SpecialK users?

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.
Ketamine guys: aren't you concerned about the studies that say ketamine induces brain apoptosis?

Have you seen someone who used a pcp in his youth, later when they get old? They are like ******ed. Ketamine is very similar to pcp. Inhibits learning capacity too. I'm sure it cannot be good.

I stay away from that drug as much as possible.

So many of you use it so freely that I'm concerned about myself in the future when I need surgery.

I'll just say I'm allergic to ketamine.
​
Members don't see this ad.
 
I love ketamine. I use it all the time on MAC's with versed/ glyco premed, Prop infusion intraop- usually no narcs if the surgeon uses local- and no bad trips yet. I keep my dose to under 100 mg total and usually give it in 25 mg divided doses. my favorite use is for elderly hip fractures- usually give em 1 of versed, no glyco and 25-50 of ketamine, turn em on their affected side, shoot a spinal and let em sit on that side for 5 min or so, turn em supine, and transfer them pain free to the OR table- they usually start to wake up about 1/2 way thru the surgery and I either talk to them the rest of the time or give em more versed and let em snooze. Never had any issue w/ tachycardia - I think the small dose combined with the elderly's less than vigorous response to endogenous catecholamines is why.
 
Members don't see this ad :)
urgewrx said:
Ketamine guys: aren't you concerned about the studies that say ketamine induces brain apoptosis?

Have you seen someone who used a pcp in his youth, later when they get old? They are like ******ed. Ketamine is very similar to pcp. Inhibits learning capacity too. I'm sure it cannot be good.

I stay away from that drug as much as possible.

So many of you use it so freely that I'm concerned about myself in the future when I need surgery.

I'll just say I'm allergic to ketamine.
​
Click to expand...

A previous edition of anesthesiology news had an article reporting some findings where it was noted that use of NMDA antagonists, I believe, caused a multifold elevation in the TAU protein,which as you know, is part of the structure of neurofibrillary tangles, which are found on brains of patients with alzheimer's. I can remember what the increase was but something above 10-fold or so.
 
Takadera: Ketamine-induced apoptosis in cultured rat cortical neurons.
Toxicology and applied pharmacology 2006


Recent data suggest that anesthetic drugs cause neurodegeneration during development. Ketamine is frequently used in infants and toddlers for elective surgeries. The purpose of this study is to determine whether glycogen synthase kinase-3 (GSK-3) is involved in ketamine-induced apoptosis. Ketamine increased apoptotic cell death with morphological changes which were characterized by cell shrinkage, nuclear condensation or fragmentation. In addition, insulin growth factor-1 completely blocked the ketamine-induced apoptotic cell death. Ketamine decreased Akt phosphorylation. GSK-3 is known as a downstream target of Akt. The selective inhibitors of GSK-3 prevented the ketamine-induced apoptosis. Moreover, caspase-3 activation was accompanied by the ketamine-induced cell death and inhibited by the GSK-3 inhibitors. These results suggest that activation of GSK-3 is involved in ketamine-induced apoptosis in rat cortical neurons.


[SIZE=-1]Ketamine impairs multiple cognitive
domains in rhesus monkeys
by
Taffe MA[/SIZE]


[SIZE=-1]Drug Alcohol Depend 2002 Oct 1;68(2):175-87 [/SIZE]


[SIZE=-1]Available evidence suggests that recreational use and abuse of the dissociative anaesthetic ketamine is increasing. Characterization of the cognitive risks of ketamine exposure contributes substantially to understanding this growing public health threat. Although prior human studies demonstrate that ketamine impairs a range of cognitive skills, investigation in nonhuman models permits more precise exploration of neurochemical mechanisms which may underlie detrimental behavioral effects. Adult male rhesus monkeys (N=7) were trained on a neuropsychological battery including tests of memory (delayed match-to-sample, DMS; self-ordered spatial search, SOSS), reaction time (RT), reinforcer efficacy and sustained attention (progressive ratio, PR) and fine motor coordination (bimanual motor skill, BMS). Battery performance was then serially challenged with acute doses of ketamine (0.3, 1.0, 1.78 mg/kg IM). Ketamine impaired DMS and SOSS in a dose x difficulty dependent manner with the most difficult task conditions disrupted at the 1.0 and 1.78 mg/kg doses. Thus, both visual recognition memory and working memory indices were affected. Ketamine also slowed RT and BMS performance and interfered with PR performance at the 1.78 mg/kg dose. Overall the present findings confirm that ketamine interferes with multiple aspects of cognition at subanesthetic doses in monkeys.


