Why does lidocaine cause seizures
Mild nausea is occasionally described. Some patients describe a degree of mild dysarthria, mild confusion, and slight memory impairment. For example, a patient might have difficulty pronouncing words or have a slightly unsteady gait, as if mildly drunk. One patient had difficulty remembering her telephone and apartment numbers.
The onset of symptoms occurred approximately 12 hours after surgery, on awakening from a nap. Serum lidocaine concentrations were not obtained. On receiving a telephone call from a patient with these symptoms, the surgeon should take a careful history and perform a rapid evaluation. Patients may admit self-medication with a sedative or a codeine-type narcotic analgesic from a prescription written by another physician.
The symptoms listed are known to occur with reactions associated with benzodiazepines or hydrocodone. For some patients the subjective symptoms have been consistent with a hyperventilation syndrome, with perioral and digital tingling and mild to moderate anxiety. Once the mild nature of the complaint is determined, I speak to the patient by telephone every 1 to 2 hours or until the symptoms improve.
I tell the patient that if the symptoms worsen, evaluation in a local ER will be necessary. The symptoms usually begin to improve noticeably within an hour or two.
Having the patient drink fluids, relax in a semirecumbent position, watch television as a distraction, or breathe into a paper bag has been helpful. They were sufficiently anxious to warrant more than a telephone evaluation.
Plasma lidocaine levels, obtained as part of an ER examination, were 2. These patients likely had much lower thresholds for subjective symptoms. Subjective CNS toxicity is most likely to occur with relatively high doses of tumescent lidocaine. Serious consequences have not been reported. It is theoretically impossible to define precisely the maximum safe dose of tumescent lidocaine. A scientific attempt to determine a maximum safe dose of tumescent lidocaine is, at best, a sophisticated process of biostatistical estimation see Chapters 6 and As noted elsewhere, a proposal that a higher dosage limit for tumescent liposuction is safe is merely a clinical hypothesis.
The surgeon who makes such a proposal has a strong ethical obligation to make a concerted statistical effort to disprove the hypothesis. In one report, In the late s and early s, procainamide Novacaine , now procaine Novocain , was virtually the only local anesthetic used in the United States. By , lidocaine had become the most widely used local anesthetic because of its superior safety and efficacy and the exceedingly low incidence of allergy.
Procain is an ester-type local anesthetic that is metabolized in the blood by plasma esterases. Lidocaine is an amide-type local anesthetic that is metabolized by CYP3A4. True allergic reactions to lidocaine are extremely rare, but a history of allergy to any local anesthesia cannot be ignored.
Most patients are not aware of the distinction between adverse drug reaction and allergic drug reaction. They make no distinction between an allergic reaction and the predictable pharmacologic event following rapid systemic absorption of epinephrine. Questions during the preliposuction history generally provide enough information to distinguish between a potentially serious anaphylactic or anaphylactoid drug reaction and a benign pharmacologic response.
If a true adverse reaction to a local anesthetic cannot be excluded by the history, or if the patient insists that a reaction was truly allergic, the patient should be referred to a specialist for consultation, allergy testing, and a written report documenting the findings and recommendations. Chemically mediated reactions are most likely related to a preservative such as sodium bisulfite.
Other local anesthetics have adverse interactions with lidocaine. The pharmacologic or toxic effects of lidocaine and any other local anesthetic are additive. Drug that share CYP3A4 as the important metabolic enzyme may have adverse interactions with lidocaine. General anesthesia with halothane plus nitrous oxide causes an elevation in lidocaine plasma concentrations. Sinus bradycardia was seen in a patient taking the oral antiarrhythmic drug amiodarone after being given lidocaine as local anesthesia.
Amiodarone competes with lidocaine for binding to CYP3A4. Dilute bupivacaine and high-dose dilute epinephrine have been associated with a death during liposuction by local anesthesia in a patient taking phentermine Fastin.
Cocaine and lidocaine interact adversely. In a rat study, the overall toxicity of cocaine was significantly increased with simultaneous exposure to lidocaine. At sufficiently high doses, beta blockers decrease cardiac output, thus decreasing hepatic blood flow and rate of lidocaine extraction by the liver.
To avoid preoperative hypertension or recurrent severe headaches, patients should continue these drugs during liposuction surgery. A study using rat liver microsomes showed that lidocaine 3-hydroxylation and propranolol ring hydroxylations are mediated by the same cytochrome P 2D isoenzymes. Phenytoin and lidocaine have been reported to have additive cardiac depressant effects. Using high-dose lidocaine in patients with seizure disorders probably carries a risk of lowering the seizure threshold.
