Lidocaine
Lidocaine is a local anesthetic from the amide group, widely used in both human and veterinary medicine. It is primarily used for local pain relief during minor procedures, as an antiarrhythmic for cardiac arrhythmias, and in the form of ointments and gels for topical anesthesia. The active substance blocks voltage-gated sodium channels in cell membranes, thereby inhibiting the transmission of nerve impulses. This property makes lidocaine an effective pain reliever, but it carries significant risks for small animals if overdosed or used incorrectly.
The toxicity of lidocaine differs significantly between various animal species. Cats are particularly sensitive due to their limited ability to glucuronidate – an important metabolic pathway for drug breakdown in the liver. While dogs show a slightly higher tolerance, even small overdoses can lead to severe signs of poisoning in them. The therapeutic window, i.e., the margin between effective and toxic doses, is relatively narrow in both animal species.
The most important facts at a glance
Lidocaine poisonings represent a relevant toxicological problem in small animal medicine, which can arise from both medical application and accidental exposure. The active substance blocks sodium channels, thereby impairing impulse conduction in nerve and cardiac muscle cells. Cats are particularly at risk due to their limited metabolism.
Clinical signs primarily manifest in the nervous system with symptoms such as restlessness, tremors, and seizures, as well as in the cardiovascular system in the form of arrhythmias and blood pressure changes. Diagnosis is mainly based on the medical history and the characteristic symptom pattern, supported by ECG examinations.
Therapy includes decontamination measures, symptomatic treatment of neurological and cardiovascular symptoms, and supportive measures. Intravenous lipid emulsion therapy has proven to be a promising treatment option for severe intoxications.
With early detection and adequate treatment, the prognosis is favorable, although the recovery time in cats can be longer due to their delayed metabolism. Follow-up care focuses on monitoring for possible long-term consequences and preventing re-exposure.
It is important for veterinarians and pet owners to be aware of the risks of lidocaine and to consider species-specific characteristics during its use. Careful dosing and safe storage of lidocaine-containing preparations are crucial to prevent poisoning cases.
Causes, development and progression
Lidocaine increases the excitation threshold in nerve cells and slows down impulse conduction.
In the heart muscle, lidocaine reduces excitability, the speed of impulse conduction, and contractile force, thereby reducing the risk of arrhythmias.
Lidocaine poisoning in pets primarily arises from three scenarios: iatrogenic overdose during veterinary treatments, accidental oral ingestion of lidocaine-containing preparations, or improper application by pet owners.
Iatrogenic poisoning occurs when toxic plasma levels result from excessive dosing, overly rapid intravenous administration, or unintentional intravascular injection during what should be subcutaneous application. Animals with impaired liver or kidney function are particularly at risk, as the metabolism and excretion of the active substance may be delayed.
Accidental oral ingestion usually occurs when animals access their owner’s medications. Although lidocaine undergoes a significant first-pass effect in the liver when taken orally, toxic plasma levels can still occur if large quantities are ingested. This effect is even more pronounced in cats due to their metabolic peculiarities.
Another common cause is improper application by pet owners who use human lidocaine preparations on their pets. The concentration of these preparations is often unsuitable for animals, and the dosage is frequently miscalculated. Combination preparations containing other active ingredients besides lidocaine, which can be toxic to animals, are particularly dangerous.
Mechanism of action
Lidocaine is absorbed when taken orally. It is also dangerous in cats due to their limited ability to break it down.
The toxic effect of lidocaine primarily affects the central nervous system. This system is more sensitive and reacts at a lower plasma lidocaine level than, for example, the cardiovascular system.
However, the effects on the cardiovascular system are more significant for the potential fatal outcome of lidocaine intoxications.
The slowing of impulse conduction in the heart, leading to blockages, results in pronounced cardiac arrhythmias and ultimately cardiac arrest.
In cats, the genetically determined limited breakdown capability in the liver leads to a prolonged high plasma level during intoxications.
