Science topic

Local Anesthetics - Science topic

Drugs that block nerve conduction when applied locally to nerve tissue in appropriate concentrations. They act on any part of the nervous system and on every type of nerve fiber. In contact with a nerve trunk, these anesthetics can cause both sensory and motor paralysis in the innervated area. Their action is completely reversible. (From Gilman AG, et. al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed) Nearly all local anesthetics act by reducing the tendency of voltage-dependent sodium channels to activate.
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The antimicrobial effect of local anesthetics has been known for more than 50 years, but it still seems to have an unclear mechanism of action. which bacteria? which concentration? etc etc. . Where can I find more literature?
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some anesthetics like procaine and benzocaine have the ability to generate oxidative stress via oxidizing free radicals. Common knowledge about these drugs. - Oxidative stress caused by amino ester anesthetics might be antiseptic toward common skin or mucosa flora just like Oxygen Water (hydrogen peroxide) and thus antimicrobial. Just a thought
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I have observed not much difference in the onset of action of different local anesthetics ( bupivacaine, lignocaine and ropivacaine) when used for peripheral nerve /plexus blocks. Although studies are warranted for proof, it is just my observation. Please share your views and experiences
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Yes, the differential blockade do really seen mostly in neuraxial techniques compared to peripheral nerve blockade.
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Dear researchers, what do you think about the idea of an inhalation therapy with Procain 1% or Lidocain 1% as an adjuvant therapy of viral pneumonia caused by SARS-CoV-2 in order to prevent ARDS?
Two very interesting links discussing the anti-inflammatory properties of local anesthetics:
page 270, Cytokines
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Dear Amjid Hammodi,
even better than Lignocaine is Procain 1% as a nasal spray, I already use this for 3 years in patients with chronic sinusitis, privinism, allergic rhinitis, viral rhinitis and so on. And not only me, there are colleagues, mainly GPs, that are specialized in neural therapy, who use this already for decades! The amount of corticoid nasal spray needed is a lot less in these patients I see (sorry, no EBM, just empirical). And there are two pharmacies in Switzerland, that are officially producing Procain 1% nasal spray.
Best regards
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I am trying to develop a simple Organic Chemistry Lab that will teach students on how to conduct Esterification reaction. The catch is that the synthesized molecule should have recognized medicinal value.
I want to synthesize Procaine as it is a widely known as a local anesthetic. However, the lab doesn't have 2-diethylaminoethanol. So, is it possible to do it from Triethanolamine instead?
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Directly, I think it is not possible. Regards,
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When Stanley Malamed, in his books and many of his papers, writes that " IANB has the highest failure rate among all local anesthetic blocks in Medicine - not only in dental local anesthesia : are there any data in the medical literature backing this assertion, or do you think it is simply a fact that he personnaly observed or experienced as a dentist-anesthesiologist, without scientific evidence ? In the first case, are there references readily availa and if so, could anybody  let me know how and where I can get it ?
Thank you for your comments.
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I thank Mr. Alok Dubey for his very ingenious metaphorical allusions to a medieval European legend ( even though there is much to discuss about the adequacy and comprehensibility of his curious parallels) and his very entertaining and subtle zoological analogies (although they sound a bit farfetched) : I do praise Mr. Dubey for his generous spirit of invention, which allows us to enjoy his devastating humor.
However, I doubt that these reflections are likely to enlighten the primary subject.
I would like to clarify -with serenity and courtesy, but without doublespeak- on both the substance and the form of Mr. Dubey’s intervention.
1-On the content itself:
I am afraid that Mr. Dubey did not read with sufficient attention the original question, nor, moreover, the various contributions, some of them, in particular those by Dr. Daniel Uzbelger Feldman, demonstrating a perfect analysis and understanding of my interrogations.
I need to stress, again, that I am not the author of the statement that “the IANB has the lowest success rate in medicine” (not only in dentistry): it is Prof. Stanley Malamed, who is, as far as I understand, a universally recognized specialist in Oral Anesthesia. Having said that, I tend to agree with Dr Malamed’s opinion; the only thing that still annoys me (a little) is the fact that he did not explain to us how he came to this conclusion, despite repeated requests (directly or via internet).
