Understanding Lidocaine and Its Primary Use
Lidocaine is a local anesthetic of the amino amide type, first synthesized in 1946 and sold since 1948. Its primary mechanism of action is blocking voltage-gated sodium channels in nerve cells. This blockage prevents the transmission of pain signals from a specific area of the body to the brain, resulting in temporary numbness. Because of its rapid onset and intermediate duration of action, it is widely used for minor surgical procedures, dental work, epidurals, and nerve blocks. It is also classified as a class Ib antiarrhythmic medication used to treat certain heart rhythm disorders like ventricular tachycardia.
How Lidocaine Enters the Bloodstream
While lidocaine is intended to act locally, it can be absorbed into the systemic circulation. Systemic toxicity occurs when the plasma concentration of lidocaine reaches a toxic level. This can happen in several ways:
- Inadvertent Intravascular Injection: The most common cause of rapid-onset toxicity is accidentally injecting the anesthetic directly into a blood vessel, like an artery or vein.
- Rapid Absorption from Highly Vascular Tissues: Injecting lidocaine into areas with a rich blood supply (like the scalp or intercostal spaces) can lead to faster absorption into the bloodstream than intended.
- Excessive Dosage: Using too large a dose of lidocaine, even when administered correctly, can overwhelm the body's ability to metabolize it, leading to a gradual rise in plasma levels.
- Application to Non-Intact Skin: Applying topical lidocaine to broken skin, burns, or large surface areas can increase absorption into the bloodstream.
The Progression of Lidocaine Toxicity (LAST)
Local Anesthetic Systemic Toxicity (LAST) typically presents with a progression of symptoms, often starting with the central nervous system (CNS) and potentially advancing to the cardiovascular system (CVS). However, atypical presentations are common, with some patients showing only cardiac signs or a delayed onset of symptoms.
Central Nervous System (CNS) Manifestations
In an awake patient, the initial signs of toxicity are often neurological. These symptoms are dose-related and can progress rapidly.
- Early/Mild Symptoms: The first signs often include numbness or tingling around the mouth (circumoral numbness), tongue paresthesia, a metallic taste in the mouth, dizziness, and ringing in the ears (tinnitus). Patients may also experience blurred vision, agitation, confusion, or nervousness.
- Moderate to Severe Symptoms: As plasma levels rise, these excitatory signs can worsen, leading to muscle twitching, tremors, and eventually generalized tonic-clonic seizures. Seizures are the most common major feature of LAST.
- Late Stage CNS Depression: With a large overdose, the initial excitatory phase is followed by CNS depression, which can manifest as drowsiness, unconsciousness, coma, and respiratory arrest.
Cardiovascular System (CVS) Manifestations
Major cardiovascular toxicity usually requires a higher concentration of lidocaine in the blood than what causes CNS symptoms. However, in some cases, especially with a direct intravascular injection, cardiac symptoms can appear suddenly and without preceding neurological signs.
- Early Signs: Initially, there may be a brief period of hypertension and tachycardia (fast heart rate).
- Progressive Signs: This is followed by more severe cardiovascular depression, including hypotension (low blood pressure) and bradycardia (slow heart rate).
- Severe Complications: At very high concentrations, lidocaine's blockage of cardiac sodium channels can lead to life-threatening arrhythmias, atrioventricular (AV) heart block, ventricular tachycardia, and eventually cardiovascular collapse or cardiac arrest (often asystole).
Central Nervous System (CNS) Symptoms | Cardiovascular System (CVS) Symptoms | |
---|---|---|
Mild/Early | Circumoral numbness, metallic taste, tinnitus, dizziness, blurred vision, agitation, confusion. | Hypertension, tachycardia. |
Severe/Late | Muscle twitching, tremors, seizures, drowsiness, coma, respiratory arrest. | Hypotension, bradycardia, arrhythmias, heart block, ventricular tachycardia, cardiac arrest. |
Prevention and Treatment of LAST
Prevention is the most critical strategy. Healthcare providers can minimize risk by using the lowest effective concentration and volume, performing incremental injections, aspirating before injecting to check for blood return, and using ultrasound guidance to avoid blood vessels.
If LAST is suspected, immediate action is required:
- Stop the Injection: The first step is to immediately stop administering the local anesthetic.
- Airway Management: Securing the patient's airway and providing 100% oxygen is crucial to prevent hypoxia and acidosis, which can worsen toxicity.
- Seizure Control: Seizures are typically managed with benzodiazepines.
- Lipid Emulsion Therapy: For any serious signs of toxicity, especially cardiovascular instability, intravenous lipid emulsion (e.g., Intralipid) is the primary treatment. This therapy acts as a "lipid sink," sequestering the lipophilic lidocaine molecules out of the plasma and away from target tissues like the heart and brain. The American Heart Association recommends this treatment for local anesthetic toxicity.
- Cardiovascular Support: If cardiac arrest occurs, standard Advanced Cardiac Life Support (ACLS) protocols are modified. Small doses of epinephrine are preferred, and certain antiarrhythmics like amiodarone may be used. Drugs that can worsen the situation, such as calcium-channel blockers, beta-blockers, and lidocaine itself, are contraindicated.
Conclusion
When lidocaine enters the bloodstream in sufficient quantity, it causes a dangerous condition called Local Anesthetic Systemic Toxicity (LAST). This toxicity presents a spectrum of symptoms, beginning with CNS excitation like dizziness and tingling, and potentially progressing to seizures, coma, and life-threatening cardiovascular collapse. While this complication is rare, its severity underscores the importance of preventative measures by healthcare professionals, such as careful injection techniques and ultrasound guidance. Should toxicity occur, rapid recognition and management—primarily involving airway support and the administration of intravenous lipid emulsion therapy—are vital to reversing the effects and ensuring patient survival.
For more information, an authoritative resource is the American Society of Regional Anesthesia and Pain Medicine (ASRA) which provides detailed guidelines on LAST. https://www.asra.com/practice-management/guidelines/local-anesthetic-systemic-toxicity