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What are the two side effects of lignocaine hydrochloride?

4 min read

Systemic toxicity from local anesthetics like lignocaine hydrochloride is estimated to occur in approximately 0.03% of peripheral nerve blocks [1.8.2]. While generally safe, it's crucial to understand the answer to 'What are the two side effects of lignocaine hydrochloride?' as they primarily involve the central nervous and cardiovascular systems [1.6.3].

Quick Summary

Lignocaine hydrochloride, a widely used local anesthetic, can cause side effects primarily affecting the central nervous system (CNS) and cardiovascular system. CNS effects range from dizziness to seizures, while cardiac effects include changes in heart rate and blood pressure.

Key Points

  • Two Main Side Effect Categories: The primary side effects of lignocaine hydrochloride impact the Central Nervous System (CNS) and the Cardiovascular System [1.6.3].

  • CNS Toxicity is Progressive: CNS symptoms often appear first, starting with mild signs like perioral numbness and tinnitus, and can progress to seizures and respiratory arrest [1.5.2].

  • Cardiovascular Risks: Cardiovascular effects, such as hypotension and arrhythmias, usually occur at higher drug concentrations than CNS effects but can be life-threatening [1.5.2].

  • Mechanism of Action: Lignocaine works by blocking sodium channels to prevent pain signals from reaching the brain [1.4.1].

  • Risk Factors Increase Susceptibility: Patients at extremes of age or with heart, liver, or kidney disease are at a higher risk for toxicity [1.6.1, 1.6.2].

  • Management is Critical: Immediate treatment for toxicity involves stopping the drug, supporting airway and circulation, and administering lipid emulsion therapy [1.9.4].

  • True Allergies are Rare: Most adverse reactions are toxic or psychogenic; true allergic reactions to lignocaine are extremely uncommon [1.11.1].

In This Article

Understanding Lignocaine Hydrochloride

Lignocaine hydrochloride, more commonly known as lidocaine, is an essential medication in modern medicine, valued for its role as a local anesthetic and a Class 1b antiarrhythmic agent [1.4.2]. It functions by blocking sodium channels in neuronal membranes, which inhibits the nerve impulses required for pain signals to travel to the brain [1.4.1]. This mechanism allows for localized numbness, making it indispensable for minor surgical procedures, dental work, and as a topical agent to relieve pain and itching from burns or insect bites [1.2.2, 1.4.1]. Beyond its anesthetic properties, it's also used intravenously to treat life-threatening ventricular arrhythmias [1.4.2]. Its rapid onset and effectiveness have secured its place on the World Health Organization's List of Essential Medicines [1.4.5].

The Two Primary Categories of Side Effects

While lignocaine is broadly safe, its side effects can be categorized into two main groups: Central Nervous System (CNS) toxicity and Cardiovascular toxicity. These effects are typically dose-dependent and often result from high concentrations of the drug in the bloodstream, which can occur from accidental intravascular injection, excessive dosage, or rapid absorption [1.6.2].

Central Nervous System (CNS) Effects

The CNS is often the first to show signs of lignocaine toxicity, especially in an awake patient [1.5.2]. The symptoms are progressive and directly related to the plasma concentration of the drug.

Early/Mild Symptoms:

  • Numbness or tingling, particularly around the mouth (circumoral numbness) and in the tongue [1.5.2, 1.5.3]
  • A metallic taste in the mouth [1.5.3]
  • Lightheadedness and dizziness [1.5.2]
  • Ringing in the ears (tinnitus) [1.5.3]
  • Blurred or double vision [1.2.1, 1.5.3]
  • Feelings of drowsiness, confusion, or agitation [1.2.4, 1.5.2]

Severe Symptoms: As plasma levels rise, these initial signs can escalate to more severe neurological effects.

  • Muscle Twitching and Tremors: Involuntary muscle movements are a key indicator of progressing toxicity [1.2.1, 1.5.2].
  • Seizures: Generalized convulsions can occur as the drug's excitatory effects on the CNS peak [1.2.4, 1.6.3].
  • Unconsciousness and Coma: At very high concentrations, the initial excitatory phase gives way to profound CNS depression, leading to loss of consciousness [1.5.2].
  • Respiratory Depression and Arrest: Ultimately, the brain's control over breathing can be suppressed, leading to respiratory failure [1.5.5, 1.6.3].

Cardiovascular Effects

Cardiovascular toxicity usually requires a higher blood concentration of lignocaine than what is needed to produce CNS symptoms [1.5.2]. However, in some cases, especially with rapid intravenous injection, cardiac symptoms can appear simultaneously with or even before CNS signs [1.6.4]. The effects result from the drug's action on the cardiac muscle's sodium channels.