Lack of communication between anesthesiologist and surgeon has contributed to deaths of patients not being treated totally by local anesthesia. Both surgeon and anesthesiologist should be aware of the total parenteral IV and subcutaneous fluid dosage. If either clinician is unaware of the fluids administered to the patient by the other, a fluid overload is highly probable.
Excessive parenteral isotonic fluids can result in hemodilution, leading to disseminated intravascular coagulation DIC , pulmonary edema, and adult respiratory distress syndrome ARDS. This requirement demands compulsively accurate record keeping, using an efficient intraoperative anesthesia flow sheet that is specifically designed for tumescent anesthesia.
I know of two superwet liposuction—related deaths resulting from pulmonary edema and lidocaine toxicity see Chapter 9. In both cases, no explicit orders were written for lidocaine. Surgeons should know that local anesthetics are toxic and that explicit orders must be written before the preparation or mixture of parenteral medications.
Surgeons and anesthesiologists must be in complete agreement regarding the exact type and dosage of drug and fluids used during liposuction. Besides excessive volumes of liposuction, lack of knowledge about IV fluid toxicity, and careless surgical technique, the greatest risk of surgical mortality with the tumescent technique is lack of precise communication between the surgeon and staff.
Surgeons, anesthesiologists, and OR staff are not accustomed to written orders for local anesthesia, but written orders are an absolute necessity for safe tumescent anesthesia. The OR staff should be instructed not to mix any tumescent anesthesia unless explicit written orders have been completed by the surgeon Box The surgeon and staff are responsible for documenting the true dose of lidocaine and epinephrine that the patient actually has received.
This is accomplished by means of a special intraoperative anesthesia flow sheet, which all surgeons performing tumescent techniques are encouraged to use Box As discussed, human error is the most likely cause of lidocaine overdose and serious toxicity.
The goal is to minimize the possibility of error through training of staff and fastidious written policies and procedures; for example, staff should have Advanced Cardiac Life Support ACLS training. If there is a significant risk that a toxic overdose has been given, the patient should not be managed in an outpatient facility. Appropriate clinical observation in an ICU, with cardiac monitoring, secure IV access, and oxygen supplementation, is necessary with a suspected or a recognized overdose of tumescent lidocaine.
A patient who has received too much lidocaine should not be treated for a seizure before it occurs. For example, preemptive treatment with a benzodiazepine such as diazepam may actually impair lidocaine metabolism by inhibiting CYP3A4, thereby increasing the risk of a seizure.
By impairing ventilation, benzodiazepines can also increase the risk of seizures. The most prudent approach is to observe the patient closely in the ICU for a potential seizure. Plasma lidocaine concentrations should be obtained every 4 to 6 hours. The patient should be discharged only after two consecutive levels indicate that 1 the peak concentration has been achieved and 2 the subsequent levels are definitely on a downward course.
When a serious lidocaine toxicity is encountered, the principal therapeutic intervention is treating seizures and maintaining adequate ventilation and oxygenation. Treatment with oxygen alone is insufficient to prevent hypoventilation and respiratory acidosis. Both the lidocaine dose and route of administration were verified and within the recommended range. A lidocaine level of 0. No further seizures were noted and the newborn was discharged on day of life 27 on multivitamins, ferrous sulfate drops and no antiseizure medications.
Neurology follow-up through 6 months of age has been within normal limits. NICU graduates and newborn male infants may have circumcision routinely performed using subcutaneous lidocaine for local anesthesia.
Many of these procedures are done just prior to discharge home. Neonatal seizures following recommended doses of lidocaine administered for local anesthesia for this extremely common procedure have not been reported to the best of our knowledge.
We report a case of tonic—clonic seizures in a day-old former premature newborn following elective circumcision with a quantified lidocaine level of 0. Based on the timing of the tonic—clonic seizures in our patient, lidocaine appeared to be the most likely cause of these seizures.
The clinical presentation was not consistent with a hypersensitivity reaction. Lidocaine-induced seizures have been reported in infants, children, and adults. Seizures have been previously reported in a neonate where intravenous lidocaine was given in conjunction with midazolam and atropine for preoperative intubation. Delayed maturation of drug metabolizing enzymes may predispose premature and term neonates to adverse effects from drugs such as lidocaine.
CYP 3A7 is the predominant isoform expressed in the fetal liver. The expression or activity of 3A7 peaks shortly after birth and then declines as it is replaced by 3A4.
Prolonged elimination half-life, increased volume of distribution and decreased protein binding may also predispose premature neonates to adverse effects. This decrease in protein binding increases the amount of unbound and active drug.