Precisely, my question was: How did Stanley Malamed come to this assertion?
The question was not: “Does the block of NAI have a reduced success rate?”, because there is a vast consensus on the subject, as shown in any up-to-date books dealing with dental anesthesia.
For example:
Alfred Reader, John Nusstein, Melissa Drum: Successful local anesthesia for restorative dentistry and Endodontics. Second edition. Hanover Park, IL: Quintessence Publishing Co Inc, 2017.
Mr. Dubey explains:
” THE AUTHOR WANT US TO BELIEVE THAT HE IS NOT AWARE OF THE EFFICACY OF THE BLOCK.” (sic)
I am perfectly aware of the efficacy of the IANB, particularly during surgeries (but the necessity of administrating a buccal nerve block might reinforce the global success rate of the IANB), and even more aware of its lack of efficacy in many cases: the authors of the book cited above, after reviewing not less than 21 articles, write, page 42:
“Table 2-1 shows the percentage of success rates in various mandibular teeth. It is important to realize that 100% of the subjects in these studies had profound lip numbness. [2–19,21–23] Success occurs most often in the molars and premolars and less often in the incisors.
IN CONCLUSION, anesthetic success varies from 51% in the first molar to 10% in the central incisor
even though patients have profound lip numbness.”
End of citation.
Anyone who treats endodontically symptomatic mandibular posterior teeth, and reads these articles knows that this question is pointless.
In chapter 2, dealing with mandibular anesthesia, no less than 19 pages (out of the 43 pages of the chapter) explain why and how IANB fails, and how to improve its success rate.
So that the conclusion drawn by Mr. Dubey seems a bit inadequate:
“Even the dumbest of the final year student who has ever given IANB in a proper manner is well versed of its efficacy. SO BASICALLY, THIS DISCUSSION IS FOR THOSE ARE NOT CLEAR WITH THEIR BASICS OF GIVING LA & WANT TO IMPOSE THEIR FAILURE/ INEFFICIENCY OVER IANB BLOCK” (re sic)
The barely subliminal message delivered by Mr. Dubey is that I am unable to administer IAN blocks (I probably compare –not favorably, I am afraid- with the “dumbest of the final year student”), solely because I dare ask a (semantic, not technical) question. He implies that he himself has a remarkable success rate in that exercise: no one doubts it and we all welcome his abilities.
At the end of his diatribe, Mr. Dubey writes:
“SO, I WOULD REQUEST ALL TO END UP THIS DISCUSSION (MISLEADING CONCEPTIONS OR SHOULD I SAY MISCONCEPTION) & DISCUSS ANY TOPIC WHICH WILL THROW SOME LIGHT ON ANY UNTOUCHED TOPIC”.
This final injunction proves to be highly comical when we read the vital and innovative questions that Mr. Dubey proposed, two months ago, at the sagacity of the scientific community (Mr. Dubey has a very personal concept of an “untouched topic”):
- “What is the amount (mg) of lignocaine in 1.8ml carpule of local anesthesia?”
- “What is the maximum recommended dose of 2% lignocaine with vasoconstrictor in a child?”
I do not intend to be unnecessarily cruel, but I must recall that Mr. Dubey is, officially, « Associate Professor in the Department of Pedodontics and Preventive Dentistry, College of Dentistry, Jazan University, Jazan, Kingdom of Saudi Arabia”, and tells us, in his Researchgate profile, that his skills include « anesthesia, pediatric anesthesia, toxicity », amongst numerous capabilities.
So that, after responding his first question, and discovering the second one, I thought it was not incongruous to wonder why an Associate Professor in Pedodontics is led to make such simplistic demands, whereas, by his function itself, this topic is precisely what he is supposed to know, and a fortiori, to teach. Therefore, considering the utterly absurd aspect of the situation, I suggested that the author of such questions probably needed to artificially increase his "visibility" on Researchgate.
I can certainly understand that Mr. Dubey is not absolutely delighted that I made such a hypothesis. For now, and awaiting further explanations, I reiterate my view and I sign.
This rather epic episode explains Mr. Dubey's wrath towards me; but it gives us no satisfactory explanation on the reasons why he asks such basic questions, considering his prominent situation in his university.
