What is the treatment for a patient experiencing lignocaine (lidocaine) toxicity?

Treatment of Lignocaine (Lidocaine) Toxicity

Immediately stop lignocaine administration, secure the airway with oxygen, and prepare to manage seizures with benzodiazepines while maintaining cardiovascular support—this is the cornerstone of managing local anesthetic systemic toxicity. 1

Immediate Recognition and Initial Management

The first priority is prevention through vigilant monitoring of cardiovascular and respiratory vital signs and the patient's level of consciousness after lignocaine administration. 1 At the first sign of toxicity, immediately administer 100% oxygen. 1

Clinical Presentation of Toxicity

Lignocaine toxicity manifests primarily through neurological and cardiovascular effects:

Neurological symptoms (typically appear first):

• Perioral numbness and numbness of lips or tongue 2
• Dizziness, confusion, and slurred speech 2
• Drowsiness and disorientation 2
• Muscle twitching and tremor 2
• Seizures (generalized convulsions) 1, 3, 4
• Respiratory depression or arrest 2
• Altered consciousness 2

Cardiovascular effects (appear with higher toxicity):

• Bradycardia and sinus arrest 2
• Hypotension 2
• Myocardial and circulatory depression 2
• Cardiac arrest 1

Toxic blood levels are generally considered >5 mg/L, though clinical toxicity correlates roughly with blood concentrations. 2

Airway and Ventilation Management

The first step in managing convulsions or respiratory compromise consists of immediate attention to maintaining a patent airway and providing assisted or controlled ventilation with oxygen using a delivery system capable of immediate positive airway pressure by mask. 1

• Ensure adequate oxygenation and ventilation to prevent hypoxia and acidosis, which can worsen toxicity 1
• Consider endotracheal intubation if difficulty maintaining a patent airway or if prolonged ventilatory support is needed 1
• Both convulsions and cardiovascular depression, if untreated, can result in hypoxia, acidosis, bradycardia, arrhythmias, and cardiac arrest 1

Seizure Management

If convulsions persist despite adequate respiratory support and the circulation permits, administer small increments of an ultra-short acting barbiturate (such as thiopental or thiamylal) or a benzodiazepine (such as diazepam) intravenously. 1 Clinicians should be familiar with these anticonvulsant drugs prior to using local anesthetics. 1

Important Caveat

Be aware that drugs used to treat convulsions can themselves depress circulation when administered intravenously, so ensure hemodynamic stability before administration. 1

Cardiovascular Support

Immediately after instituting ventilatory measures, evaluate the adequacy of circulation. 1

Supportive treatment of circulatory depression includes:

• Administration of intravenous fluids 1
• Vasopressor therapy (e.g., ephedrine) as directed by the clinical situation 1
• Standard cardiopulmonary resuscitative measures if cardiac arrest occurs 1

Lipid Emulsion Therapy

For severe local anesthetic systemic toxicity, particularly when cardiovascular collapse occurs, lipid emulsion therapy should be administered to reverse the effects of the anesthetic. 5 This represents the most specific antidote available for severe lignocaine toxicity, though the FDA label does not specifically mention it as it predates this treatment modality. 5

What NOT to Do

• Dialysis is of negligible value in treating acute lignocaine overdosage and should not be pursued as a treatment strategy 1
• Do not delay airway management while attempting other interventions 1

Prevention Strategies

The maximum dose of lignocaine should be limited to 8.2 mg/kg in adults (approximately 29 ml of a 2% solution for a 70 kg patient), with extra care in the elderly or those with liver or cardiac impairment. 2

Special populations requiring dose reduction:

• Patients >70 years of age 2
• Patients with congestive heart failure, cardiogenic shock, or hepatic dysfunction 2
• Patients with severe renal dysfunction 2
• Patients with preexisting neurologic dysfunction 2

With prolonged or high infusion rates or changes in neurologic condition, measure serum lignocaine levels. 2 Lignocaine is eliminated primarily by hepatic metabolism, and clearance is significantly reduced in cardiac failure and liver disease. 6 In patients with cardiac failure, blood lignocaine concentrations may continue to rise for 24-48 hours. 6