Initial Symptoms:

  • Hypotension (Low Blood Pressure): Lidocaine can cause vasodilation, leading to a drop in blood pressure [1.2.4, 1.4.5].
  • Bradycardia (Slow Heart Rate): The drug can slow the heart's electrical conduction, resulting in a decreased heart rate [1.5.3, 1.6.3].

Severe Symptoms:

  • Arrhythmias: Serious disturbances in heart rhythm, such as atrioventricular (AV) block, ventricular tachycardia, or fibrillation can occur [1.5.2, 1.2.4].
  • Cardiovascular Collapse: In the most severe cases, the heart's ability to pump blood effectively is compromised, leading to circulatory collapse and cardiac arrest [1.5.2, 1.6.3].

Risk Factors for Toxicity

Certain patient populations and conditions increase the risk of developing lignocaine toxicity. These include:

  • Extremes of age: Infants and the elderly are more susceptible [1.6.2, 1.6.1].
  • Pre-existing conditions: Patients with heart disease, liver disease, or kidney disease are at higher risk as they may not metabolize or clear the drug effectively [1.6.1, 1.10.4].
  • Pregnancy: Pregnant women may have increased sensitivity [1.6.1].
  • Low muscle mass: Dosage calculations can be affected, leading to higher effective concentrations [1.6.4].
  • Site of injection: Injection into a highly vascular area increases the rate of absorption and the risk of systemic effects [1.6.3].

Comparison of Local Anesthetics: Lignocaine vs. Bupivacaine

Feature Lignocaine (Lidocaine) Bupivacaine
Onset of Action Fast (1-5 minutes) [1.7.4] Slower (10-15 minutes) [1.7.4]
Duration of Action Short (1-2 hours) [1.7.4] Long (2-4+ hours) [1.7.1]
Primary Use Procedures requiring rapid onset and shorter duration. Procedures requiring prolonged pain control [1.7.1].
Toxicity Profile CNS toxicity typically precedes cardiovascular toxicity [1.6.4]. Higher risk of cardiotoxicity, which can occur simultaneously with CNS symptoms [1.7.1, 1.6.4].
Side Effects More likely to cause transient neurological symptoms. More cardiotoxic compared to lidocaine [1.7.1].

Management and Conclusion

The immediate management of lignocaine toxicity involves stopping the administration of the drug and focusing on airway management, breathing, and circulation (the ABCs) [1.9.4]. Oxygen should be administered, and seizures are typically managed with benzodiazepines [1.9.2]. In cases of severe cardiovascular toxicity or cardiac arrest, Advanced Cardiac Life Support (ACLS) protocols are initiated. Intravenous lipid emulsion therapy has become a standard treatment, acting as a "lipid sink" to absorb the lipid-soluble anesthetic from the plasma, thereby reducing its toxic effects on the heart and brain [1.9.2, 1.9.4].

In conclusion, while lignocaine hydrochloride is a vital and generally safe local anesthetic, the two main categories of its side effects—central nervous system and cardiovascular toxicity—are serious and require immediate recognition and management. Understanding the progressive nature of these symptoms, from initial signs like metallic taste and dizziness to severe events like seizures and cardiac arrest, is critical for any healthcare provider administering the drug. Patients with known risk factors require careful dosing and monitoring to ensure a safe and effective outcome.


For more information from a certified authority, please visit the National Institutes of Health's page on Lidocaine Toxicity.

Frequently Asked Questions

The earliest signs of lignocaine toxicity often involve the central nervous system and include numbness or tingling around the mouth and tongue, a metallic taste, dizziness, and ringing in the ears (tinnitus) [1.5.2, 1.5.3].

Yes, in cases of severe toxicity, lignocaine hydrochloride can cause profound cardiovascular effects, including severe arrhythmias, cardiovascular collapse, and cardiac arrest [1.2.4, 1.6.3].

No, a true allergic reaction to lignocaine is extremely rare. Most adverse reactions are psychogenic (related to fear/anxiety) or toxic (due to high blood levels of the drug) [1.11.1].

Treatment involves immediately stopping the drug, managing the patient's airway and circulation, and administering specific treatments like benzodiazepines for seizures and intravenous lipid emulsion therapy to counteract systemic toxicity [1.9.2, 1.9.4].

Lignocaine toxicity typically presents with CNS symptoms first, while bupivacaine is more cardiotoxic and can cause severe cardiac events to occur at the same time as or even before CNS symptoms appear [1.6.4, 1.7.1].

Patients at the extremes of age (infants and the elderly), pregnant women, and individuals with pre-existing heart, liver, or kidney disease are at an increased risk for developing toxic side effects [1.6.1, 1.6.2].

Yes, using excessive amounts of topical lidocaine can be dangerous. The medication can be absorbed through the skin into the bloodstream, potentially leading to systemic toxicity with serious side effects like seizures or irregular heartbeat [1.3.1, 1.5.5].

References

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.