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I am sharing my own knowledge and experience with you. In Canada, only anesthesiologists are allowed to administer this treatment. It is a medical act therefore it requires someone who is knowledgeable with an MD graduate and an anesthesiology specialty. I encourage you to seek a doctor who knows and is proficient in the administration of lidocaine infusion and to seek medical information from the doctor.
Before administering this treatment, the anesthesiologist will determine if the lidocaine is for you. A simple test will be administered. A syringe of lidocaine and a syringe of saline will be given separately, to determine if the lidocaine is actually effective. Simple and safe. Then your weight will be captured in order to use the formula which will determine how much lidocaine you require for targeting the pain safely. Vital signs are taken during the infusion, Blood pressure, pulse, oxygen level.
The anesthesiologist will usually start the treatment at its lowest dosage which is:
4.5 mg of lidocaine 2% per kilogram of your weight
This will start you on a safe journey. Your next appointment is very important because you will be able to tell the length of the relief you obtained from the infusion. I recommend you keep track , between the infusions, the pain levels, what unusual events happened, your mood, or anything that is out of ordinary. Once you have determined that the length of the relief you experienced, you will give this valuable info to your doctor so he can titrate the lidocaine according to your pain level. The lidocaine can be increased at each visit until you reach a comfortable level.
It is important to remember that achieving complete pain control is very difficult, therefore it is better to stay at a lower level of dosage such as 5mg as an example for as long as you can. The body always gets accustomed to medication so you want to make sure you keep this alternative viable for you.
There are other ways to achieve pain relief which complement the infusion. We will talk about this .
- Oral/tongue numbness, metallic taste
- Double vision
- Dizziness, lightheadedness
- Seizures are rare
In order to contravene the side effects I drink an orange juice or have a chocolate bar during the infusion, to keep my blood sugar levels up. This way it eliminates and/or decrease the pesty side effects. The side effects disappear rapidly after the infusion is finished. Driving is contraindicated. The lidocaine makes me very tired so after a good night sleep, I am back to normal and go back to my normal life without pain or almost without. My pain level is at about 1 or 2 level from 10 being the worst.
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Lidocaine & other anesthetics
Mechanism of action: Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action.
Hemodynamics: Excessive blood levels may cause changes in cardiac output, total peripheral resistance, and mean arterial pressure. With central neural blockade these changes may be attributable to block of autonomic fibers, a direct depressant effect of the local anesthetic agent on various components of the cardiovascular system and/or the beta-adrenergic receptor stimulating action of epinephrine when present. The net effect is normally a modest hypotension when the recommended dosages are not exceeded.
Pharmacokinetics and metabolism: Information derived from diverse formulations, concentrations and usages reveals that lidocaine is completely absorbed following parenteral administration, its rate of absorption depending, for example, upon various factors such as the site of administration and the presence or absence of a vasoconstrictor agent. Except for intravascular administration, the highest blood levels are obtained following intercostal nerve block and the lowest after subcutaneous administration.
The plasma binding of lidocaine is dependent on drug concentration, and the fraction bound decreases with increasing concentration. At concentrations of 1 to 4 mcg of free base per mL, 60 to 80 percent of lidocaine is protein bound. Binding is also dependent on the plasma concentration of the alpha-1-acid glycoprotein.
Lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion.
Lidocaine is metabolized rapidly by the liver, and metabolites and unchanged drug are excreted by the kidneys. Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the amide linkage, and conjugation. N-dealkylation, a major pathway of biotransformation, yields the metabolites monoethylglycinexylidide and glycinexylidide. The pharmacological/toxicological actions of these metabolites are similar to, but less potent than, those of lidocaine. Approximately 90% of lidocaine administered is excreted in the form of various metabolites, and less than 10% is excreted unchanged. The primary metabolite in urine is a conjugate of 4-hydroxy-2, 6-dimethylaniline.
The elimination half-life of lidocaine following an intravenous bolus injection is typically 1.5 to 2.0 hours. Because of the rapid rate at which lidocaine is metabolized, any condition that affects liver function may alter lidocaine kinetics. The half-life may be prolonged two-fold or more in patients with liver dysfunction. Renal dysfunction does not affect lidocaine kinetics but may increase the accumulation of metabolites.
Factors such as acidosis and the use of CNS stimulants and depressants affect the CNS levels of lidocaine required to produce overt systemic effects. Objective adverse manifestations become increasingly apparent with increasing venous plasma levels above 6.0 mcg free base per mL. In the rhesus monkey arterial blood levels of 18-21 mcg/mL have been shown to be threshold for convulsive activity.
Indications and Usage
Lidocaine Hydrochloride Injection, USP is indicated for production of local or regional anesthesia by infiltration techniques such as percutaneous injection and intravenous regional anesthesia by peripheral nerve block techniques such as brachial plexus and intercostal and by central neural techniques such as lumbar and caudal epidural blocks, when the accepted procedures for these techniques as described in standard textbooks are observed.
Lidocaine is contraindicated in patients with a known history of hypersensitivity to local anesthetics of the amide type.