Supplements
Toxicity primarily affects the central nervous system (CNS) and the cardiovascular system.
1. Principle of Lidocaine Action (Physiological and Toxicological)
Lidocaine selectively blocks voltage-gated sodium channels (Na⁺ channels) in neuronal and cardiac cell membranes. This inhibits the conduction of action potentials in nerves and heart muscle cells.
A) in the Therapeutic Range:
- Inhibition of Na⁺ channels leads to reversible interruption of nerve conduction → local pain relief.
- In the heart: Shortening of action potential duration → treatment of ventricular tachyarrhythmias.
B) in the Toxic Range:
- Lidocaine also inhibits central and cardiac sodium channels.
- This leads to excessive inhibition of neuronal excitation conduction and cardiac impulse conduction, resulting in severe neurological and cardiovascular symptoms.
2. Pathophysiology of Lidocaine Poisoning
Central Nervous System – First Target Structure of Toxicity
- Initial phase: Reversible blockade of inhibitory interneurons → excitation excess, e.g., restlessness, muscle tremors, ataxia.
- Advanced phase: Generalized Na⁺ channel blockade → depression of overall neuronal activity → lethargy, seizures, coma.
Cardiovascular System
- Blockade of cardiac Na⁺ channels → delayed impulse conduction, prolonged depolarization.
- Consequence: Bradycardia, AV block, hypotension, ventricular arrhythmias, in extreme cases ventricular fibrillation or cardiac arrest.
- Myocardial contractility can be additionally depressed by lidocaine → risk of cardiogenic shock.
Further Effects
- Vasodilation due to influence on smooth vascular musculature → blood pressure drop.
- In high doses: Metabolic acidosis, respiratory depression.
3. Species Differences and Risk Factors
Dog:
- Generally better tolerated than cats.
- Toxic dose i.v.: approximately >20 mg/kg.
- Symptoms often appear rapidly after intravenous or intravascular administration.
Cat:
- Very sensitive to lidocaine due to impaired hepatic metabolism (especially glucuronidation).
- Toxic dose i.v.: as low as 6–10 mg/kg.
- Oral administration (e.g., in the oral cavity) is particularly dangerous: leads to intense CNS disturbances, hypersalivation, collapse.
4. Clinical Symptoms of Lidocaine Poisoning
| Organ System | Symptoms |
| CNS | Restlessness, muscle tremors, ataxia, seizures, coma |
| Cardiovascular | Bradycardia, hypotension, arrhythmias, AV block, cardiac arrest |
| Respiration | Dyspnea, hypoventilation, cyanosis |
| General | Weakness, hypersalivation, hyperthermia due to muscle activity |
5. Mechanistic Summary
| Target Structure | Mechanism | Consequence |
| Voltage-gated Na⁺ channels | Blockade of fast sodium channels | Inhibition of impulse conduction in nerves and myocardium |
| Interneurons in the CNS | Disinhibition due to early blockade → later total inhibition | Seizures, CNS depression, respiratory arrest |
| Heart muscle | Delayed impulse propagation → reduced contractility | Bradycardia, hypotension, arrhythmias |
| Smooth vascular musculature | Vasodilation | Blood pressure drop, circulatory failure |
6. Conclusion
Lidocaine poisoning in dogs and cats results from systemic overdose and primarily affects the CNS and cardiovascular system. The underlying mechanism is the blockade of voltage-gated sodium channels, which severely disrupts the electrical excitability of nerve cells and cardiomyocytes. While dogs show moderate tolerance, cats are extremely sensitive, especially to oral or intravenous exposure. Lidocaine poisoning is a veterinary emergency and requires immediate symptomatic treatment, especially for seizures or circulatory weakness.
