Introduction
A temporary loss of sensory, motor, and autonomic function occurs when Lidocaine is injected into or administered to the area around neural tissue. It is the most widely used local anesthetic in practically all medical disciplines. As an antiarrhythmic drug, it is also frequently used to suppress ventricular arrhythmias (heartbeats with an abnormal rhythm). Since they can lower the minimum alveolar concentration of volatile anesthetics by up to 40 percent and alleviate discomfort in the peri-operative period, Lidocaine (and procaine) have been used to enhance general anesthetic procedures. It belongs to the group of local anesthetics known as amide local anesthetics, which, in contrast to ester-type local anesthetics, are typically well tolerated with only very infrequent allergic responses.
When used to induce anesthesia by injection, inhalation, or topical application, Lidocaine provides a good safety margin before hazardous blood levels are reached. To reduce its systemic toxicity, however, care must be made to monitor the total amount given because it might be administered differently to the same patients. Additionally, as hazardous doses appear to be cumulative, doctors should consider the dose of any additional local anesthetics that may have been given to the same patient. Lidocaine toxicity is influenced by the overall amount (about 4.5 mg/kg) and the rate of absorption, which depends on the tissue's blood flow. Vasoconstrictors (a drug that causes the narrowing of blood vessels), such as Epinephrine 1:200000, are widely used to decrease blood flow to the injection site and, consequently, the absorption rate; this can raise the hazardous dose to 7 mg/kg.
Lidocaine toxicity to muscles and peripheral or neuraxial nerves is possible at the injection site. In addition, numerous reports of transient neurologic symptoms (TNS) following high-concentration Lidocaine spinal anesthetics have prompted either the reduction of the dose's concentration or the use of a different medication.
What Is the Etiology (Causes) of Topical Lidocaine Toxicity?
The prolonged application of high drug concentrations or the impact of preservatives in the local anesthetic solution, or maybe both, is thought to cause toxicity to local nerves and muscles. High systemic plasma levels of Lidocaine, which result from the absorption of large doses of Lidocaine and mainly depend on blood flow at the injection site, cause systemic local anesthetic toxicity. Additionally, systemic Lidocaine toxicity can result from the blind injection of high volumes into a sizable muscle region, such as for lumbar plexus or sciatic nerve blocks. Spinal anesthetics' overall volume is deficient and does not produce systemic Lidocaine toxicity. Even at doses below the systemic toxic threshold, accidental intra-arterial injections may result in local anesthetic toxicity in the tissue beds supplied by that artery. Injections into the neck are the most common site for this problem, frequently resulting in central nervous system (CNS) symptoms during or immediately after the injection without escalating to cardiac toxicity.
What Is the Epidemiology (Distribution) Of Topical Lidocaine Toxicity?
Lidocaine poisoning has an equal impact on both sexes. However, patients at the extremes of age and pregnant women are likely more vulnerable to local anesthetic toxicity. Depending on the block type, rates of severe systemic toxicity (seizures with or without cardiac arrest) range from 1:10,000 for epidurals to up to 1:2000 for peripheral nerve blocks.
What Is the Toxicokinetic (How the Body Handles a Chemical) Associated With Topical Lidocaine?
The capacity of the local anesthetic molecule to pass across membranes in a hydrophobic environment, or lipid solubility, correlates with potency.
Lipid solubility and protein binding both have an impact on how long an effect lasts. Local anesthetics that are highly lipid-soluble and protein-bound last longer because blood flow is less likely to eliminate them from the body. High plasma protein binding is present in highly lipid-soluble local anesthetics, primarily to alpha-1-acid glycoprotein and, to a lesser extent, albumin. As a result, their clearance is slowed down. The blood flow determines the plasma level and the absorption rate to the region where the local anesthetic is deposited.
However, it will also move local anesthetics away from the affected tissue, lowering the chance of direct nerve damage. In addition, Lidocaine has a 90 percent hepatic metabolism and an elimination half-life of 1.5 to 2 hours; in individuals with severe liver disease, this half-life can be increased by up to 3.5 times.
What Are the Signs and Symptoms of Topical Lidocaine Toxicity?
