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Understanding What is the last syndrome of lidocaine?

4 min read

Local Anesthetic Systemic Toxicity (LAST) is a rare, life-threatening complication of local anesthetics, including lidocaine, with severe instances occurring in as few as 1 in 10,000 epidurals. Understanding what is the last syndrome of lidocaine? is crucial for prompt recognition and treatment to prevent serious morbidity or mortality.

Quick Summary

A severe and potentially fatal complication of local anesthetic use, LAST primarily affects the central nervous and cardiovascular systems due to excessive systemic absorption. Prompt intervention is critical to mitigate the risk of severe outcomes.

Key Points

  • Local Anesthetic Systemic Toxicity (LAST): LAST is a serious, rare, and potentially fatal complication of local anesthetic administration, including lidocaine.

  • Causes of LAST: It most often results from inadvertent intravascular injection or overdose, leading to high systemic concentrations of the anesthetic.

  • CNS Effects of Lidocaine LAST: Symptoms often progress from mild signs like metallic taste and tinnitus to severe signs such as seizures and coma.

  • Cardiovascular Effects of Lidocaine LAST: High concentrations can lead to cardiac depression, bradycardia, hypotension, and life-threatening arrhythmias.

  • Atypical Presentations: LAST may present with atypical symptoms, including isolated cardiovascular collapse or a delayed onset, requiring high clinical suspicion.

  • Treatment is Immediate: Management requires immediate cessation of the anesthetic, supportive care, and administration of intravenous lipid emulsion.

  • Prevention is Key: Best practices for prevention include using the lowest effective dose, incremental injection with aspiration, and using ultrasound guidance.

In This Article

What is Local Anesthetic Systemic Toxicity (LAST)?

Local Anesthetic Systemic Toxicity, or LAST, is a rare but life-threatening adverse event that results from an excessive systemic concentration of a local anesthetic, such as lidocaine. While local anesthetics are designed to block nerve signals locally to produce numbness, if they are inadvertently injected into the bloodstream, absorbed rapidly, or administered in a dose that is too high, they can cause systemic toxicity. This occurs because the anesthetic agent then travels throughout the body, affecting other voltage-gated sodium channels in the central nervous system (CNS) and the cardiovascular system (CVS). When LAST is associated with lidocaine, symptoms often follow a classic pattern of CNS effects preceding cardiovascular collapse, though atypical presentations are increasingly reported.

The Classic Progression of Lidocaine LAST

Lidocaine toxicity is characterized by a dose-dependent progression of symptoms that begins with CNS manifestations and, in severe cases, leads to cardiovascular dysfunction.

Central Nervous System (CNS) Effects

For awake patients, CNS signs are typically the earliest indicators of an overdose. The classic progression includes:

  • Early warning signs: Patients may report symptoms such as circumoral (around the mouth) numbness, a metallic taste, tinnitus (ringing in the ears), dizziness, lightheadedness, and slurred speech (dysarthria).
  • Excitatory phase: As plasma concentrations rise, patients may develop restlessness, agitation, confusion, or visual disturbances. This can escalate to muscle twitching, tremors, and finally, generalized tonic-clonic seizures.
  • Depressive phase: With very high plasma levels, the initial excitatory phase is overwhelmed, leading to CNS depression, unconsciousness, coma, and respiratory arrest.

Cardiovascular (CV) Effects

Cardiac toxicity often manifests after CNS signs in lidocaine toxicity, but it represents the most critical and life-threatening aspect of LAST. Cardiovascular symptoms include:

  • Initial hypertension and tachycardia.
  • As toxicity worsens, myocardial contractility is depressed, and cardiac conduction is blocked.
  • This leads to profound hypotension, bradycardia, and various arrhythmias, including ventricular tachycardia (VT), ventricular fibrillation (VF), and asystole.
  • Ultimately, this can result in cardiovascular collapse and death.

Causes and Risk Factors for Lidocaine LAST

Causes

The most frequent cause of LAST is the inadvertent injection of a local anesthetic directly into a blood vessel. Other contributing factors include:

  • Administering a dose that exceeds the maximum recommended dose (overdose).
  • Rapid systemic absorption from highly vascularized injection sites (e.g., intercostal, caudal, or large nerve blocks).
  • Repeat dosing or continuous infusion methods can lead to accumulating toxic levels.

Risk Factors

Certain patient and procedural factors can increase the risk of developing LAST:

  • Patient Factors:
    • Extremes of age (<6 years or >60 years).
    • Low muscle mass (infants, elderly, frail).
    • Preexisting cardiovascular disease, liver or kidney disease.
    • Pregnancy.
    • Metabolic or respiratory acidosis.
    • Lower levels of protein binding (e.g., liver disease).
  • Procedural Factors:
    • Peripheral nerve blocks, particularly those involving large volumes.
    • Techniques where intravascular injection is more likely or absorption is rapid.
    • Failure to use ultrasound guidance or aspiration before injection.

