prolonged (30-45 min) because some anesthetics are very lipid soluble and require a long time for redistribution. However, some of these patients can be successfully treated with properly conducted cardiopulmonary resuscitation (CPR).

If cardiac arrest occurs, the ASRA recommends standard Advanced Cardiac Life Support (ACLS) with the following modifications:

  • If epinephrine is used, small initial doses (10-100 μg boluses in adults) are preferable
  • Vasopressin is not recommended
  • Avoid calcium channel blockers and beta-blockers
  • If ventricular arrhythmias develop, amiodarone is preferable

In patients with cardiac toxicity, avoiding the use of lidocaine and related class IB antidysrhythmic agents (eg, mexiletine, tocainide) is crucial because they may worsen toxicity. Lidocaine has been used successfully in bupivacaine-induced dysrhythmias, but its additive CNS toxicity is still a major concern.

In patients who do not respond to standard resuscitative measures, some case reports have indicated that the use of cardiac pacing and cardiopulmonary bypass may improve the outcome.[2] Cardiopulmonary bypass may serve as a bridging therapy until tissue levels of the local anesthetic have cleared.[1]

In a Korean study, combined boluses of glucose, insulin, and potassium were successful in reversing bupivacaine-induced cardiovascular collapse.[8] However, the 2 units/kg dose of insulin used in this protocol may be challenging to use in clinical practice because of physicians' reluctance to administer such unusually high doses. In China, shenfu, an extract of traditional Chinese herbal medicines, was shown to reduce the CNS and cardiovascular toxicity of bupivacaine on rats.[9]


Lipid Emulsion Therapy

IV infusion of a 20% lipid emulsion (eg, Intralipid 20%) has become an accepted part of treatment for systemic toxicity from local anesthetics, and particularly for cardiac arrest that is unresponsive to standard therapy. ASRA guidelines recommend considering the use of lipid emulsion therapy at the first signs of systemic toxicity from local anesthetics, after airway management.[1]

The proposed mechanism is that lipid infusion creates a lipid phase that extracts the lipid-soluble molecules of the local anesthetic from the aqueous plasma phase (lipid sink hypothesis). A beneficial energetic-metabolic effect may also occur.[10] An in vitro study demonstrated high solubility of local anesthetics in lipid emulsions and high binding capacity of these emulsions.[11]

In an animal model, Weinberg et al demonstrated the successful application of lipid emulsion infusion in the resuscitation of bupivacaine-induced cardiac arrest.[12, 13] Rosenblatt and colleagues were the first to report use of a 20% lipid infusion to resuscitate a patient from prolonged cardiac arrest that followed an interscalene block with bupivacaine and mepivacaine.[14]

Subsequent case reports from other researchers documented successful use of lipid emulsion in the treatment of both cardiovascular and neurologic toxicity, including asystole, cardiovascular collapse, and seizures. Local anesthetic agents involved in these cases have included ropivacaine, mepivacaine and prilocaine, and levobupivacaine.[15, 16, 17, 18, 19, 20]

Marwick and colleagues reported a case of successful lipid rescue in which systemic toxicity recurred after 40 minutes. Since additional lipid supply was not available, amiodarone was used for the recurrent dysrhythmia. This case highlights the importance of the availability of a sufficient quantity of lipid emulsion (1000 mL) when regional anesthesia is performed.[21]

Weinberg and colleagues, using an intact animal model of bupivacaine overdose, have shown that lipid emulsion therapy provides superior hemodynamic and metabolic recovery from bupivacaine-induced cardiac arrest than do either epinephrine or vasopressin.[22, 23] Both of these vasopressors were associated with adverse outcomes.

However, several reports question the efficacy of lipid rescue treatment. Mayr et al, working with a porcine model of bupivacaine toxicity, reported that vasopressin combined with epinephrine resulted in higher coronary perfusion pressure during CPR and better short-term survival rates than lipid emulsion.[24] Harvey et al showed that lipid emulsion/ACLS resulted in lower coronary perfusion pressure and lower rates of spontaneous circulation compared with ACLS alone in a rabbit model of asphyxial cardiac arrest.[25]

A range of adverse events have been reported after acute infusion of lipid emulsion. These have included acute kidney injury, cardiac arrest, ventilation-perfusion mismatch, acute lung injury, venous thromboembolism, hypersensitivity, fat embolism, fat overload syndrome, pancreatitis, extracorporeal circulation machine circuit obstruction, allergic reaction, and increased susceptibility to infection.[26]