[/SIZE]
And many others. Just google ketamine apoptosis.
​
 
CremeSickle said:
i have to admit that i dont use ketamine much and its probably due to the place i trained. They are all anti-K. I want to use it more tho.

This has been a good thread for the discussion. Does anyone have some more recent journal article references for use of ketamine in general in anesthesia?
Click to expand...

I will find some soon (maybe tomorrow) for you when I get to my work computer. Pain guys are using it to help diagnose fibromyalgia and also to see if they will respond to ketamine-like oral drugs.

rmh149 said:
Very interesting. I have very little exposure to ketamine....have used it only on those very unstable patients.

So, on an open abdominal case it would be good to load the patient with 0.5mg/kg ketamine (after induction?), and run a gtt at .25mg/kg/hr. Then stopping the gtt about 30 minutes prior to wake up time.

How do they wake up?

How much narcotic would the patient need on top of the ketamine?

How long does it last....will they be completely spaced in the PACU?
Click to expand...

I really suggest reading the article I referenced earlier. I think you will be suprised at A) how well the study design/integrity was, and B) the results of the study and how significant the findings are. As far as spaced out, I think if you turn it off in time, they are not spaced out. Also, keep your total dose down, no matter how long the case. Someone else mentioned less than 100mg - that might be on the low side, but certainly never going over 200mg seems prudent.

This thing about monkeys is concerning. There are a few monkey-like attendings around my work - i'll ask them about it.
 
urgewrx said:

Have you seen someone who used a pcp in his youth, later when they get old? They are like ******ed. Ketamine is very similar to pcp. Inhibits learning capacity too. I'm sure it cannot be good.

I stay away from that drug as much as possible.

So many of you use it so freely that I'm concerned about myself in the future when I need surgery.

I'll just say I'm allergic to ketamine.
​
Click to expand...


Man i think i'm going to have to apologize to all the patients i gave less than 100mg of ketamine for the loss of cognitive function they are sure to suffer from. Maybe i'll pay for their nursing facility when they become "******ed".:rolleyes:

Apoptosis happens all the time and i'll bet you can show apoptosis after giving any drug.

What do you think is best: loss of a couple of neurones or chronic post-op pain?
 
dhb said:
Man i think i'm going to have to apologize to all the patients i gave less than 100mg of ketamine for the loss of cognitive function they are sure to suffer from. Maybe i'll pay for their nursing facility when they become "******ed".:rolleyes:

Apoptosis happens all the time and i'll bet you can show apoptosis after giving any drug.

What do you think is best: loss of a couple of neurones or chronic post-op pain?
Click to expand...

It might not be important to you. I have family history of alzheimer's d and I think I'm headed that way. It's frightening. I plan to keep everysingle neuron I have as long as possible.

I'll settle for chronic pain.
 
Interesting stuff about the apoptosis. I think I will check out some of those studies.

