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ketamine or nitrous oxide for dental procedure?

~*geNeRaTiOn E*~

~*geNeRaTiOn E*~

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the reason i'm posting this here is because i'm mostly looking for citations on which is safer and more effective for pediatric dental procedures. any help in the form of full journal articles or even abstracts would be great. thank you :)
 
I think you're going to have trouble. I don't believe ketamine has ever been seriously evaluated for such a use. It just doesn't make much sense. Most dental procedures take about 30-60 minutes. In these settings nitrous oxide just makes much more sense. Within 20 minutes of discontinuing it, the patient will be back to normal, ready to drive home.

Ketamine is administered such that complete aneasthesia is reached, more or less total unconsciousness. From a single dose, it will take about an hour before consciousness is starting to be restored, and could take up to three hours before complete sobriety is reestablished.

There's no doubt that nitrous oxide is much safer than ketamine, either in adults or children.
 
N2o

Nitrous oxide is much safer than ketamine the only damage a properly administered dose of N2O can do is cause a vitamin b12 deficiency which can be prevented with a b12 supplement whereas ketamine is known to cause Olney's lesions / NAN (brain damage)... there is no serious damage without prolonged abuse however I still prefer N2O over ketamine.


Also as hammilton mentioned I've never seen ketamine used as a dental anesthesia.
 
onmyway said:
well i can tell you this:
in the US most ER docs will not use nitrous for conscious sedation on any paitent, much less peds. however, ketamine is used for conscious sedation on kids frequently.

http://www.medscape.com/viewarticle/510622
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I live in Canada and I have never seen N2O used for anything medically. For dental work they jab us with a needle of.. I can't think of the drug name right now. (in the gums around the area they intend to do work on) and make us sit through any dental work awake unless it is a MAJOR surgery.
 
Yerg said:
IIRC they've never been observed in humans.
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You are correct, however this is because no testing on humans has ever been done. I imagine it is difficult to get people to line up to get their brain cut in half. Never mind the permission to perform such research :O


It has not and never will be proven because of that fact, the only argument disbelievers have is they think animal testing is not a reliable way to prove or disprove them. So I guess its personal preference if you choose to believe or not.

In my opinion animal testing has proven a very reliable and effective means of medical research for things we can not do to humans (for obvious ethical reasons). That and the fact I have seriously abused ketamine in the past and definitely killed more than one brain cell in the process.
 
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N2O is one of the oldest inhalant anesthetics still used today at least in the US. It is great for dental procedures as it produces stage I anesthesia rapidly. Also it is removed from the body almost 100% unchanged. I know it is very common for most dental procedures such as wisdom tooth removal, cavity filling, etc as it is fast acting and is devoid of any serious side effects during brief exposure. It is also used as preliminary anesthetic to a more potent/active inhalant anesthetic whose action is slow, though I'm not sure how common it is. I just know it has and can be used for that function.

I read somewhere about case studies about the use of ketamine in pediatric emergency cases. I can't seem to find the article atm. I'll look and see if I can find it.

Also ketamine used in procedures of under 3 hours is shown to not produce any neurological damage in the frontal cortex in developing monkeys brains.

Prolonged exposure to ketamine increases neurodegeneration in the developing monkey brain.

Zou X, Patterson TA, Divine RL, Sadovova N, Zhang X, Hanig JP, Paule MG, Slikker W Jr, Wang C.

Division of Neurotoxicology, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.