In conscious patients, premonitory overdose symptoms are located in the CNS. Early signs include dizziness, tongue paresthesia (burning sensation), and circumoral numbness. Vision blurriness and tinnitus (ringing noises) are examples of sensory problems. Muscle cramps and seizures may develop from agitation symptoms, including restlessness, agitation, anxiousness, or paranoia. Large overdoses can ultimately result in CNS depression, including unconsciousness and coma. In addition, when neuraxial blockade or nerve blocks are done close to the CNS, relative local anesthetic overdoses can potentially cause hypotension and bradycardia as side effects.
Significant cardiovascular toxicity typically calls for blood lactate (LA) concentrations higher than those that cause seizures. Unintentional intravascular injection of local anesthetics during regional anesthesia causes severe cardiotoxic reactions, typically the first symptoms of local anesthetic toxicity during general anesthesia. These reactions include hypotension, atrioventricular heart block, idioventricular rhythms, and life-threatening arrhythmias like ventricular tachycardia and fibrillation.
How Is the Evaluation of Topical Lidocaine Toxicity Done?
A clinical diagnosis is made. The significant variables to consider while thinking about systemic symptoms are the timing, dosage, and location of the Lidocaine injection. It is crucial to remember that even low amounts accidentally injected into a brain artery can result in CNS symptoms.
The concentration and injection site will aid in diagnosing immediate local manifestations, such as discomfort experienced in TNS. The diagnosis of TNS cannot be made with a computed tomography (CT) or magnetic resonance imaging (MRI) scan of the spine. However, it will be helpful to rule out additional factors that could compress the spinal structures. These factors could also result in significant pain following neuraxial blocking and necessitate an immediate surgical decompression. It is possible to measure the plasma level of Lidocaine, but it will take too long for the results to help make treatment choices.
What Is the Treatment Given for Topical Lidocaine Toxicity?
Raising the seizure threshold with pharmacologic interventions, such as giving benzodiazepines, barbiturates, or Propofol, is how local anesthetic systemic toxicity (LAST) is treated. High oxygen dose hyperventilation decreases cerebral blood flow.
Delivering lipid emulsions reduces the concentration of free, readily available local anesthetic in the plasma, which is the other basis of treatment. The infusion of lipid emulsions will bind freely to circulating local anesthetics and lower the plasma levels because of the high lipid solubility. The American Society of Regional Anesthesia and Pain Medicine has the following treatment protocol:
Call For Help: Even premonitory CNS systems may develop into severe cardio-respiratory compromise, necessitating the completion of numerous tasks at once, such as retrieving code carts and the lipid emulsion.
Management of Cardiac Arrhythmias:
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Medicines will need to be adjusted, and primary and advanced cardiac life support (ACLS) may require extended effort.
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Avoid using vasopressin, beta-blockers, calcium channel blockers, and local anesthetics.
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Lower each person's Epinephrine dosage to 1 mcg/kg.
Lipid Emulsion (20 percent) therapy:
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100mL bolus administered intravenously at 1.5 mL/kg (lean body mass).
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Ongoing infusion 0.25 mL/kg/min (18 mL/min; roller clamp-adjustable).
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Repeat the bolus once or twice if the cardiovascular collapse continues.
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If blood pressure remains low, double the infusion rate to 0.5 mL/kg/min.
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Once the circulatory system has stabilized, keep infusing for at least 10 minutes.
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Over the first 30 minutes, an upper limit of around 10 mL/kg lipid emulsion is advised.
Successful outcomes have been recorded even after lengthy resuscitation, which may be partially explained by evidence from animal models suggesting that adding Bupivacaine to the cardioplegia solution improves function and lessens cellular damage in isolated rat hearts after extended, cold storage.
What Is the Differential Diagnosis in the Case of Topical Lidocaine Toxicity?
The diagnosis will most likely be made based on the timing of the onset of symptoms after receiving or applying significant amounts of Lidocaine. The diagnosis could be complicated by coincidental seizures brought on by a seizure disease or panic episodes accompanied by hyperventilation.
To rule out other reasons, such as hematoma, which could compress structures in the spinal canal and necessitate urgent surgical decompression, one must first rule out immediate local toxicity symptoms following Lidocaine injection, such as radicular discomfort. That diagnosis would be improbable due to the timing of an epidural abscess about a central neuraxial block. However, most epidural abscesses develop independently and could occur concurrently with the injection.
Conclusion
After topical Lidocaine has been applied, patients may experience dizziness and paresthesia. These side effects might proceed to seizures and cardiorespiratory depression, which can ultimately result in death.