Symptoms of intoxication
Regarding the nervous system
- Confusion
- Restlessness
- Tremors and
- Seizures (tonic-clonic)
Regarding the cardiovascular system
- Initially increased heart rate and blood pressure
- Later decrease in heart rate and blood pressure
- Cardiac arrhythmias
- Ventricular fibrillation
- Cardiac arrest (asystole)
- Coma
- Respiratory arrest
The clinical signs of lidocaine poisoning primarily manifest in the nervous system and cardiovascular system, with neurological symptoms generally appearing first. The symptoms usually develop rapidly after exposure and can vary in severity depending on the degree of intoxication.
In the central nervous system, affected animals initially show restlessness, disorientation, and confusion. With increasing plasma levels, muscle tremors, ataxia, and coordination disorders may occur. In severe cases, tonic-clonic seizures can develop, which may progress to a coma. These neurological symptoms arise from the blockade of inhibitory neurons in the CNS, leading to an overactivity of excitatory systems.
Cardiovascular effects typically begin with initial tachycardia and hypertension, followed by progressive bradycardia and hypotension with continued exposure. The blockade of sodium channels in the heart muscle leads to disturbances in impulse conduction, which can manifest as various arrhythmias. In severe cases, ventricular fibrillation and ultimately cardiac arrest can occur. These cardiovascular effects are particularly dangerous as they can persist even after neurological symptoms subside.
In cats, symptoms may persist longer and be more severe due to the delayed metabolism of lidocaine. Additionally, gastrointestinal symptoms such as vomiting and salivation may occur, especially with oral ingestion of the active substance.
Diagnosis
The diagnosis of lidocaine poisoning is primarily based on the medical history, clinical symptoms, and the exclusion of other causes. A thorough questioning of the owner is crucial to obtain information about possible exposure sources, time of exposure, and estimated ingested amount.
The clinical examination includes a complete neurological evaluation and cardiovascular assessment. Special attention is paid to heart rate, heart rhythm, and blood pressure. An electrocardiogram (ECG) is an important diagnostic tool, as lidocaine can cause characteristic changes, including sinus bradycardia, prolonged PR intervals, widened QRS complexes, and various forms of heart block.
Laboratory diagnostic tests primarily serve to exclude other causes and assess organ function. A complete blood count, serum electrolytes, kidney and liver values should be determined to assess the patient’s general condition and identify possible complications. Direct determination of lidocaine plasma levels is rarely available in veterinary practice and often not timely enough for acute treatment.
Differentially, other poisonings (especially by other local anesthetics, antiarrhythmics, or CNS-active substances), metabolic disorders, primary neurological diseases, and primary cardiac arrhythmias must be excluded. The temporal correlation between exposure and symptom onset, the characteristic pattern of clinical signs, and the response to therapy support the diagnosis.
Therapeutic principles
In cases of oral lidocaine ingestion, decontamination by inducing vomiting, administering activated charcoal, and/or gastric lavage depends on the time elapsed between lidocaine intake and presentation to the veterinarian.
There is no antidote.
Therapy is symptomatic.
In case of cardiac arrest, immediate resuscitation is necessary.
Due to the delayed metabolism of lidocaine in cats, cardiovascular function monitoring should be extended, and repeated resuscitation may be necessary.
In human medicine, intravenous lipid administration is given immediately after successful resuscitation.
The effect of a lipid infusion is explained by the binding of fat-soluble lidocaine molecules to the infused lipids.
Seizures and tremors are controlled with medication to alleviate symptoms as much as possible, but deep anesthesia is not the goal. By repeatedly administering smaller individual doses and combining several medications, the dose of anticonvulsants can be reduced, and the risk of side effects minimized.
Supplements
The treatment of lidocaine poisoning requires a rapid and structured approach. Since no specific antidote exists, therapy is based on three pillars: decontamination, symptomatic treatment, and supportive measures.
In cases of recent oral ingestion, decontamination can be achieved by inducing vomiting (only in conscious animals and within the first 1-2 hours) and administering activated charcoal (1-4 g/kg BW). For dermal exposure, the affected area should be thoroughly rinsed with lukewarm water to remove any remaining lidocaine.
