Lidocaine Toxicity Clinical Presentation

The symptoms of lidocaine toxicity tend to follow a predictable progression. The toxicity begins with numbness of the tongue, lightheadedness, and visual disturbances and progresses to muscle twitching, unconsciousness, and seizures, then coma, respiratory arrest, and cardiovascular depression.

CNS toxicity

When the lidocaine dose is increased from 1 mg/kg to 1.5 mg/kg, the risk of CNS toxicity increases from 10% to 80%. Symptoms include the following:

• Lightheadedness, dizziness
• Visual disturbance
• Headache
• Perioral tingling, numbness or tingling of tongue
• Sedation
• Impaired concentration
• Dysarthria
• Tinnitus
• Metallic taste
• Muscular twitching, tremors

With progression of toxicity, the patient may experience tonic-clonic seizures and, eventually, unconsciousness and coma. Seizures generally do not occur with lidocaine levels of less than 10 mcg/mL.

CNS symptoms may be masked in patients premedicated with anticonvulsants such as benzodiazepines or barbiturates. The first sign of toxicity in these premedicated patients may be cardiovascular system (CVS) depression. When blood levels are high enough to block inhibitory and excitatory pathways, convulsions cease and the patient experiences respiratory depression or arrest and cardiovascular depression. Large bolus injections may increase peak anesthetic levels to the point where the CNS and CVS are simultaneously affected.

Cardiovascular

Excessive lidocaine concentration can cause cardiovascular toxicity, although this is less common than CNS toxicity. Lidocaine is somewhat less cardiotoxic than lipophilic local anesthetics such as bupivacaine. Risk of cardiac toxicity is greatest in those patients with underlying cardiac conduction problems or after myocardial infarction. Potential cardiovascular effects are included below.

Negative inotropic effects include effects on vascular tone (with low doses having vasoconstrictive effects and higher doses causing relaxation of vascular smooth muscle). Effects on cardiac conduction include widened PR interval, widened QRS duration, sinus tachycardia, sinus arrest, and partial or complete atrioventricular dissociation. Cardiac arrest has been reported after intraurethral administration of lidocaine.^[2]

Cardiac toxicity is potentiated by acidosis, hypercapnia, and hypoxia, which worsen cardiac suppression and increase the chance of arrhythmia. This is important to consider since seizure makes this metabolic picture more likely.

Plasma lidocaine levels of less than 5 mcg/mL are unlikely to have cardiovascular toxicities. levels of 5-10 mcg/mL can cause hypotension by inducing both cardiac suppression and vascular smooth muscle relaxation. levels of more than 30 mcg/mL are associated with cardiovascular collapse.

Lidocaine should be avoided in persons with Wolff-Parkinson-White syndrome.

The most common cause of lidocaine toxicity is dosing error.

The maximum recommended dose of lidocaine without epinephrine is 3-5 mg/kg; if given with epinephrine, up to 7 mg/kg may be given. Note that dosing may require modification based on patient characteristics and site of administration.

• Although lidocaine toxicity is ultimately a simple matter of excessive blood concentration, several factors can influence the development of these reactions. Influential factors include the speed of the injection, the dose of the local anesthetic injected, acid-base status, hypercapnia, hypoxia, plasma protein level, and hepatic function.
• Concurrent administration of other drugs, such as benzodiazepines, may mask the development of CNS symptoms but not CVS symptoms.
• Lidocaine crosses the placenta.