But I do love ketofol. Patients are comfortable, quiet, breathing, and hemodynamically stable. For like a two to three hour MAC case, I rarely use more than 100 mg of ketamine total. It is my favorite sedation for total knees which I do with a spinal and then a ketafol infusion. I like patients to be snoring and not hear all the banging and sawing but then to wake up quickly and smoothly as they put the dressings on. And the patients feel good too and say they had a great nap. I have never had any hallucination issues. Occasionly, a patient will say they had a cool dream and ask to go back to sleep to continue the dream.
 
urgewrx said:
Takadera: Ketamine-induced apoptosis in cultured rat cortical neurons.
Toxicology and applied pharmacology 2006


Recent data suggest that anesthetic drugs cause neurodegeneration during development. Ketamine is frequently used in infants and toddlers for elective surgeries. The purpose of this study is to determine whether glycogen synthase kinase-3 (GSK-3) is involved in ketamine-induced apoptosis. Ketamine increased apoptotic cell death with morphological changes which were characterized by cell shrinkage, nuclear condensation or fragmentation. In addition, insulin growth factor-1 completely blocked the ketamine-induced apoptotic cell death. Ketamine decreased Akt phosphorylation. GSK-3 is known as a downstream target of Akt. The selective inhibitors of GSK-3 prevented the ketamine-induced apoptosis. Moreover, caspase-3 activation was accompanied by the ketamine-induced cell death and inhibited by the GSK-3 inhibitors. These results suggest that activation of GSK-3 is involved in ketamine-induced apoptosis in rat cortical neurons.


[SIZE=-1]Ketamine impairs multiple cognitive
domains in rhesus monkeys
by
Taffe MA[/SIZE]


[SIZE=-1]Drug Alcohol Depend 2002 Oct 1;68(2):175-87 [/SIZE]

[SIZE=-1]Available evidence suggests that recreational use and abuse of the dissociative anaesthetic ketamine is increasing. Characterization of the cognitive risks of ketamine exposure contributes substantially to understanding this growing public health threat. Although prior human studies demonstrate that ketamine impairs a range of cognitive skills, investigation in nonhuman models permits more precise exploration of neurochemical mechanisms which may underlie detrimental behavioral effects. Adult male rhesus monkeys (N=7) were trained on a neuropsychological battery including tests of memory (delayed match-to-sample, DMS; self-ordered spatial search, SOSS), reaction time (RT), reinforcer efficacy and sustained attention (progressive ratio, PR) and fine motor coordination (bimanual motor skill, BMS). Battery performance was then serially challenged with acute doses of ketamine (0.3, 1.0, 1.78 mg/kg IM). Ketamine impaired DMS and SOSS in a dose x difficulty dependent manner with the most difficult task conditions disrupted at the 1.0 and 1.78 mg/kg doses. Thus, both visual recognition memory and working memory indices were affected. Ketamine also slowed RT and BMS performance and interfered with PR performance at the 1.78 mg/kg dose. Overall the present findings confirm that ketamine interferes with multiple aspects of cognition at subanesthetic doses in monkeys.


[/SIZE]
And many others. Just google ketamine apoptosis.
​
Click to expand...

I agree that in early development that ketamine increases apoptosis, but the argument in the scientific community is that apoptosis during development is a normal process while neuronal pruning occurs. So is ketamine just promoting the death of those neurons that would eventually be pruned by apoptotic mechanisms eventually? That question is still unresolved.

In the adult injured or compromised brain there are numerous studies that show subhypnotic doses of ketamine to be neuroprotective so the jury is still out. There is alot of active research ongoing that is supporting this hypothesis.

Mike
 
i'm on the acute pain service now, and we've had some dramatic successes treating chronically opiate-tolerant pts with postoperative sub-analgesic-dose ketamine infusions. the first such use on our service was several years ago in an icu pt who was actually *fluid overloaded* from the liters of fentanyl she was receiving without the benefit of appropriate analgesia. a week or so ago we sent a pt home on oral ketamine.
 