May I also stress that his intervention did not allow any sort of progress for my initial questioning.
2-On the form:
Mr. Dubey probably believes that stressing all his text by using capital letters provides it with some additional profoundness. For example:
“LAST BUT NOT THE LEAST:
THE CHEETAH WHO BAGS FINAL POSITION IN THE RACE WITH OTHER CHEETAHS MIGHT BE LAST .....
BUT THAT WOULD BE OUR STUPIDITY TO DISCUSS "DOES THE CHEETAH IN FINAL POSITION KNOW HOW TO RUN?"
I am reasonably confident that -nearly – all readers in Researchgate globally understand what they are reading, and do not need any typographic alteration to detect the main points in a text.
As a rule, the greatest statements are rarely shouted. It is considered disrespectful and rude to others using all caps. People "in the know", those who are convinced of the accuracy of their speech do not use all caps. The so-called “Netiquette” very wisely suggests refraining from using all capitals ...Moreover, ultimately, underlining a whole text stresses nothing: it is of no use or interest.
Finally, as proof that I am not a bad bugger, and in order to conclude in a pleasant positive way, I will give Mr. Dubey a personal opinion (this is not a tip, I would not dare!): to treat your pediatric patients, rather than using an IANB, try to administer an intraosseous anesthesia, using a Quicksleeper : immediate onset, profound analgesia, and lack of lip, tongue, cheek anesthesia, perfectly well tolerated by children, possibility of treating in more than one quadrant, minimal amount of anesthetic solution... And it works with a remarkable success rate for MIH. Who could reasonably ask for anything more? You will thank me, for sure…
If you would like further details, I will be more than happy to provide you with all the necessary information.
Dr Thierry COLLIER.
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Local anesthetics produce anesthesia by inhibiting excitation of nerve endings or by blocking conduction in peripheral nerves.
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Ali,
The mechanism of action for local anesthetics involves the inhibitions of sodium channels resulting in the inability of normal function. (That is the influx and outflow of sodium which results in the propagation of impulses along the nerve.) The sodium channels are "stuck" in one of three phases; 1) open, 2) closed or 3) partially closed. The speed of onset is predicated by the pKa of the local anesthetic and the pH of the tissue it is injected. The closer the two values, the faster the un-ionized portion can permeate the cell membrane (the ionized is the active portion, but does not permeate the cell membrane). As a note, the pKa is the pH at which 50% of the solution is ionized. The balancing act occurs on either side of the membrane. 
So, on to your question: the initial influx of sodium would be measured as a stimulation. As the sodium channels become inactive, depression would be measured.
Refards,
Christopher
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1. Epinephrine may cause acute hypertensive crisis (dangerously high blood pressure)
2. Interaction of epinephrine and some antihypertensive medications may cause acute hypertensive or hypotensive crisis.
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Anesthetic agents whether it is Lidocaine, Prilocaine, Mepivacaine solution with vasoconstrictor can be used safely in hypertensive patients attending dental clinic. However It is of utmost importance that dental clinicians need to select anesthetic solution in hypertensive patients considering their cardiovascular effect in order to provide comfort to the patients and knowing safety
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the drug is tested and is safe to use. It is used clinically for different purposes. However, it has some local anesthetic properties which we would like to test clinically. is there any known protocol that is used in such type of research?
please advise. Thanks
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Hello Laila, 
could you provide some more information about which aspect of the drug should be tested? Are you interested in the kinetics after the administration or in the dynamics, the anesthetic effect related to the administered dose? Is it topically applied or injected. Would you be happy with a "simple" pain score test?
I think there so many different protocols which can be found in literature. So, for an appropriate advise, you should give us more information. 
Best, Thomas
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Is there any well documented study(ies) supporting the statement by John Meechan in his book “Practical dental anesthesia” that epinephrine added to dental local anesthetic formulations modifies the distribution of blood in the body and sends relatively more to the brain, so that epinephrine might increase the toxicity of local anesthetic molecules on the Central Nervous System ?
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In theory John Meechan's comments make sense as the effects of the adrenaline as described can increase the delivery of lignocaine to brain. But i am not sure the small amount of epinephrine injected locally (1 in 80,000 adrenaline is 12.5 microgm per ml) can cause a significant systemic effect. 