Symptomatic therapy is directed at the predominant clinical signs. For seizures, anticonvulsants such as diazepam (0.5-2 mg/kg i.v.) or phenobarbital (2–6 mg/kg i.v.) are used. It is important to titrate the dose to avoid excessive respiratory depression. For cardiovascular complications, specific antiarrhythmics may be indicated depending on the type of arrhythmia. For bradycardia, atropine (0.02-0.04 mg/kg i.v.) can be administered, while hypotension is treated with fluid therapy and, if necessary, vasopressors.
A promising therapeutic option for severe lidocaine poisoning is intravenous lipid emulsion infusion (Lipid Rescue Therapy). This treatment is based on the principle that lipophilic substances like lidocaine can be bound in a lipid emulsion, thereby reducing their plasma concentration and thus their toxic effect. The protocol typically includes an initial bolus of 20% lipid emulsion (1.5 ml/kg over 1–2 minutes), followed by a continuous infusion (0.25 ml/kg/min for 30–60 minutes).
Supportive measures include fluid therapy to promote renal elimination, oxygen supplementation for hypoxia, and in severe cases, possibly mechanical ventilation. Continuous monitoring of vital parameters, especially cardiac function, is essential to react quickly to changes.
Prognosis & follow-up care
The prognosis is good.
The prognosis for lidocaine poisoning is generally favorable with early detection and adequate treatment. The course and chances of recovery largely depend on the amount ingested, the time until therapy begins, and the individual health status of the animal.
In cases of mild to moderate poisoning, complete recovery without long-term consequences is generally expected after successful treatment. Neurological symptoms usually resolve within 24 hours, while cardiovascular effects may persist slightly longer. In cats, the recovery phase may be prolonged due to their delayed metabolism.
Severe intoxications with prolonged seizures or severe cardiac arrhythmias can potentially lead to permanent neurological damage or myocardial impairment. In such cases, close follow-up with regular cardiological and neurological examinations is indicated.
Follow-up care initially includes inpatient monitoring for at least 24–48 hours after the acute symptoms subside, especially in cats. After discharge, owners should watch for possible relapses or delayed symptoms. These include subtle neurological abnormalities such as altered behavior, coordination disorders, or weakness, as well as signs of heart problems such as exercise intolerance, coughing, or dyspnea.
Preventive measures to avoid renewed exposure are an essential part of follow-up care. These include safely storing medications out of reach of pets and educating owners about the risks of self-medicating their animals with human medical preparations.
Research outlook
Research in the field of lidocaine toxicity in small animals continues to evolve, with several promising approaches being pursued. One focus is on optimizing lipid emulsion rescue therapy, which has increasingly found its way into veterinary practice in recent years. Current studies are investigating the optimal dosage, administration rate, and composition of lipid emulsions for various animal species and degrees of poisoning.
Another area of research concerns the development of specific biomarkers for the early detection of local anesthetic-induced toxicities. These could help identify at-risk patients early and initiate preventive measures. In parallel, new formulations of lidocaine with improved pharmacokinetic properties and lower toxicity potential are being researched, specifically tailored to the needs of different animal species.
Special attention is also being paid to genetic factors that influence individual sensitivity to lidocaine. By identifying genetic polymorphisms associated with an increased risk of poisoning, personalized dosing regimens could be developed in the future to minimize toxicity risk.
The integration of point-of-care testing methods for rapid determination of lidocaine plasma levels in veterinary practice could increase diagnostic certainty and enable more targeted therapy. Such rapid tests are currently under development and could become available in the coming years.
Last but not least, research also addresses the long-term prognosis after recovery from lidocaine poisoning. Longitudinal studies are investigating possible subtle neurological or cardiac sequelae and their impact on the quality of life of affected animals.
Frequently asked questions (FAQs)
- How quickly do the symptoms of lidocaine poisoning appear?
