Mindblown

[Kaisu]

I went back to school because I love to learn things. I know that there is so much about medicine that we don't know. I lost interest in EMS when the really cool things I was learning about medicine either were of no use to me in the field (protocols, short transport times, etc.) or painted a target on my back because I didn't fit in with the herd.

Room temperature IQs that had memorized the protocols advanced in the ranks and perpetuated the stupidity. Refusing to backboard kyophotic geriatrics for their slip and falls on the carpet had me dodging bullets.

I loved the field. The field did not love me back.

[Just Plain Ruff]

yeah, try to backboard and collar a terribly kyphotic elderly patient, that works wonders for the patient. Those patients are truly poster children for re-evaluation of boarding and collaring. Just how the hell do you board patients like that without causing more damage to them?

I also refused to collar and board them as well. at least my docs I worked understood my rationale on why I didn't and supported me.

[Kaisu]

Every time the protocol police lost their minds and made a fuss, the medical director backed me. It did nothing to improve my popularity. I felt more and more isolated. I figured it was only a matter of time before I made a mistake and the sharks swarmed in for the kill. I guess I am still hurting.

[Just Plain Ruff]

Screw em Kaisu, we've talked about this type of crap before. Any time a valuable and smart provider threatens lesser providers, that smarter provider becomes a target and have to be removed. IT's the nature of the game. Most of the time that smarter provider ends up at a service that truly wants that provider but it may take several attempts to find the right service.

Sadly to say, many of those smart providers just languish out there in negativity land and they suffer until they just say F it and get lazy and don't care anymore. I mean why should they care anymore when no-one else does.

[triemal04]

Interesting stuff, nicely done. Since it's part of the same subject, I'd suggest looking into both lipid emulsion therapy and high-dose insulin for beta-blocker OD's; both are extremely promising, and may eventually show themselves to be more beneficial/preferred to large doses of glucagon. For some people I think they allready have.

A final note, I'd be very interested in seeing exactly where the "33% remain asymptomatic" came from. My only potential area of concern is that they are lumping all OD's together (as I suppose is appropriate) and the people who took small amounts yet were still technically overdose's account for a large number of the asymptomatic patient's. Without seeing the numbers it is something to think about; if the patient was otherwise healthy then it would stand to reason that it wasn't their prescription, so they may only have taken a few pills but thus been called "an overdose." I'm willing to bet that the same person who takes a couple of hundred milligrams and is technically overdosed will fair differently than if they took a couple of grams. I could be wrong, but it is an area of concern for me.

I will admit that I did treat a teenager who popped some of daddie's metoprolol (dont' remember how much) after his girlfriend broke up with him...granted it was early on, but other than a moderately low heartrate he was asymptomatic...

[chbare]

Thanks for the comments everybody. A discussion regarding additional therapies is definetly in order:

Regarding lipid emulsions: This therapy shows promise and at least has efficacy in experimental models using animals. However, the mechanism of action is not well known. It may possible be one of four concepts; a sponge or 'fat sink" action, alteration of intracellular processes, interaction with stong ion channels and perhaps it may be as simple as reativating enzymes through the law of mass action. Most of the research has been bupivacaine induced toxicity in animals. I am not aware of significant human studies. However, large studies do not exist for glucagon significant observation evidence exists and few people would be willing to turn a cardiotoxic patient into a control when glucagon is generally accepted to work in spite of the lack of robust studies.

Bottom line, there is promise but the data is lacking and it is unclear if lipids would be any more effective than glucagon.

[chbare]

Iphone special, please forgive typographical errors.

[triemal04]

I don't think the mechanism is that unknown; it generally seems to work best in lipophilic drugs so I'd think that was the main reason, though there are other possibilities. I don't know of any real human studies either, but there have been a fair amount of case reports of it being used in various toxic overdoses (not just beta-blockers) with good results, and in many hospitals it is being used with some regularity. In all the ones I can remember it was always used in conjuction with standard therapies though, (which would seem to be appropriate) so how effective it would be alone is very debatable. Just my personal opinion, but if it and other therapies continue to show promise at some point a study will be done; I don't think it would be unethical either. Just make the control group standard treatments, and the experimental group those same treatments plus lipids, or whatever.

[DartmouthDave]

Hello,

I have seen lipids use twice for -caine toxicity (Ropivacaine I think) from epidurals. It seemed to work quite well.

I have seen lipids used for two different mixed OD (CCB and beta blockers). As noted by Triemal04 it was started when standard therapy was failing. One turned around and the other died.

Intersting case.

By the way, Chris, I like your YouTube channel.

It may be time to see if I can find a copy of Goldfrank's Toxicology.

Cheers

[chbare]

True, but I think we have different definitions of what an adequately understood mechanism of action is. With what I am currently doing, it is not uncommon to use differential equations and compartment modelling to make very accurate predictions about how things work and what they do. (Mostly pharmacokinetic models at this point). If there is a lack of highly accurate and precise models that can be used to make predictions that match experimentation, I would say the mechanism is not totally understood, even though it may be understood when taking a very broad approach. However, in the case of lipid emulsions, there are multiple proposed mechanisms with experimentation perhaps favouring some hypotheses over other hypotheses.

For example, using fairly simple algebra in the form of Henderson-Hasselbalch, I can make very good predictions about the amount of ion trapping that will occur with ASA depending on it's pH. With that said, some may say that I do not have a good understanding because if you dig deep enough, you can eventually find things that are not well understood. Perhaps it is more interpretation bias and semantics in some cases?

Dave, Goldfrank's is the boss when it comes to toxicology IMHO. It is easily my first go to resource when working on various assignments and projects. If your O-chem and biochem is weak, some of the concepts can be confusing as it assumes you have a pretty good understanding of basic sciences. Occasionally, my lack of chemistry preparation shows through. For example, I had a difficult time understanding how Florine acts as a good leaving group when dealing with Sarin. I simply did not appreciate the fact that the Florine is attached to a Phosphorous atom which is in turn attached to Oxygen atoms. This results in a rather polarised Phosphorous atom (Oxygen is highly electronegative like the Florine) that allows for the abstraction of fluorine under substitution with a hydroxyl group (ACHE molecule). Anyway, long winded, but basically, it's a great book but I find myself reaching form my gen chem and O-chem textbooks fairly often.