Why is lignocaine (lidocaine) used intravenously in patients with impaired renal function (elevated creatinine)?

Lidocaine Use in Renal Impairment

Direct Answer

Lidocaine is used intravenously in patients with renal impairment because it is metabolized almost exclusively by the liver, not the kidneys, making it safer than renally-cleared antiarrhythmics for treating ventricular arrhythmias in this population. 1, 2

Hepatic vs. Renal Clearance

• Lidocaine undergoes approximately 90% hepatic metabolism through oxidative N-dealkylation and ring hydroxylation, with less than 10% excreted unchanged in urine. 1
• The primary route of elimination is hepatic biotransformation to metabolites (MEGX and GX), which are then renally excreted. 1, 2
• Renal dysfunction does not affect lidocaine kinetics or clearance in patients receiving regular hemodialysis, whose pharmacokinetic parameters remain similar to those with normal renal function. 1, 2

Dosing Adjustments Required

Severe Renal Insufficiency (Not on Hemodialysis)

• Patients with severe renal insufficiency (creatinine clearance <30 mL/min/1.73 m²) who are NOT receiving hemodialysis require dose reduction: clearance is approximately half that of normal subjects (6.01 vs 11.87 mL/min/kg), and half-life is doubled (4.55 vs 2.24 hours). 2
• For these patients, reduce both loading and maintenance doses by approximately 50%. 2

Patients on Hemodialysis

• No dose adjustment is necessary for patients receiving regular hemodialysis, as their lidocaine clearance and half-life remain normal. 2
• This represents a critical distinction often missed in clinical practice. 2

Standard Dosing for Ventricular Arrhythmias

• Initial bolus: 1.0-1.5 mg/kg (75-100 mg) IV over 2 minutes. 3, 4
• Additional boluses: 0.5-0.75 mg/kg (25-50 mg) every 5-10 minutes if needed, up to maximum total of 3 mg/kg. 3
• Maintenance infusion: 2-4 mg/min (20-50 μg/kg/min). 3, 4

Metabolite Accumulation Concerns

• Glycinexylidide (GX) levels are more than doubled in all patients with chronic renal failure, regardless of hemodialysis status. 2
• However, GX accumulation does not inhibit lidocaine metabolism—its inhibition constant (52 μmol/L) is 2 orders of magnitude higher than in vivo concentrations. 2
• MEGX levels remain independent of renal function. 2

Additional Dose Reductions Required

Beyond renal function, reduce infusion rates in: 3

• Patients >70 years of age (higher risk of toxicity). 3
• Congestive heart failure or cardiogenic shock (reduced hepatic blood flow decreases clearance). 3, 1
• Hepatic dysfunction (primary elimination pathway impaired). 3, 1
• Prolonged infusions >24 hours (half-life increases over time; discontinue within 24 hours when possible). 5

Monitoring for Toxicity

• Early CNS toxicity appears at plasma levels >6 μg/mL: perioral numbness, dizziness, confusion, slurred speech, muscle twitching. 3, 1
• Severe toxicity includes seizures, respiratory depression/arrest, cardiovascular collapse. 3, 1
• Measure serum levels with prolonged or high infusion rates, or if neurologic changes occur. 3

Clinical Pitfall

The most common error is failing to distinguish between patients with severe renal insufficiency who are NOT on hemodialysis (who require dose reduction) versus those receiving regular hemodialysis (who do not). 2 This distinction is critical because hemodialysis patients maintain normal lidocaine clearance despite absent renal function, likely due to compensatory mechanisms or the effects of dialysis on hepatic blood flow. 2