Our case report raises the following important questions: 1 are premature newborns more likely to exhibit adverse effects to recommended doses of lidocaine secondary to immature hepatic function and increased drug bioavailability; 2 should lower doses of lidocaine or other anesthetics altogether be used in premature newborns undergoing circumcision; and 3 should there be a longer observation period prior to discharge for premature neonates after circumcision?
Until further studies are available, we now recommend that former premature newborns undergoing elective circumcisions and other procedures using local anesthetics be performed at least 24 hours prior to planned discharge. Recurrent seizures in a neonate after lidocaine administration. J Perinatol ; 18 — Lidocaine induced seizures in patients with history of epilepsy: effect of antiepileptic drugs. Anesthesiology ; 97 — Article Google Scholar. Lidocaine toxicity secondary to postoperative bladder instillation in a pediatric patient.
Urology ; 53 Pediatr Emerg Care ; 16 — Neurologic conditions may be associated with occupational or environmental exposures to heavy metals, such as lead and manganese. Conditions resulting from metal exposure may mimic routine neurologic disease, such as encephalopathy, movement disorders, neuropathy, or seizures. Neurotoxic illness is often a diagnosis of exclusion after considering other more common presentations for a condition.
Botulinum toxin has been approved for treatment of migraine headache, cervical dystonia, strabismus and blepharospasm, and upper and lower limb spasticity. It is a neuromuscular blocking agent that functions by inhibiting the release of acetylcholine. Movement Disorders. Parkinsonism is a common side effect of all the atypicals except quetiapine and clozapine, certain calcium channel blockers, tetrabenazine, and its derivative vesicular monoamine transporter type 2 VMAT2 blockers.
It may also be seen with valproic acid and lithium. Although most drugs causing parkinsonism do so in a dose-related manner, there is an enormous variation in individual susceptibility. Sleep Disorders. Valproic acid is used as an anticonvulsant drug to treat multiple seizure types, as well as for prevention of migraine and treatment of bipolar disorder.
It is structurally unrelated to other antiepileptic drugs. The aim of therapy is to control seizures, continued for as long as seizure control is required.
Sign Up for a Free Account. Go to Pubmed. Updated Local anesthesia: neurologic complications. Overview This article focuses on the neurologic complications of drugs used for local anesthesia as well as the procedures involved. Key points Local anesthetics may cause adverse effects either by action on the nerves and muscles or neurotoxicity following systemic absorption. Injection injury of neural structures may result from the procedure.
Historical note and terminology Local anesthetics are substances that produce a reversible loss of sensation or analgesia when applied to body tissues. Presentation and course Neurologic adverse effects of local anesthetics may be confined to peripheral or cranial nerves in proximity to the site of application.
Adverse effects may involve the CNS directly. CNS adverse effects may be due to systemic toxicity involving other body systems. Table 1. Prognosis and complications The prognosis of recovery from complications of local anesthesia is generally good.
Peripheral nerves may be injured by the injection needle. Etiology and pathogenesis Neurologic complications have been reported with all currently used local anesthetics. The causes of neurologic damage associated with spinal anesthesia include the following: Trauma of lumbar puncture with subarachnoid hemorrhage. Chemical and bacterial contamination of the local anesthetic solution. Toxic reaction to the local anesthetic. Examples of technical factors leading to neurologic complications are: Accidental intrathecal injection of local anesthetic during trigger-point injection therapy, resulting in respiratory depression and hemiplegia.
Paralysis of diaphragm, due to upward migration of local anesthetic after brachial block. The following pharmacokinetic interactions increase the toxicity of local anesthetics: Calcium antagonists reduce the protein binding and increase the free fraction of local anesthetics. Beta blockers decrease clearance of local anesthetics. Cimetidine decreases the metabolism of lidocaine, thus, increases its toxicity.
Acetazolamide prolongs the half-life of procaine. The following pharmacodynamic interactions increase the neurotoxicity of local anesthetics: Baclofen lowers the threshold for seizures.
Flumazenil may increase the convulsive activity of bupivacaine. Risks of permanent neurologic injury and systemic toxicity with local anesthesia are low. The best approach to the management of local anesthetic complications is prevention. Concomitant use of drugs that may interact with local anesthetics should be avoided. Confusing conditions Complications need to be differentiated from other causes of similar complaints.
Associated or underlying disorders The risk of severe postoperative neurologic dysfunction in patients with preexisting peripheral sensorimotor neuropathy, diabetic polyneuropathy, or spinal canal pathology who undergo neuraxial anesthesia or analgesia is higher than the risk in the general population.
Blood examination including levels of local anesthetics ECG EEG A patient with neurologic complications of local anesthetics should have a blood sample examined for serum concentration of the suspected anesthetic, as well as a normal hematological examination to assess the effects of local anesthetics on platelets, leukocytes, and the morphology of erythrocytes.
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