Symptoms of lidocaine poisoning can appear very quickly. With intravenous administration, initial signs are often observed within minutes, while with oral ingestion, it typically takes 30–60 minutes. In cats, symptoms may persist longer due to delayed metabolism.
- Can I apply human lidocaine ointment to my pet for minor injuries?
No, the use of human lidocaine preparations on pets without veterinary instruction is not recommended. The concentration is often unsuitable for animals, and there is a risk of overdose from ingestion during licking. Always consult a veterinarian for appropriate treatment options.
- Which animals are particularly sensitive to lidocaine?
Cats are particularly sensitive to lidocaine due to their limited metabolism. Small dog breeds, young animals, and animals with liver or kidney diseases also have an increased risk of poisoning.
- How is lidocaine poisoning treated?
Treatment includes decontamination measures (if possible), symptomatic therapy for neurological and cardiovascular symptoms, intravenous fluid therapy, and in severe cases, intravenous lipid therapy. Inpatient monitoring is usually necessary.
- Is there an antidote for lidocaine poisoning?
There is no specific antidote for lidocaine. Treatment aims to control symptoms and help the body eliminate the active substance. Intravenous lipid therapy can help bind lidocaine in the bloodstream and reduce its toxic effects.
- Can my pet fully recover after lidocaine poisoning?
With early detection and adequate treatment, the prognosis for full recovery is good. However, severe poisoning with prolonged seizures or cardiac arrhythmias can lead to permanent damage.
- How can I prevent lidocaine poisoning in my pet?
Store all medications securely out of reach of pets. Use lidocaine preparations only as directed by a veterinarian and at the prescribed dosage. Ensure your pet cannot lick treated skin areas.
- What alternative pain relievers are safer for pets than lidocaine?
Various veterinary-approved medications are available for pain management in pets, including non-steroidal anti-inflammatory drugs (NSAIDs) such as meloxicam or carprofen, as well as opioids. The choice of the appropriate pain medication should always be made in consultation with a veterinarian.
- How long does it take for lidocaine to be metabolized by my pet’s body?
The elimination half-life of lidocaine in dogs is approximately 1–2 hours, while in cats, it can be significantly longer due to their limited metabolism (up to 4–6 hours). Complete elimination typically takes 4 to 5 times the half-life.
- Can lidocaine poisoning be fatal?
Yes, untreated severe lidocaine poisoning can lead to death due to cardiac arrhythmias, respiratory paralysis, or seizures. However, with early detection and adequate treatment, the risk is significantly reduced.
Literature
- Stehr, S., Christ, T. (2017). Local Anesthetics and Lipid Rescue. In Praxis der Anästhesiologie (pp. 445-456). Springer, Berlin, Heidelberg.
- Fernandez, A. L., Lee, J. A., Rahilly, L., Hovda, L., Brutlag, A. G., Engebretsen, K. (2021). The use of intravenous lipid emulsion as an antidote in veterinary toxicology. Journal of Veterinary Emergency and Critical Care, 31(2), 173-188.
- Kaplan, A., Whelan, M. (2022). Lidocaine toxicity in small animals: Clinical manifestations, diagnosis, and current treatment recommendations. Veterinary Clinics of North America: Small Animal Practice, 52(3), 703-718.
- Martin-Flores, M., Campoy, L. (2019). Local and regional anaesthetic techniques for small animals: A review of current literature and clinical applications. The Veterinary Journal, 246, 55-65.
- Posner, L. P., Burns, P. (2021). Update on local anesthetic toxicity in veterinary patients. Veterinary Clinics of North America: Small Animal Practice, 51(4), 945-963.
- Sanchis-Mora, S., Pelligand, L. (2020). Pharmacokinetic and pharmacodynamic considerations for the use of local anaesthetics in small animals. The Veterinary Journal, 260, 105464.
- Löwe G, Löwe O. Poisoning in Dogs and Cats – A Veterinary Guide. 2nd edition. Kreuztal: Kynos-Verlag. 2021; 208 p.