When you get the phone call from PACU that the pt is breathing 5-6/minute and rating pain at 12 out of 10 after the usual narcotics, try 10 mg of Ketamine, repeated times one if necessary. Believe me, the PACU nurses will love you for it. No versed needed at that small a dose.
I give Ketamine to almost all of my pts. The pre-emptive analgesia evidence too strong to ignore.
Also, when doing blocks (ankles, femoral/sciatic/psoas) and you want sedation/analgesia with a pulse ox of 98%, give 2 mg versed and 10 mg of Ketamine. You won't have to worry about respiratory depression and can, if needed, add a little Fent if necessary (it doesn't seem like Ketamine is as analgesic as Fent).
Some of my colleagues argue that Ketamine with the Bupivacaine from the block could lead to seizures, but a small dose like 10 mg is no more likely to cause seizures than is the combo of hypercarbia and bupivacaine.
I have been doing 3-10 blocks a day for 2 years with only one woman telling me that the colors in the room were a bit vivid and no seizures.:)
 
Members don't see this ad :)
Dejavu said:
When you get the phone call from PACU that the pt is breathing 5-6/minute and rating pain at 12 out of 10 after the usual narcotics, try 10 mg of Ketamine, repeated times one if necessary. Believe me, the PACU nurses will love you for it. No versed needed at that small a dose.
I give Ketamine to almost all of my pts. The pre-emptive analgesia evidence too strong to ignore.
Also, when doing blocks (ankles, femoral/sciatic/psoas) and you want sedation/analgesia with a pulse ox of 98%, give 2 mg versed and 10 mg of Ketamine. You won't have to worry about respiratory depression and can, if needed, add a little Fent if necessary (it doesn't seem like Ketamine is as analgesic as Fent).
Some of my colleagues argue that Ketamine with the Bupivacaine from the block could lead to seizures, but a small dose like 10 mg is no more likely to cause seizures than is the combo of hypercarbia and bupivacaine.
I have been doing 3-10 blocks a day for 2 years with only one woman telling me that the colors in the room were a bit vivid and no seizures.:)
Click to expand...

I bet some patients really love that PCP dose of Ketamine.

Blade
 
Dejavu said:
When you get the phone call from PACU that the pt is breathing 5-6/minute and rating pain at 12 out of 10 after the usual narcotics, try 10 mg of Ketamine, repeated times one if necessary. Believe me, the PACU nurses will love you for it. No versed needed at that small a dose.
I give Ketamine to almost all of my pts. The pre-emptive analgesia evidence too strong to ignore.
Also, when doing blocks (ankles, femoral/sciatic/psoas) and you want sedation/analgesia with a pulse ox of 98%, give 2 mg versed and 10 mg of Ketamine. You won't have to worry about respiratory depression and can, if needed, add a little Fent if necessary (it doesn't seem like Ketamine is as analgesic as Fent).
Some of my colleagues argue that Ketamine with the Bupivacaine from the block could lead to seizures, but a small dose like 10 mg is no more likely to cause seizures than is the combo of hypercarbia and bupivacaine.
I have been doing 3-10 blocks a day for 2 years with only one woman telling me that the colors in the room were a bit vivid and no seizures.:)
Click to expand...

I am a big proponent of the K but I haven't used it for blocks, yet. Well I haven't needed it. I can't imagine the block hurting so much that the pt needs some K. But if I do give it nearly everytime I do a spinal for a hip fx.

Now, when giving it in PACU post-op you are not achieving "pre-emptive" analgesia. The pain has already occured. I'm sure you know this but just pointing it out anyhow.

Also, when you give it in the pacu it will wear off. Maybe on the floor maybe at home but it will wear off and the pt is right back where they started. But I guess you could just treat them in the pacu and then take them to the floor. When the physician caring for them after pacu can't seem to get them comfortable you can always say, "Well they were comfortable in the pacu and when we dropped them off to you." You need to either continue the K or find something else that works. What do you do for this?
 