I am sure you already know that epinephrine added to lignocaine is known to cause local vasoconstriction which helps to minimise the bleeding and also decrease the systemic absorption of lignocaine thus causing decreased plasma levels while improving the depth and duration of block. Hence the actual risks of increased toxicity if there are any as suggested by him hopefully would be nullified. I haven't come across any studies or any other expert opinion to support that there is risk of increased toxicity when combining adrenaline with lignocaine. The confounding factors, i suppose, are the higher dose that is allowable with adrenaline and inadvertent intravascular injection of some of it.  
At the end of the day, the sensible thing to do is to keep the dose to as minimum as possible and exercising caution in detecting and avoiding intravascular spillage especially when using LA combinations in highly vascular areas.   
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How to reduce pain in laparoscopic appendectomy?
Local anesthetic use
Duration of operation.
Position of patients
Expiriences of Surgeons
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laparoscopic appendectomy is generally well tolerated with low levels of post-opetive pain. To further improve the postoperative comfort is useful to infiltrate the place of the trocars with ropivacaine 7.5%, and avoid placing pelvic tubular drain at inflated abdomen,or avoid to place it at all.
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As in the majority of the hospitals, we use a blood management program. We use postsurgery blood recovery system in some situations: low presurgery Hb level, tranexamic acid contraindication..., but, if the surgeon practices an intraarticular infiltration of local anesthetic, within a fast recovery system, we won't be able to use it, . What is more important in your opinion, faster recovery or lower possibility of blood transfusion?
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It is indeed a difficult question.
One option is collecting retransfusion blood for 4-6 hours, and then changing to introduction of local anesthetic solutions. If you you spinal or general anesthesia the first hours are already covered by pain relief.
Kindest regards,
Robert Slappendel
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There are some patients have a resistance to local anesthesia .Although a proper injection techinque is performed ,those patients cant anaesthetized. 
Are there certain drugs or a milk of camal female makes you resistant to local ansthesia? 
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Some humans have a variance in their sodium channel that make them less perceptible for local anesthetic. The drug can not connect properly on the channel, and is therefore unable to block it.
I read once that up to 5%(?) of the populations are slow responder to local anesthetic. Delaying the time for full effect for a couple of minutes.
However, I have no paper readily avaliable to show you right now.
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Most local anaesthetics are weak bases, with a pKa between 8 and 9, so that they are mainly but not completely ionised at physiological pH.your comments
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Yes, you need to go back to the Henderson-Hasselbalch equation. LAs are bases and thus are highly ionised in acidic pH. pH-pK=log unionised species/ionised species. Since the pK of many LAs are around 8, then if the pH of the infected tissue is 2 (say) then 10 to the power of 6 times more of the LA will be in the ionised form. Not good for tissue penetration and binding to Na channels as pointed out above. In addition, the hyperaemia of infection will also tend to disperse the LA more quickly. A double whammy!
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A nerve block is a treatment used to both treat and diagnose severe pain. We often use local anesthetic like lidocaine for exemple.
Have you some references about peripheral nerve blocks wtih alcohol for chronic pain?
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Once I personally saw alcohol injection in epidural catheter. It was extremely painful procedure. The level Th8-Th9. Lidocaine injection followed by Alcohol injection. I observed abdominal muscle fibrillation for 3-4 minutes and then pain relief.
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Thanks
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It´s depends of what kind of local anesthetics your are talking obout? For Lidocaine without adrenaline is up to 5 mg/kg and whit it up to 7 mg/kg, it´s depends too to the way of administrations. I recomend you be more specific with the question.
Regards
Dr. Ernesto Rodríguez
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what is the effect of local anesthesia on the respiratory, cardiovascular system in pregnancy women ? and what about the fetus safety?