Recommended dosing regimen

Lipid emulsion therapy is performed with a 20% solution.[7] First, administer a bolus of 1.5 mL/kg over 1 minute.[27, 6, 1] Then convert to an infusion at a rate of 0.25 mL/kg/min for 20 minutes,[6] 30-60 minutes,[27] or until hemodynamic stability is restored.[1]

If this regimen does not provide adequate resuscitation, several options have been suggested. Bolus doses may be repeated up to 2 times, possibly at 5-minute intervals,[6] or repeated at 5-minute intervals until stable rhythm is restored. Alternatively, the infusion rate may be increased[27] (eg, to 0.5 mL/kg/min for 10 minutes[1, 6] ). The recommended upper limit of lipid emulsion is approximately 10 mL/kg over the first 30 minutes.[1]

Note that propofol is not a component of lipid rescue. It is formulated in a 10% lipid emulsion, and, therefore, an overdose of propofol (gram quantities) would be necessary to provide an adequate dose of lipid emulsion. Propofol is contraindicated when any evidence of cardiovascular toxicity is present.[1]


Treatment of Allergic Reactions

Although allergic reactions to local anesthetics are extremely rare, these are treated according to severity. Mild cutaneous reactions may be treated with oral or intravenous (IV) diphenhydramine (Benadryl, 25-50 mg for adults, 1 mg/kg for pediatric patients).

For more serious allergic reactions, administer subcutaneous epinephrine (0.3 mL of 1:1000 dilution) and closely monitor for further decompensation. Corticosteroids (125 mg methylprednisolone IV push, or 60 mg prednisone orally) should be given to the patient with severe allergic reactions (eg, respiratory distress, hypotension).



The following suggestions may help avoid complications related to local anesthetic use, especially in emergency department patients:

  • Consider obtaining and documenting informed consent in individuals with a prior history of anesthetic reactions
  • Document the amount and type of anesthetic used during the procedure
  • Always obtain an adequate history and physical examination to identify risk factors and allergies
  • Do not use class IB antidysrhythmics (including phenytoin) for seizures or dysrhythmias believed to be due to cocaine toxicity
  • Consider changes in neurologic signs or symptoms as a possible manifestation of anesthetic toxicity
  • Admit patients with serious or unresolved symptoms

Know the toxic dose of the local anesthetic being used. Use the lowest concentration and volume of local anesthetic that still produces good results. Add epinephrine at a ratio of 1:200,000 to slow vascular uptake through vasoconstriction.

Describe the early symptoms of local anesthetic overdose to patients and instruct them to inform the physician if they experience any of these effects. Be sure that patients understand the effects of local anesthetics and that they should tell the physician if symptoms occur.

A careful injection method may help prevent toxic reactions. Perform high-volume (>5 mL) injections slowly, in 3-mL increments. Stop to aspirate and observe for blood in the syringe after every 3 mL injected. Injecting local anesthetic in this manner reduces the chances of a large-volume intravascular injection.

Maintain verbal contact with the patient during the procedure. This helps detect subtle symptoms, such as dysarthria, as well as more severe ones, such as changes in mental status.

Because benzodiazepines raise the threshold for CNS symptoms but not for cardiovascular symptoms, heavy benzodiazepine premedication is likely to result in a patient progressing directly to cardiovascular toxicity without showing preliminary signs of CNS toxicity.

For more information, see Infiltrative Administration of Local Anesthetic Agents.

Dosage guidelines

Lower concentrations of local anesthetics are typically used for infiltration anesthesia.

Variation in local anesthetic dose depends on the procedure, the degree of anesthesia required, and individual patient circumstances. Use of a reduced dose is indicated in the following patients:

  • Debilitated or acutely ill patients
  • Very young children or geriatric patients
  • Patients with liver disease, atherosclerosis, or occlusive arterial disease
Contributor Information and Disclosures

Raffi Kapitanyan, MD Assistant Professor of Emergency Medicine, Rutgers Robert Wood Johnson Medical School

Raffi Kapitanyan, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Mark Su, MD, MPH, FACEP, FACMT Consulting Staff and Director of Fellowship in Medical Toxicology, Department of Emergency Medicine, North Shore University Hospital

Mark Su, MD, MPH, FACEP, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.


