Anesthetics seizures caused

The only other anesthetic to cause serious toxicity for which a metabolic drug interaction has been reasonably well characterized is the local anesthetic and antiarrhythmic agent lidocaine. Amiodarone decreased lidocaine systemic clearance in a patient (primarily by inhibition of CYP3A4 N-dealkylation of lidocaine) and yielded concentrations of lidocaine that led to seizures (78,79). 

Of the effects listed, the most important in local anesthetic overdose (of both amide and ester types) concern the CNS. Such effects can include sedation or restlessness, nystagmus, convulsions, coma, and respiratory depression. Diazepam is used for seizures caused by local anesthetics, usually without significant effects on ventilation or circulation. The answer is (E). 

Which one of the following drugs has spasmolytic activity and could also be used in the management of seizures caused by overdose of a local anesthetic ... 

In a retrospective analysis of 334 patients with a history of seizure disorder undergoing 411 regional blocks, local anesthesia was implicated in seizure activity in only five of 24 seizures, judging by the time-course of the events [5 ]. There was no proof that the local anesthetic had caused the seizure. Depending on the classification of these five cases, the authors estimated the incidence of... 

PCP receptor (NMDA charmel) GRINl Agonism Anesthetic properties, may induce psychosis (schizophrenia like). hallucination, delirium and disoriented behavior, may cause seizures, neurotoxicity. 

Transcranial magnetic stimulation (TMS) is a novel treatment for psychiatric illness (George et ah, 1999 Pridmore and Belmaker, 1999). In the procedure, a current is passed around an insulated coil held in contact with the patient s head, causing a magnetic field to pass into the first few millimeters of cortex. Unlike ECT, a specific area of the brain is stimulated, the procedure does not require a general anesthetic, and a seizure does not occur. 

In the cardiovascular system, arrhythmias and, in extreme situations, arrest may occur, usually secondary to the combination of seizure activity and anesthetic agent. The mortality rate per course of ECT treatments is in the range of 1 per 10,000 or 0.01%. This risk is less than the overall morbidity and mortality rate (i.e., 3 to 9 per 10,000) seen in severely depressed patients who go untreated or receive inadequate medication trials, and is less than the anesthetic risk for labor and delivery during childbirth. Thus, those who receive an adequate trial of ECT may actually be at a reduced risk of dying from a variety of causes. 

As we will see in part V, the Recreational Drugstore, many of the abused stimulant drugs that cause seizures during acute use are highly sleep suppressant through their direct action on neuromodulatory systems. Alcohol, by contrast, is a general central nervous system suppressant. As such, and in contrast to the stimulants, alcohol causes euphoria only as a relatively brief consequence of its essentially anesthetic action on the brain. By numbing the brain it induces relaxation, lifts cortical inhibition, and produces a temporary sense of comfort with the self and with society. 

With the exception of one case of grand mal seizure possibly associated with the topical application of benox-inate, no cases of serious systemic reactions caused by topically instilled ocular anesthetics have occurred. However, because 98% or more of systemic reactions to local injectable anesthetics are due to drug overdose, such systemic toxic reactions can potentially occur with the excessive administration of topical anesthetics to the eye. Topically applied anesthetics are rapidly absorbed into the systemic circulation, and their blood levels rise almost as rapidly as after intravenous injection. 

The cardiovascular system is more resistant to the toxic effects of local anesthetics than the nervous system. Mild circulatory depression can precede nervous system toxicity, but seizures are more likely to occur before circulatory collapse. The intravenous dose of lidocaine required to produce cardiovascular coUapse is seven times that which causes seizures. The safety margin for racemic bupivacaine is much lower. The stereospecific levorotatory isomers levobupivacaine and ropivacaine are less cardiotoxic, and have a higher safety margin than bupivacaine, but not lidocaine in the case of ropivacaine this may be at the expense of reduced anesthetic potency (14,15). Toxicity from anesthetic combinations is additive. 

Central nervous system effects of low concentrations of local anesthetics are mainly sedation and confusion high concentrations are more likely to cause seizures (18). 

The authors postulated vertebral artery injection of local anesthetic as the cause of the seizure and loss of consciousness. 

Anesthetic induction agents These (e.g. methohexital, propofol, thiopental sodium) rapidly induce hypnosis, without significantly shortening seizure activity or causing hemodynamic instability, and thus allow for rapid emergence from anesthesia. 

In the 1960s GHB was developed as an anesthetic s ent. Like PGP, it had serious side effects (seizure-like activity) and its use y/as discontinued. In the 1980s GHB was sold in the health food industry as a growth hormone stimulator and was supposed to help body builders gain muscle mass. It was also sold as a sleep aid. It became a popular recreational drug because in low doses it can have an aphrodisiac effect as well as cause relaxation and euphoria. However, at higher doses it causes coma and amnesia. These effects made it effective as a date rape ... 

In the first case the authors assumed that the seizure was due to absorption of the local anesthetic into the systemic circulation rather than direct intravascular injection, because of the delayed development. In the second case the enlarged pupils were caused by total spinal anesthesia most probably due to absorption of a large volume of local anesthetic into the cerebrospinal fiuid rather than direct intrathecal injection, in view of the very slow onset during surgery. 

Evaluate for toxicity due to intravascular placement symptoms such as lightheadedness, dizziness, a metallic taste, ringing in the ears, or perioral numbness signify potential intravascular injection and risk for toxicity. Local anesthetic toxicity can also cause late symptoms such as hypotension, blurry vision, seizures, and cardiac arrhythmias. Stay with the patient for the first 10 minutes after a test dose or bolus. 

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