I researched a lot for this topic and I cannot find satisfied articles and information
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While regional anesthesia can be safe to use the impact to the fetus is not always readily appreciated.  The un-medicated laboring mother produces endorphins and has some hyperventilation to offset the acidosis and hypoxic components as well as the discomfort of being "squashed" by the uterus that is  experienced by the fetus during intense uterine contractions. When maternal pain is blocked her adaptations for her discomfort are decreased if not abolished entirely however the process nevertheless continues for the fetus - now without any accommodation.  The longer laboring mothers receive regional relief the more potential for embarrassment the fetus can experience - so as a neonatologist I see babies whose activity is reduced, cord blood ph is lower, some appear stunned or "hyperalert" -they are  nothing like the robust infant of a "natural" childbirth.  Epidurals/spinals when poorly timed can prolong labor can change the course of fetal rotation and may end up necessitating an operative delivery - ie vacuum or, forceps assisted delivery or even Csection deliveiry),  The use of regional anesthesia should be carefully considered and should never be accepted as routinely necessary.
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Dear Dr. Piccini and colleagues,
Many thanks for sending e a full text version of Paraesthesia after Local Anaesthetics: An Analysis of Reports to the FDA Adverse Event Reporting System. It is a very important work.
You may be interested in my continued research subsequent to my 2006 paper that you kindly referred in your article.
If you send me your e mail address, I would be more than happy to send you my recent works, a combined clinical- and registry study, and an animal experiment.
Kind regards
Søren Hillerup, PhD, Dr Odont.
Professor em., Maxillofacial Surgery
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I already had it, but thank you very much for thinking of sending it to me.
I understand you prefer not to give us your final opinion on Malet, Faure, Haas, and Lambert's work...And what about Stanley Malamed efforts to prove the inocuity of articaine in paresthesias ( he had a fierce opposition from Dr Haas - from Toronto)
But I would be very interested in your advice : may be by using my email address for privacy ? Or, is the question taboo?
Thierry
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Hello,
RV or LV Catheterization Protocol for Swine (50-70 kg) Yorkshire recovery procedure.
Based on your best results, what is the most up to date protocol (published or internal) for using Amiodarone in combination with Lidocaine. Please post, if possible your insights or experience with using both drugs in swine post-LV or RV cath recovery.
What is the best dose regiment for i.v. for Amiodarone (alone or in combo with Lido)? Also is per os (2-3 days before catetherization) better than i.v. dosing and why for recovery procedures? 
Much appreciated,
Filip 
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Hi Filip, you did not mention data about ejection fraction. If your experimental model is applied to severely depressed cardiac function pigs, I would recommend amiodarone as antiarrhythmic/prophilactic drug for preventing VT/VF or slow down heart rate in case of supraventricular tachyarrhythmias occurrence.
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Dexmedetomidine is used as an adjuvant to intrathecal  local anesthetic                     (Bupivacaine/ Ropivacaine ). Does it help in prolonging duration of spinal anesthesia? How would you rate it on comparison to fentanyl/ morphine?
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Have never used it, coz this is the place where it can be carried to CNS and its vital tissues directly. However, in the epidural route and peripheral blocks the absorption characteristics are variable. But free accessibility of this drug to CNS structures while floating in CSF has not been studied extensively and mainly Indian studies are available only. Even the dose calculation is little weird when it is used intrathecally. Concerns from FDA are likely to come up soon regarding its intrathecal use.
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We have done test doses so far, but not a single person had a reaction. And it is time wasting to wait and do the procedure. Are there any recommendations.
do comment
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thank you for your opionion we still follow so i needed a consensus.
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Position plays a vital role in subarachnoid blockade specially while using hyperbaric local anesthetic agents. Sitting or supine position may affect the final height of the block. Is there any modification of positioning while using isobaric local anesthetic agents?
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Contrary to hypo- and hyperbaric solutions, a true isobaric solution does not exist. This has to do with the variation in the density of c.s.f. between individuals. Hyperbaric solutions are defined as having a density > 1.0015, and these solutions will be hyperbaric in all individuals. Hypobaric solutions are defined as having a density < 0.9990, and these solutions will be hypobaric in all individuals as well. The traditional definition of an isobaric solution is a solution with a density between 0.9990 and 1.0015, but it is obvious that a solution with a density of, say, 0,9992 will be hypobaric in an individual with a c.s.f. density of, say, 1.0012. Conversely, a solution with a density of 1.0012 will be hyperbaric in an individual with a c.s.f. density of 0.9993. Another complicating factor is that the density of a solution is inversely related to temperature. Since local anesthetics are usually injected at room temperature, the density of that solution will decrease during equilibration to body temperature. With a true hypo- or hypobaric solution this change in density will not have much impact, but with a solution that has a density in the range of 0.9990 - 1.0015 the change in density may also cause a change in baricity. This has been amply demonstrated with plain bupivacaine, a solution considered to be isobaric: When plain bupivacaine is stored in a refrigerator an injected with a temperature of 6 degrees Celsius, the solution shows a hyperbaric distribution pattern. When the solution is warmed to body temperature immediately prior to injection, it shows a clearly hypobaric distribution pattern.