John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Russell F Kelly MD, Assistant Professor, Department of Internal Medicine, Rush Medical College; Chairman of Adult Cardiology and Director of the Fellowship Program, Cook County Hospital

Russell F Kelly is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Lance W Kreplick, MD, FAAEM, MMM Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC

Lance W Kreplick, MD, FAAEM, MMM, is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physician Executives

Disclosure: Nothing to disclose.

Harold L Manning, MD Professor, Departments of Medicine, Anesthesiology and Physiology, Section of Pulmonary and Critical Care Medicine, Dartmouth Medical School

Harold L Manning, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Ruben Peralta, MD, FACS Professor of Surgery, Anesthesia and Emergency Medicine, Senior Medical Advisor, Board of Directors, Program Chief of Trauma, Emergency and Critical Care, Consulting Staff, Professor Juan Bosch Trauma Hospital, Dominican Republic

Ruben Peralta, MD, FACS is a member of the following medical societies: American Association of Blood Banks, American College of Healthcare Executives, American College of Surgeons, American Medical Association, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Massachusetts Medical Society, Society of Critical Care Medicine, and Society of Laparoendoscopic Surgeons

Disclosure: Nothing to disclose.

Michael R Pinsky, MD, CM, FCCP, FCCM Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Association of University Anesthetists, European Society of Intensive Care Medicine, Shock Society, and Society of Critical Care Medicine

Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership; Edwards Lifesciences Honoraria Consulting

Karl A Poterack, MD Consulting Staff, Department of Anesthesiology, Mayo Clinic Scottsdale

Karl A Poterack, MD is a member of the following medical societies: American Society of Anesthesiologists

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Table 1. Epinephrine Content Examples
Solution Volume 1:100,000 (1 mg/100 mL) 1:200,000 (1 mg/200 mL)
1 mL 0.01 mg 0.005 mg
5 mL 0.05 mg 0.025 mg
10 mL 0.1 mg 0.05 mg
20 mL 0.2 mg 0.1 mg
Example: 50 mL of 1% lidocaine with epinephrine 1:100,000 contains lidocaine 500 mg and epinephrine 0.5 mg.
Table 2. Local Anesthetic Agents Used Commonly for Infiltrative Injection
Agent Duration of Action Maximum Dosage Guidelines (Total Cumulative Infiltrative Injection Dose per Procedure*)
Procaine (Novocaine) Short (15-60 min) 7 mg/kg; not to exceed 350-600 mg
Chloroprocaine (Nesacaine) Short (15-30 min) Without epinephrine: 11 mg/kg; not to exceed 800 mg total dose

With epinephrine: 14 mg/kg; not to exceed 1000 mg

Lidocaine (Xylocaine) Medium (30-60 min) Without epinephrine: 4.5 mg/kg; not to exceed 300 mg
Lidocaine with epinephrine Long (120-360 min) With epinephrine: 7 mg/kg
Mepivacaine (Polocaine, Carbocaine) Medium (45-90 min) Long (120-360 min with epinephrine) 7 mg/kg; not to exceed 400 mg
Bupivacaine (Marcaine) Long (120-240 min) Without epinephrine: 2.5 mg/kg; not to exceed 175 mg total dose
Bupivacaine with epinephrine Long (180-420 min) With epinephrine: Not to exceed 225 mg total dose
Etidocaine (Duranest)

No longer available in United States

Long (120-180 min) Without epinephrine: 0.4 mg/kg; not to exceed 300 mg total dose

With epinephrine: 8 mg/kg

Prilocaine (Citanest) Medium (30-90 min) Body weight < 70 kg: 8 mg/kg; not to exceed 500 mg

Body weight >70 kg: 600 mg

Ropivacaine (Naropin) Long (120-360 min) 5 mg; not to exceed 200 mg for minor nerve block
*Nondental use, administer by small incremental doses; administer the smallest dose and concentration required to achieve desired effect; avoid rapid injection.
Table 3. Minimum Intravenous Toxic Dose of Local Anesthetic in Humans [2]
Agent Minimum Toxic Dose (mg/kg)
Procaine 19.2
Tetracaine 2.5
Chloroprocaine 22.8
Lidocaine 6.4
Mepivacaine 9.8
Bupivacaine 1.6
Etidocaine 3.4
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