Ketamine, a widely used pediatric anesthetic, has been associated with enhanced neuronal toxicity in the developing brain, but mechanisms and neuronal susceptibility to neurotoxic insult leading to neuronal cell death remain poorly defined. One of the main goals of this study was to determine whether there is a duration of ketamine-induced anesthesia below which no significant ketamine-induced neurodegeneration can be detected. Newborn rhesus monkeys (postnatal day 5 or 6) were administered ketamine intravenously for 3, 9 or 24h to maintain a steady anesthetic plane, followed by a 6-h withdrawal period. The 9- and 24-h durations were selected as relatively long and extremely long exposures, respectively, while the 3-h treatment more closely approximates a typical duration of pediatric general anesthesia. Animals were subsequently perfused under anesthesia and brain tissue was processed for analyses using silver and Fluoro-Jade C stains and caspase-3 immunostain. The results indicated that no significant neurotoxic effects occurred if the anesthesia duration was 3h. However, ketamine infusions for either 9 or 24h significantly increased neuronal cell death in layers II and III of the frontal cortex. Although a few caspase-3- and Fluoro-Jade C-positive neuronal profiles were observed in some additional brain areas including the hippocampus, thalamus, striatum and amygdala, no significant differences were detected between ketamine-treated and control monkeys in these areas after 3, 9 or 24h of exposure. These data show that treatment with ketamine up to 3h is without adverse effects as determined by nerve cell death. However, anesthetic durations of 9h or greater are associated with significant brain cell death in the frontal cortex. Thus, the threshold duration below which no neurotoxicity would be expected is somewhere between 3 and 9h.
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The same scenario but for rats.

Toxicol Sci. 2009 Mar;108(1):149-58. Epub 2009 Jan 6.
Potential neurotoxicity of ketamine in the developing rat brain.

Zou X, Patterson TA, Sadovova N, Twaddle NC, Doerge DR, Zhang X, Fu X, Hanig JP, Paule MG, Slikker W, Wang C.

Division of Neurotoxicology, National Center for Toxicological Research, U.S. Food & Drug Administration, Jefferson, Arkansas 72079, USA.

Ketamine, an N-methyl-D-aspartate (NMDA) receptor ion channel blocker, is a widely used anesthetic recently reported to enhance neuronal death in developing rodents and nonhuman primates. This study evaluated dose-response and time-course effects of ketamine, levels of ketamine in plasma and brain, and the relationship between altered NMDA receptor expression and ketamine-induced neuronal cell death during development. Postnatal day 7 rats were administered 5, 10, or 20 mg/kg ketamine using single or multiple injections (subcutaneously) at 2-h intervals, and the potential neurotoxic effects were examined 6 h after the last injection. No significant neurotoxic effects were detected in layers II or III of the frontal cortex of rats administered one, three, or six injections of 5 or 10 mg/kg ketamine. However, in rats administered six injections of 20 mg/kg ketamine, a significant increase in the number of caspase-3- and Fluoro-Jade C-positive neuronal cells was observed in the frontal cortex. Electron microscopic observations showed typical nuclear condensation and fragmentation indicating enhanced apoptotic characteristics. Increased cell death was also apparent in other brain regions. In addition, apoptosis occurred after plasma and brain levels of ketamine had returned to baseline levels. In situ hybridization also showed a remarkable increase in mRNA signals for the NMDA NR1 subunit in the frontal cortex. These data demonstrate that ketamine administration results in a dose-related and exposure-time dependent increase in neuronal cell death during development. Ketamine-induced cell death appears to be apoptotic in nature and closely associated with enhanced NMDA receptor subunit mRNA expression.
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also in prevention of the neurotoxicity in ketamine,

Science. 1991 Dec 6;254(5037):1515-8.

NMDA antagonist neurotoxicity: mechanism and prevention.

Olney JW, Labruyere J, Wang G, Wozniak DF, Price MT, Sesma MA.

Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110.

Antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor, including phencyclidine (PCP) and ketamine, protect against brain damage in neurological disorders such as stroke. However, these agents have psychotomimetic properties in humans and morphologically damage neurons in the cerebral cortex of rats. It is now shown that the morphological damage can be prevented by certain anticholinergic drugs or by diazepam and barbiturates, which act at the gamma-aminobutyric acid (GABA) receptor-channel complex and are known to suppress the psychotomimetic symptoms caused by ketamine. Thus, it may be possible to prevent the unwanted side effects of NMDA antagonists, thereby enhancing their utility as neuroprotective drugs.
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It has not and never will be proven because of that fact, the only argument disbelievers have is they think animal testing is not a reliable way to prove or disprove them. So I guess its personal preference if you choose to believe or not.
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Ummm...no. Most people seem to have issues with the fact that Onley's lesions have never been induced in experimental animals at sub-anesthetic doses of ketamine.

ebola
 
I've been on the other side of Olney's lesions argument and I knew id catch flak for trying to defend it but again I'll state:

eurolite said:
That and the fact I have seriously abused ketamine in the past and definitely killed more than one brain cell in the process.
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Anyone I've known to go on a heavy ketamine binge agrees it does some serious shit to your brain takes months to recover sometimes... Which is what makes me think Onley's lesions since the small amount of research I could find about them said they self repair.

