Introduction to Lidocaine and Systemic Absorption
Lidocaine is a widely used local anesthetic from the amide class, valued for its ability to temporarily block pain signals by inhibiting sodium channels in nerve cells. While generally safe when applied correctly, a primary concern is the risk of excessive absorption into the bloodstream. This can occur due to an accidental intravascular injection, application of amounts of medication that are too large, use on highly vascular areas, or prolonged exposure. When systemic plasma levels become too high, it leads to a potentially life-threatening condition known as Local Anesthetic Systemic Toxicity (LAST). This toxicity is dependent on the amount of medication in the body and affects the entire body, most notably the central nervous system (CNS) and the cardiovascular system.
The Progression of Systemic Toxicity (LAST)
LAST symptoms typically manifest in a biphasic pattern, starting with CNS excitation and progressing to depression, which can then be followed by cardiovascular compromise.
Central Nervous System (CNS) Effects
The CNS is usually the first to show signs of toxicity because lidocaine can quickly cross into the brain.
- Early Symptoms: Initial, often subtle, signs include numbness around the mouth (circumoral numbness), tongue paresthesia, a metallic taste, dizziness, and lightheadedness. Sensory issues like tinnitus (ringing in the ears) and blurred or double vision are also common.
- Excitatory Phase: As toxicity progresses, patients may exhibit signs of CNS excitation, such as restlessness, agitation, confusion, muscle twitching, and tremors. This phase can escalate rapidly to generalized tonic-clonic seizures, which are a hallmark of severe neurotoxicity.
- Depressive Phase: Following the excitatory phase, or with very large amounts of medication, CNS depression occurs. This can lead to drowsiness, unconsciousness, respiratory depression, and eventually, coma and respiratory arrest.
Cardiovascular (CV) Effects
Cardiovascular toxicity generally requires a higher concentration of lidocaine in the blood than what causes seizures and is often preceded by CNS symptoms. However, in some cases, cardiac symptoms can appear suddenly, especially if there was an accidental intravenous injection.
- Initial Signs: The effects can be varied, including both an increased heart rate (tachycardia) and a slowed heart rate (bradycardia), as well as hypertension or hypotension.
- Severe Complications: As toxicity worsens, it can lead to severe cardiac issues such as atrioventricular (AV) heart block, life-threatening arrhythmias (like ventricular tachycardia and fibrillation), and profound hypotension. Ultimately, this can result in cardiovascular collapse and cardiac arrest.
Preventing Systemic Toxicity
To prevent toxicity, adherence to appropriate administration guidelines is recommended. These guidelines can vary depending on factors such as the use of a vasoconstrictor, which slows absorption and can influence the amount that can be administered safely.
Considerations for Lidocaine Administration | Detail |
---|---|
Use of Vasoconstrictor | Can influence the recommended amount of lidocaine |
Total Amount Administered | Guidelines exist for the maximum total amount |
It is crucial to note that these are general guidelines, and patient-specific factors can alter the toxic threshold. Always consult with a healthcare professional for specific recommendations.
Risk Factors and Prevention
Certain factors increase the risk of developing LAST.
- Patient Factors: Extremes of age (very young or elderly), pregnancy, low muscle mass, and pre-existing conditions like heart, liver, or kidney disease increase susceptibility.
- Procedural Factors: The site of injection plays a major role; absorption is fastest in highly vascular areas (tracheal > intercostal > caudal > epidural > brachial plexus > subcutaneous). High-volume blocks and failure to use ultrasound guidance also increase risk.
Prevention is the most critical aspect of managing LAST. Key strategies include:
- Using the lowest effective amount.
- Injecting slowly in small, incremental amounts (3-5 mL at a time).
- Aspirating before each injection to check for blood, indicating vessel puncture.
- Using ultrasound guidance to avoid intravascular injection.
- Continuous patient monitoring for at least 30 minutes after injection.
Management of Lidocaine Toxicity
If LAST is suspected, it is a medical emergency requiring immediate action.
- Stop the Injection: The first step is to immediately stop administering lidocaine.
- Airway Management: Ensure the patient has a clear airway and provide 100% oxygen to prevent hypoxia, which worsens toxicity.
- Seizure Control: Benzodiazepines are used to control or prevent seizures.
- Lipid Emulsion Therapy: For moderate to severe toxicity, intravenous infusion of a 20% lipid emulsion is the primary antidote. This therapy acts as a "lipid sink," sequestering the lidocaine molecules from the plasma and reducing their effect on the heart and brain.
- Cardiovascular Support: If cardiac arrest occurs, standard CPR protocols should be initiated, with some modifications. Small amounts of epinephrine may be used, but vasopressin and local anesthetic anti-arrhythmics should be avoided.
Conclusion
When lidocaine is absorbed into the bloodstream at high levels, it can cause severe, life-threatening systemic toxicity. The effects progress from initial CNS signs like dizziness and perioral numbness to seizures, coma, and cardiovascular collapse. Understanding the risk factors, adhering to preventative measures like correct administration amounts and injection techniques, and being prepared for rapid emergency management with lipid emulsion therapy are essential for ensuring patient safety when using this common local anesthetic. For more detailed clinical guidelines, you can refer to the American Society of Regional Anesthesia and Pain Medicine (ASRA).