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Ok so you don’t have any. Gotcha.
Ketamine for RSI in hypertensive patients
- Thread starter SandpitMedic
- Start date
If I posted evidence based studies would you actually change your mind? I seriously doubt it. This comes from the person who posted that etomidate presents epileptiform eeg tracings and mycolonic activity, but that it doesn't cause seizures.
VFlutter
Flight Nurse
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I do not think Remi was imply that epileptiform eeg activity with concurrent myoclonic jerks are not seizures however they are commonly independent of each other. There are many reasons for myoclonus other that epileptic seizures and there are patients with epileptiform eeg activity without clinical seizure activity. So a patient whom has myoclonus after etomidate is not necessarily seizing even if it may he interpreted as such.
And i get the the rationale to avoid Etomidate in the head injury or epileptic patient however your statement that it should never be used without a barbiturate or Benzo is a little extreme. Lowering the seizure threshold is not going to induce spontaneous seizures in patients except of those mentioned.
“Etomidate is a hypnotic nonbarbiturate, ultra–short-acting anesthetic agent associated with involuntary muscle movements in 10–70% of patients. These movements can be violent and mimic seizure activity. Etomidate is often administered because of its cardiovascular stabilizing effect. In patients without epilepsy, surface electrode recordings during the myoclonic movements are not associated with epileptiform activity.54
In epilepsy patients, etomidate (0.2 mg/kg) can activate seizure foci within 30 seconds55 and has been used intraoperatively for this purpose.
Despite the lack of evidence that etomidate causes seizures in nonepileptic patients, epileptiform activity occurred in 6 of 30 nonepileptic patients who were induced with etomidate for heart valve replacement.”
https://www.epilepsy.com/learn/prof...ilepsy-patients/general-anesthetics/etomidate
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E tank
Caution: Paralyzing Agent
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And just for the record..."data" is a loaded term....
VentMonkey
Family Guy
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An extremely ironic post in a thread chocked full of the heavy-hitters on this forum with regards to EBM. You don’t know what you don’t know.
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I gotta be honest, I don't even know what you are talking about. Why don't you stop being so cryptic and just say what it is that you think I'm wrong about? And if you have evidence to support why you think I'm wrong, post it. Just saying "but, but, your wrong and there's evidence" and then failing to produce the evidence makes it look like you really can't support your position. Anyone can claim that there is evidence to support any opinion. Claims of proof without providing the proof are meaningless. Put up or shut up.
OK, so part of the problem here seems to be that you are confused about some basic neurophysiology. Let me break it down for you:
1. Just like PAC's or PVC's or a first-degree conduction block on an EKG often has no clinical meaning, an "epileptiform" EEG pattern does not mean that the patient is having a seizure.
2. The myoclonus that propofol and etomidate causes is completely distinct from seizure activity. Myoclonus of this type is caused by disinhibition of the extrapyramidal medullary tracts, which influence balance and coordination and fine motor control. Most types of seizure activity are caused by ectopic neural discharge in the cortex. Completely different parts of the brain, completely different physiology.
3. Etomidate and ketamine both lower the seizure threshold. This does not mean they cause seizures. The brain of an epileptic is always on the verge of a seizure and as soon as you nudge it in that direction, it will. Quite a few drugs and stimuli do that, not just these two drugs. This does not happen in non-epileptics.
4. What happens with etomidate is someone will read that it lowers the seizure threshold, and then they use it maybe ten times, and 4 or 5 out of those ten times they'll see pretty pronounced myoclonus, and they go tell people "etomidate causes seizures, and I've seen it" when no, they did not.
To summarize: etomidate does not cause seizures. It does lower the seizure threshold, but that only results in seizures in epileptics. And guess what? Your beloved ketamine does the exact same thing.
I was going to post yesterday but after browsing this thread I realized I’d better not bring a knife to a gun-fight...
So I have evidence! (sort of)
‘The Walls Manual of Emergency Airway Management — Fifth Edition’ has the following to say...
“In 2009, Jabre et al. Published the largest clinical trial to date involving ketamine 2mg per kg for RSI in adults, and comparing it to etomidate 0.3mg per kg, both with succinylcholine as the NMB agent. There were no significant hemodynamic differences between the two groups. The study concluded ketamine is a safe alternative to etomidate for endotracheal intubation in critically ill patients... This study has been followed by others supporting the same conclusion” p. 257
If Etomidate is the gold-standard of hemodyamically stable induction agents and these studies are finding ‘no significant differences’, I don’t see any reason why you wouldn’t use it in hypertensive patients.
So I have evidence! (sort of)
‘The Walls Manual of Emergency Airway Management — Fifth Edition’ has the following to say...
“In 2009, Jabre et al. Published the largest clinical trial to date involving ketamine 2mg per kg for RSI in adults, and comparing it to etomidate 0.3mg per kg, both with succinylcholine as the NMB agent. There were no significant hemodynamic differences between the two groups. The study concluded ketamine is a safe alternative to etomidate for endotracheal intubation in critically ill patients... This study has been followed by others supporting the same conclusion” p. 257
If Etomidate is the gold-standard of hemodyamically stable induction agents and these studies are finding ‘no significant differences’, I don’t see any reason why you wouldn’t use it in hypertensive patients.
I don't think you are wrong, but that like most medics (including myself several years ago) tend to think of RSI as a field procedure without really thinking about the effects when they are in the ED or ICU. Things like the after effects of drugs and which hospital EMS goes to can make a huge determination in patient outcome, these are things that are not well taught in P school. I have also learned that most medics don't really care that much what the patient outcomes are once they are out of their care.
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What you'll generally find on this forum is folks who do think about outcomes and do want to learn and integrate the best practices into what they do, to the greatest extent that they are able to.
I'll discuss airway management and the related pharmacology all day long, and I welcome differing opinions. I learn plenty from the discussions on here. Show some good quality evidence that contradicts what I think is true, and I''l definitely re-evaluate. I welcome opportunities to learn and improve.
But it is unhelpful when people spout off about how others are wrong because their favorite podcaster or blogger has a different opinion on how things should be done. Just because an internet personality - or 5 of them - says something doesn't make it fact. Just because something appears in a published article doesn't mean it is high quality evidence that should change practice. Even if high-quality evidence does arise that supports something, it still doesn't mean that something is always the best option in every scenario. Medicine is complex and can't be boiled down to rigid protocols.
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