Again like I said it is my personal opinion.
 
1. Damage from Onley's lesions should be permanent, although neural plasticity may allow for adaptive compensation in some cases.
2. Your one anecdote doesn't strong evidence make.
3. It might be your personal opinion, but it is an opinion on a matter of fact.
4. It is irrelevant that you are partial to ketamine. I actually dislike ketamine...but it doesn't make my take on the matter more likely true.
 
Alright..

Alright you all seem to be right, I'm not going to argue anymore. This has gone way off topic from the original post. Brain Lesions or not I still stand by my statement that N2O is a safer more practical dental anesthetic which was really the only point I was trying to make.
 
There's actually very little evidence for olney's lesions in humans. Okay, the truth is: none.

I admit I haven't looked into it for a long long time, but as I recall, they haven't been produced in any primates, only rodents. The sorts of brain damage that primates and rodents experience are very different. Just look at MPTP.
 
for the record, in case anyone missed it, this is for a child, not an adult. i really just want the safest (and most effective) anesthesia option for my child when she goes in to have a minor dental procedure done. the whole reason she's having to be sedated/knocked out is bc she was previously extremely uncooperative with the dentists and rather than restrain her in a papoose we're going for the route of least resistance.

i appreciate all of the info and input, thank you again :)

 
If you are trying to knock them out, N2O wouldn't be the best bet for that as it doesn't reach Stage III anesthesia. It isn't potent enough to be safe in those realms.
 
oral midazolam and n2o are more than likely what they'll give her. i want her to be knocked out so she doesn't remember what happened bc she's extremely sensitive to "traumatic" situations and i also want to ease her discomfort as much as possible, in the safest manner possible. i guess i'm just a freaked out parent that's being paranoid bc i've never had to deal with this before. not only am i worried about her safety, i'm worried about the after-effects. seeing your child in pain is brutal :(
 
How old is your daughter if you don't mind me asking? very young ages and anesthetics make me paranoid to the point I think any non life threatening situations that require surgery should be halted until an older age.
 
^Why do you say that, eurolite? Both ketamine and N2O have awesome safety records with children-- they are both extensively tested, widely used, and have been deemed as harmless and extremely valuable tools. Sure, there are definitely some anesthetics I would never give to a child, but ketamine and N2O are just fine.

~*geNeRaTiOn E*~ said:
oral midazolam and n2o are more than likely what they'll give her. i want her to be knocked out so she doesn't remember what happened bc she's extremely sensitive to "traumatic" situations and i also want to ease her discomfort as much as possible, in the safest manner possible. i guess i'm just a freaked out parent that's being paranoid bc i've never had to deal with this before. not only am i worried about her safety, i'm worried about the after-effects. seeing your child in pain is brutal :(
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I think it'll be just fine, Kay. (You sound like an awesome mom, btw. :))

I'm sure your dentist has tons of experience with doing work on kids, and I'm sure the procedure will go smoothly. Just give your lil' girl plenty of love, and she'll be fine. :)
 
Roger&Me said:
^Why do you say that, eurolite? Both ketamine and N2O have awesome safety records with children-- they are both extensively tested, widely used, and have been deemed as harmless and extremely valuable tools. Sure, there are definitely some anesthetics I would never give to a child, but ketamine and N2O are just fine.



I think it'll be just fine, Kay. (You sound like an awesome mom, btw. :))

I'm sure your dentist has tons of experience with doing work on kids, and I'm sure the procedure will go smoothly. Just give your lil' girl plenty of love, and she'll be fine. :)
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Child and infant are two different things I'm pretty sure no drug has any absolute level of safety in a child younger than 1y

When I said real young I meant infant young.
 
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