LIDOCAINE HYDROCHLORIDE INJECTION, FOR INFILTRATION AND NERVE BLOCK, SHOULD BE EMPLOYED ONLY BY CLINICIANS WHO ARE WELL VERSED IN DIAGNOSIS AND MANAGEMENT OF DOSE-RELATED TOXICITY AND OTHER ACUTE EMERGENCIES THAT MIGHT ARISE FROM THE BLOCK TO BE EMPLOYED AND THEN ONLY AFTER ENSURING THE IMMEDIATE AVAILABILITY OF OXYGEN, OTHER RESUSCITATIVE DRUGS, CARDIOPULMONARY EQUIPMENT, AND THE PERSONNEL NEEDED FOR PROPER MANAGEMENT OF TOXIC REACTIONS AND RELATED EMERGENCIES (See also ADVERSE REACTIONS and PRECAUTIONS). DELAY IN PROPER MANAGEMENT OF DOSE-RELATED TOXICITY, UNDERVENTILATION FROM ANY CAUSE AND/OR ALTERED SENSITIVITY MAY LEAD TO THE DEVELOPMENT OF ACIDOSIS, CARDIAC ARREST AND, POSSIBLY, DEATH.
Intra-articular infusions of local anesthetics following arthroscopic and other surgical procedures is an unapproved use, and there have been post-marketing reports of chondrolysis in patients receiving such infusions. The majority of reported cases of chondrolysis have involved the shoulder joint; cases of gleno-humeral chondrolysis have been described in pediatric and adult patients following intra-articular infusions of local anesthetics with and without epinephrine for periods of 48 to 72 hours. There is insufficient information to determine whether shorter infusion periods are not associated with these findings. The time of onset of symptoms, such as joint pain, stiffness and loss of motion can be variable, but may begin as early as the 2nd month after surgery. Currently, there is no effective treatment for chondrolysis; patients who experienced chondrolysis have required additional diagnostic and therapeutic procedures and some required arthroplasty or shoulder replacement.
To avoid intravascular injection, aspiration should be performed before the local anesthetic solution is injected. The needle must be repositioned until no return of blood can be elicited by aspiration. Note, however, that the absence of blood in the syringe does not guarantee that intravascular injection has been avoided.
Local anesthetic solutions containing antimicrobial preservatives (e.g., methylparaben) should not be used for epidural or spinal anesthesia because the safety of these agents has not been established with regard to intrathecal injection, either intentional or accidental.
KETALAR® (ketamine as hydrochloride) has been studied in over 12,000 operative and diagnostic procedures involving over 10,000 patients from 105 separate studies. During the course of these studies, KETALAR® was administered as the sole agent, as induction for other general anaesthetic agents, or to supplement low potency agents. In these studies, the anaesthesia was rated either “excellent” or “good” by the anaesthetist and the surgeon at 90% and 93% respectively. In a second method of evaluation, the anaesthesia was rated “adequate” in at least 90% and “inadequate” in 10% or less of procedures. Specific areas of application have included the following:
- debridement, painful dressings and skin grafting in burn patients as well as other superficial surgical procedures;
- neurodiagnostic procedures such as pneumoencephalograms, ventriculograms, myelograms and lumbar punctures;
- diagnostic and operative procedures of the eye, ear, nose and mouth including dental extractions;
- diagnostic and operative procedures of the pharynx, larynx or bronchial tree;
Note: muscle relaxants with proper attention to respiration, may be required (see
WARNINGS AND PRECAUTIONS)
- sigmoidoscopy and minor surgery of the anus and rectum and circumcision;
- extraperitoneal procedures used in gynaecology, such as dilation and curettage;
- orthopaedic procedures such as closed reductions, manipulations, femoral pinning, amputations and biopsies;
- as an anaesthetic in poor-risk patients with depression of vital functions;
- in procedures where the intramuscular route of administration is preferred;
- in cardiac catheterisation procedures.
Ketamine is rapidly absorbed following parenteral administration. Peak plasma levels averaged 0.75μg/ml and CSF levels were about 0.2μg/ml one hour after dosing.1 The plasma half-life is in the range of 2 to 4 hours.2,3,4 After IM administration (absorption half-life 2-17 minutes) it is up to 93 % bioavailable.1
Ketamine (as hydrochloride) is rapidly and extensively distributed throughout the body into highly perfused tissues including the brain. 3,4 Mean volume of distribution is reported to range from approximately 1 to 3 L/kg, and the distribution half-life is approximately 7 to 11 minutes. Ketamine (as hydrochloride) is approximately 20-50% bound to plasma proteins.6 Ketamine is likely to be excreted in breast milk, but this is unlikely to be clinically relevant. The drug crosses the placenta in induction doses but in amounts that have no adverse effects on the neonate5 (see Use in Pregnancy and Use in Lactation).
Ketamine undergoes extensive hepatic metabolism. The biotranformation includes N- dealkylation to norketamine (metabolite I), hydroxylation of the cyclohexone ring (metabolites III and IV), conjugation with glucuronic acid and dehydration of the hydroxylated metabolites to form the cyclohexene derivative (metabolite II). Norketamine (metabolite I) has about 1/6 of the potency of ketamine and is formed at concentrations in the plasma similar to those of the parent compound.
After intravenous bolus administration, ketamine shows a bi- or triexponential pattern of elimination. The alpha phase lasts about 45 minutes with a half-life of 10 to 15 minutes. This first phase, which represents the anaesthetic action of ketamine, is terminated by redistribution from the CNS to peripheral tissues and hepatic biotransformation to an active metabolite. The beta phase half-life is about 2.5 hours.2,3,4 About 90% of ketamine is excreted in the urine, mostly as metabolites, with only about 2 to 4 % as the unchanged drug. Approximately 5% is recovered in the faeces.7 The renal clearance of ketamine hydrochloride is 15 ± 5 mL/min/kg.8