6 replies to this topic

[StrangeAeons]

I've proposed the idea of using piracetam in the emergency setting to offset neurological ischemia/infarction, but after more research and deliberation I've thought of two more specific uses:
1. Parenteral racetams as adjuncts to fibrinolysis:
Most specifically in the incidence of thrombotic stroke, as well as myocardial infarction or pulmonary embolism resulting in altered mental status or decreased level of consciousness. The main concern with using piracetam (and I'm not sure how much this applies to other racetams) in just any old instance of brain tissue dying is the possibility of aggravating hemorrhage. On the other hand, a fibrinolysis candidate has already been screened for hemorrhagic risk factors; one need merely titrate the heparin preparation to a lower dose to offset the anti-coagulant properties of the piracetam.
2. Romazecon and Levitiracetam (Keppra)
Naloxone (Narcan) is a hell of a drug. It essentially undoes opioids. Easy as pie, save for the occassional ticked off junkie. Benzodiazepines are just as prone to being overdosed (probably more) and they also have a drug that undoes them, Flumazenil. One little catch: it can cause seizures. This is where Keppra is great: it's a non-GABAergic parenteral anticonvulsant with a great safety profile and minimal sedation. I'm not sure how well it would work as prophylaxis while wantonly antagonizing GABA, though; that's where the whole racetams' "unknown mechanism of action" thing makes this a wild guess. Guess we should start having fun with mouse seizures!
Anyways, I'm not very well trained in pharmacology, I'm just a paramedic student who likes to pretend he knows something. I'd really like some input from somebody that actually does know something...

[Cassox]

I don't think the only lack of info is that of piracetams mode of action. Most of the agents used for thrombolysis (like urokinase, streptokinase,etc.) are not well reserached systemically. Basically, are they p450 metabolized? Is piracetam? So perhaps racetams prevent the metabolism of the thrombolysis agent?

There was some research that showed promise for use of racetams to inhibit damage from hypoxia, so what your saying is a given. Just thrombolysis agents need more research as well.

But flumazenil only causes seizures in those being treated with benzodiazepines FOR seizures. Even chronic benzo abusers only suffer withdrawal symptoms, nothing too serious. Don't really think that its much of an issue. Preventative intervention to stop overadministration would probably be more of a concern.

[StrangeAeons]

I come from an EMS education, so what I'm referring to specifically is a protocol in place where you don't have access to the patient's history as often happens in the field. I've also heard tell that severe benzo addicts are prone to seizures, but I've never actually seen that pan out. I'm also a little curious how Keppra would work in place of benzo's on cocaine OD, now that I think about it.
As per the thrombolytics, I just assumed that these agents were well-understood; obviously all these doubts call for some thorough studies on many levels; but the potential gain could be quite significant.

[Cassox]

I come from an EMS education, so what I'm referring to specifically is a protocol in place where you don't have access to the patient's history as often happens in the field. I've also heard tell that severe benzo addicts are prone to seizures, but I've never actually seen that pan out. I'm also a little curious how Keppra would work in place of benzo's on cocaine OD, now that I think about it.
As per the thrombolytics, I just assumed that these agents were well-understood; obviously all these doubts call for some thorough studies on many levels; but the potential gain could be quite significant.

I get what your saying. I would feel a bit leery about, because at least anecdotally, piracetam potentiates other substances. For example, alcohol, weed, etc have a greater effect. I remember some journal article about the racetams having a significant positive effect on rats that were subjected to extreme cold and drowning. I know that the anti-hypoxia effects are pretty well documented. I could see this being a great reason for having it in an EMS setting.

Now Keppra (levitiracetam) has been shown to occasionally cause a drop in WBC count, and lowered neutrophil count. Benzodiazapenes, have a side effect of shifts in heart rate, which is probably worse. I think I'm confused as to what your suggesting. Are you saying, use Keppra instead of benzodiazapenes for a drug comedown? Or are you saying to use Keppra instead of flumazenil for benzodiazapene overdoses?

[StrangeAeons]

Compared to all the other drugs we carry on the trucks and their long list of side-effects and contraindications, you'd think having something like piracetam would by comparison look to be a no-brainer (albeit not having the piracetam results in some very literal no-brainers).
What I'm insinuating with the Keppra is that one:
a) uses it as an adjunct to Flumazenil in the instance of benzodiazepene OD without known patient history;
and
b) uses it in place of benzodiazepines in the instance of cocaine OD.
Benzo's are used as seizure prophylaxis in cocaine OD's, not for the comedown; in both cases I propose Keppra as seizure prophylaxis but in one you're actively "exchanging" the Keppra with a benzo, whereas in the latter you're merely substituting it. Obviously as an anxiolytic and sedative benzos will remain a drug of choice; I'd imagine just for practicality and cost they should remain the first line anticonvulsant in the field as well.
As per the neutropenia, well... inform the personnel that Keppra carries a relative contraindication in AIDS and allogenic transplant patients, etc.

[spacey]

I can't hardly imagine alot of people ODing on benzos, one of the reasons they replaced barbiturates is just cause of their low toxicity even for people with low tolerance.

[Cassox]

I can't hardly imagine alot of people ODing on benzos, one of the reasons they replaced barbiturates is just cause of their low toxicity even for people with low tolerance.

Its generally an exeption case, not the rule when it occurs. An example is that people have a paradoxical reaction where it actually acts like a stimulant. Kindof strange, but it occurs. Also, its used for those that overdose on stimulant drugs like cocaine so sometimes people self-administer while high. Obviously not the greatest idea. Because some (not all) benzos involve the cytochrome p450 system, competition with other compounds can prevent it from being removed. Versed in particular is known to produce muscle tremors, tachycardia, etc. Also, although it has higher specificity than barbiturates, its still a CNS depressant. I don't think toxicity is really the issue as much as simply the drug doing what its meant to do.

I think the majority of overdoses actually occur with a parenteral IV, as the result of administration error. If thats the case, than the EMT issue is moot. But p-rose states that according to his (her?) experience, its very common. I don't know why that would be. Maybe simply people that really want to frickin sleep. Insomnia does suck. lol