Is there nothing to say then about position and "isobaric" solutions? Yes there is. Plain bupivacaine is slightly hyperbaric at room temperature, but hypobaric at body temperature. During thermal equilibration, which will take an assumed 1-2 minutes, the baricity of the solution changes. This is best demonstrated by the following: When injecting plain bupivacaine in the lateral decubitus position, the maximum level of sensory blockade is unpredictable and may vary from very low to high, making this technique only reliable for lower limb surgery. However, injecting plain bupivacaine in the sitting position and maintaining this position for 2 minutes will usually result in a maximum level of sensory blockade above the tenth thoracic dermatome.
An important thing to remember: Position may be used as a tool to affect the maximum level of sensory block, but it is not suitable for accurate "steering" of the maximum level. Postion mainly affects the initial spread during the first minutes. It usually takes 10-15 min to determine if the maximum level of sensory block is going to be adequate, too high or too low; at that time, changes in position will have a minimal or no additional effect on the maximum level, asuming that a normal dose of local anesthetic has been used.
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Another theory for anesthetic action should be evoked.
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Thank you for modification , that what i mean
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I'm looking for a review about percentages and statistical data about which are the most commonly used anesthetic.
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Lignocaine was the first of the amides to be popularly used and has dominated as the choice for about nearly half a century now. Inspite of the newer anesthetic agents coming up, lignocaine is still very commonly used all over the world.
Recent introduction of aritcaine has found favour among a few section of dentists especially for local infiltration. (There are evidences that 4% Articaine when used a block has high risk of local anesthetic agent induced paresthesia and has found disfavour of late for use as block. But it's being favoured for infiltration purposes.)
To start with these articles might be of some help:
More in the list:-
1: Gaffen AS, Haas DA. Survey of local anesthetic use by Ontario dentists. J Can
Dent Assoc. 2009 Nov;75(9):649. PubMed PMID: 19900354.
2: Haas DA, Lennon D. Local anesthetic use by dentists in Ontario. J Can Dent
Assoc. 1995 Apr;61(4):297-304. PubMed PMID: 7736333.
3: Moore PA, Nahouraii HS, Zovko JG, Wisniewski SR. Dental therapeutic practice
patterns in the U.S. I. Anesthesia and sedation. Gen Dent. 2006
Mar-Apr;54(2):92-8. PubMed PMID: 16689062.
4: Cheatham BD, Primosch RE, Courts FJ. A survey of local anesthetic usage in
pediatric patients by Florida dentists. ASDC J Dent Child. 1992
Nov-Dec;59(6):401-7. PubMed PMID: 1491077.
5: Kohli K, Ngan P, Crout R, Linscott CC. A survey of local and topical
anesthesia use by pediatric dentists in the United States. Pediatr Dent. 2001
May-Jun;23(3):265-9. PubMed PMID: 11447962.
6: Rowson JE, Preshaw PM. The use of lignocaine in dental practice: results of a
survey of a group of general and hospital dental practitioners. J Dent. 1997
Sep;25(5):431-3. PubMed PMID: 9241962.
7: Malamed SF, Gagnon S, Leblanc D. A comparison between articaine HCl and
lidocaine HCl in pediatric dental patients. Pediatr Dent. 2000
Jul-Aug;22(4):307-11. PubMed PMID: 10969438.
8: Ram D, Amir E. Comparison of articaine 4% and lidocaine 2% in paediatric
dental patients. Int J Paediatr Dent. 2006 Jul;16(4):252-6. PubMed PMID:
16759322.
Regards,
Dr. Akilesh. R
India