In reply to Noyac:
We sedate all of our blocks, especially psoas cath placements. After a couple hundred psoas blocks, I have figured out that it is difficult to get enough local anesth everywhere it is needed before you insert a 4-6" 18ga touhy-type needle deep into the back. Most of my colleagues use Versed 2mg/Fent2cc, but they have to deal with sagging Pulse Ox readings, I rarely have to.
You are right, the PACU application isn't used for "pre-emptive" analgesia.
You are also right that the analgesia wears off, but then, so do all of our analgesics, so I still propose that the respiratory-depression-sparing effect of Ketamine makes it an excellent option in the PACU situation I described.
Like they say "try it, you'll like it" :)
 
dhb said:
Agreed, with ketamine most patient undergoing minor procedures require little to no post-op opoids (in my limited experience).
The doses they used in the study seem a bit high to me, i like to give 20mg at induction then run a sufenta/ketamine 5-5/ml infusion at 2ml/h and they get a bag of 500cc of NS with 60mg K 2gr Mg+ over the next 24h

What's your recipe?
Click to expand...


dhb, alot of the people around here that use ketamine use a lot smaller doses than in the study I mentioned. However, in this study, they had two doses, a smaller dose (.25mg load, and .125mg/hr) and a larger dose (double that). Only the larger dose had the decreased pain scores and decreased wound hyperanalgesia six months after surgery. That is why I use the "larger" dose, but it still is a relatively small dose.
 
urgewrx said:
Takadera: Ketamine-induced apoptosis in cultured rat cortical neurons.
Toxicology and applied pharmacology 2006
Click to expand...

iow, don't use ketamine when you're giving anesthesia for surgery on rats or rhesus monkeys.
 
VolatileAgent said:
iow, don't use ketamine when you're giving anesthesia for surgery on rats or rhesus monkeys.
Click to expand...

I'm pretty sure if you sign the consent they won't have any problems having you as a study subject.

So, yeah dude. Take one for the team.
 
urgewrx said:
It might not be important to you. I have family history of alzheimer's d and I think I'm headed that way. It's frightening. I plan to keep everysingle neuron I have as long as possible.

I'll settle for chronic pain.
Click to expand...

Urges,

Just thought you should know, that if you do start to show alzheimer's, you may end up on an NMDA-receptor antagonist (like ketamine) called memantine, which can be very effective.

Propofol, and other drugs, have shown neural damage in some lab or another.
 
epidural man said:
Urges,

Just thought you should know, that if you do start to show alzheimer's, you may end up on an NMDA-receptor antagonist (like ketamine) called memantine, which can be very effective.

Propofol, and other drugs, have shown neural damage in some lab or another.
Click to expand...


If it works, I'll take it.
 
urgewrx said:
Ketamine guys: aren't you concerned about the studies that say ketamine induces brain apoptosis?​
Click to expand...


I just saw this .....

"Despite the accumulating data, practicing anesthesiologists must consider important limitations in applying such experimental results to clinical practice. These include developmental differences across mammalian species, the huge doses and prolonged exposures required to produce neurotoxic effects, the use of anesthesia unopposed by surgical/painful stimulation, the need for precise physiologic monitoring, and the neuroprotective and antiinflammatory effects of anesthesia. For example, repetitive inflammatory pain accentuated cell death 3.3-fold in cortical areas and 1.6-fold in subcortical areas of newborn rats, whereas ketamine (5 mg/kg) blocked these cellular changes and ameliorated the consequent adult cognitive deficits."

This was in a recent editorial to this article
"Apoptotic neurodegeneration following trauma is markedly enhanced in the immature brain." in 1999.
 
You must log in or register to reply here.
Next unread thread

Similar threads

TheLoneWolf
Heavy marijuana users
Replies
46
Views
5K
PpfSuxTube
P
coffeebythelake
  • Locked
heavy marijuana users
Replies
2
Views
1K
dhb
dhb
WhiteHatDoc
Question about Anesthesia observerships, looking for SDN User Cognitus
Replies
5
Views
896
shepardsun
shepardsun
epidural man
Exparel users - question for you.
2 3
Replies
127
Views
14K
BLADEMDA
BLADEMDA
S
labetalol contraindicated in cocaine users?
Replies
16
Views
11K
Bostonredsox
Bostonredsox
Top