Lidocaine LAST vs. Bupivacaine LAST: A Comparison

Feature Lidocaine Bupivacaine
Onset of Toxicity Typically exhibits CNS symptoms before progressing to cardiovascular effects. More potent and cardiotoxic, so CNS and cardiovascular symptoms may appear simultaneously or with minimal preceding CNS signs.
CNS Toxicity Produces CNS excitatory effects (tremors, seizures) at lower concentrations than those causing severe cardiac effects. High affinity for cardiac sodium channels means CNS excitation may be subtle or absent before cardiovascular collapse.
Cardiovascular Toxicity High doses lead to myocardial depression, bradycardia, and hypotension. Associated with more malignant and refractory arrhythmias, such as ventricular fibrillation, due to slow dissociation from cardiac sodium channels.
Resuscitation Difficulty Cardiac toxicity is generally more responsive to standard resuscitation efforts. Cardiac arrest from bupivacaine toxicity is notoriously difficult to resuscitate.

Diagnosis and Management of a Lidocaine-Induced LAST

Diagnosis of LAST is primarily a clinical one, as immediate action is required without waiting for laboratory results.

Immediate Actions

  • Immediately stop the administration of the local anesthetic.
  • Call for help and activate the emergency response system.
  • Manage the airway, administer 100% oxygen, and provide ventilation as necessary to prevent hypoxia and acidosis, which worsen toxicity.

Pharmacological Treatment

  • Intravenous Lipid Emulsion (ILE): This is a cornerstone of LAST treatment and is administered early in severe cases. It is thought to work by creating a “lipid sink” that sequesters the lipophilic local anesthetic from its target sites in the heart and brain.
  • Seizure Control: Benzodiazepines (e.g., midazolam) are the first-line treatment for seizures caused by LAST.
  • Cardiovascular Support: A modified Advanced Cardiac Life Support (ACLS) protocol is followed. This includes using low-dose epinephrine and avoiding other lidocaine formulations as antiarrhythmics.
  • Advanced Support: In refractory cases of cardiac arrest, extracorporeal membrane oxygenation (ECMO) should be considered.

Prevention of LAST

Preventing LAST involves meticulous technique and heightened awareness of risks. Key strategies include:

  • Use the Lowest Effective Dose: Use the lowest volume and concentration of local anesthetic required for the procedure.
  • Incremental Injection and Aspiration: Inject in small aliquots (e.g., 3–5 mL) with pauses in between, and aspirate before each injection to check for blood, although this has a small false-negative rate.
  • Use of Ultrasound Guidance: Ultrasound-guided nerve blocks significantly reduce the risk of LAST by allowing clinicians to visualize the needle tip and avoid intravascular injection.
  • Monitor High-Risk Patients: Special attention should be paid to patients with known risk factors for at least 30–45 minutes after receiving potentially toxic doses.

Conclusion

Local Anesthetic Systemic Toxicity (LAST) is a critical but treatable emergency that can follow the use of lidocaine. The syndrome typically involves a progressive clinical picture, starting with CNS effects like perioral numbness and tremors, which can advance to seizures, followed by serious cardiovascular complications like hypotension, bradycardia, and cardiac arrest. Early recognition, immediate cessation of the local anesthetic, supportive care, and the rapid administration of intravenous lipid emulsion are the mainstays of effective management. By adhering to safe injection practices, leveraging ultrasound technology, and remaining vigilant, healthcare providers can minimize the risk of LAST and ensure patient safety during procedures involving local anesthetics. Additional information on best practices for preventing and managing LAST is available from authoritative bodies like the American Society of Regional Anesthesia and Pain Medicine (ASRA).

Frequently Asked Questions

Treatment for LAST involves immediate cessation of the anesthetic, managing the patient's airway, controlling seizures with benzodiazepines, and administering intravenous lipid emulsion to counteract the systemic effects of lidocaine.

The initial signs of lidocaine toxicity in an awake patient typically include circumoral (around the mouth) numbness, a metallic taste, tinnitus (ringing in the ears), and dizziness.

The primary cause of LAST is an excessive systemic concentration of a local anesthetic, which is most often caused by accidental injection into a blood vessel (intravascular injection) or by administering an overdose.

While both can cause LAST, bupivacaine is considered more cardiotoxic and its associated cardiac arrest is more difficult to resuscitate. Lidocaine primarily causes CNS toxicity before affecting the heart.

Yes, LAST can occur with topical lidocaine, particularly with high concentrations, prolonged exposure, or application to a large surface area or compromised skin barrier, leading to excessive systemic absorption.

The 'lipid sink' theory proposes that intravenous lipid emulsion creates a separate lipid phase in the bloodstream that sequesters the lipophilic local anesthetic, reducing its availability to act on the heart and brain and mitigating its toxic effects.

Ultrasound guidance significantly reduces the risk of LAST during nerve blocks by allowing the clinician to visually confirm the needle's location and avoid inadvertent intravascular injections.

References

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.