Talk:Suxamethonium chloride

Page in mess!!!

This page introduces total confusion between succinylcholine and its chloride. Those two MUST BE SEPARATED! Either there is a chlorine in the molecule or not, the name must reflect it! This looks like a major rework or redirects, etc. I leave then only an alert here. Sometimes Wikipedia is scary!

I have tagged the article accordingly. By the way, for future reference, please sign your comments. Thank you for the feedback. 38.100.34.2 17:18, 28 March 2007 (UTC)

As far as I know, succinylcholine is presented with chloride as a counterion to maintain neutrality, as it is a charged molecule. Is there anything else you feel could be improved on this page? I would appreciate more feedback. Fvasconcellos 00:40, 3 April 2007 (UTC)

Naming

One dose frequently used in clinical practice is 2 mg/kg. (At least that is the dose I usually use in my clinical practice). John Doyle. (djdoyle)

I guess the substance under discussion is Succinylbischoline (with a "bis" in it) aka Suxamethonium. I´m not entirely sure which of the two is correct so I won´t change it right now. Could somebody please check the proper pharmacological name? Kosebamse 12:54 Jan 28, 2003 (UTC)

I think the only "proper" name is the IUPAC chemical name, which is not in everyday use. Suxamethonium, scoline, and succinylcholine seem to be the commonest names this compound is referred by - Malcolm Farmer

I looked it up in a pharmacology textbook and the substance is listed under succinylbischoline (with a bis). But it's true that in everyday use it is succinylcholine (without a bis) or even succi so I really don't know where it should properly go. With hypertext however I believe it might be feasible to have substances dealt with under their IUPAC name and have common names linked there. Perhaps there is a wikipedia policy for this? Kosebamse

My pharm book has it listed as Succinylcholine. My vote on the "proper" name would be the International Nonproprietary Name which is set by the WHO. I don't know if Succinylcholine is the INN or the USAN (My book is american).Matt 04:38, 23 Jun 2004 (UTC)

It seems that the INN is suxamethonium chloride with CAS no. 71-27-2.

Far more common than malignant hyperthermia and prolonged block is anaphylaxis. I thought that it was implicated in anaphylaxis more than any other anaesthetic drug and that this was the leading cause of death due to it's use. Should we not edit the page to reflect this in the side effect paragraph?

Go ahead. Do you have incidence figures. JFW | T@lk 10:59, 23 October 2005 (UTC)

Tom Clancy's "Teeth of the Tiger"

This drug--spelled succinylcholine throughout the book--is used to assassinate several "bad guys" in Clancy's 2003 novel Teeth of the Tiger, though the symptoms and speed of death (cardiac arrest) vary somewhat from the description in the article. --Robertkeller 23:28, 11 September 2006 (UTC)

I'd trust Clancy before wiki, I mean Clancy knows his shit, CIA doesn't let dumbies lecture at Langley. Supra guy 07:25, 22 July 2007 (UTC)

Except that death is not invariably a result if sux administration, as he suggests. The effects don't last long enough in most patients to cause hypoxic myocardial death. I'm not saying it can't happen, just that it's nothing like as reliable as portrayed. Dlh-stablelights (talk) 11:49, 30 January 2008 (UTC)

9 minutes of apnea very well can lead to cardiac arrest. — Preceding unsigned comment added by 184.1.224.18 (talk) 17:12, 21 July 2013 (UTC)

History

A nice, freely accessible review which may help with the writing of a "History" section. Fvasconcellos 01:12, 3 April 2007 (UTC)

Some thoughts

I am not an expert but as far as I am aware Phase 2 block does not normally occur with suxamethonium at normal doses. It occurs when repeated doses of sux are given. Also, talking about the "anaesthetic effects" of sux (in the same Phase 2 paragraph) is not really accurate, as sux is a neuromuscular blocker, not an anaesthetic. Also talking about an endplate potential less than the action potential (as mentioned in the Phase 1 paragraph) does not really make sense either. I would get stuck in right now but haven't got the time. I have removed the drug doses though as wiki shouldn't be giving drug doses (vandals might cause great harm.) I'll come back when I've got a bit more spare time.Mmoneypenny 13:36, 17 April 2007 (UTC)

He's right

The description given in the article as 'phase 2 block' is actually phase 1 block; phase 2 block generally occurs with repeated administration/overdose. The two can be distinguished using a nerve stimulator. Sorry I don't have time to rewrite the section at the moment but any textbook of anaesthetics/ anaesthetic pharmacology will confirm this. Johnhglen (talk) 09:05, 22 December 2007 (UTC)

Righto; I have editted the 'Phase 1 Block' / 'Phase 2 Block' Section. I forgot to login, so it is under an IP address, but it was me. The section can still benefit from some cleaning up; not everything is linked; specifically a link to normal muscle depolarisation would probbly be appropriate and may cut down some of the text. Cheers, Maniaccs2 (talk) 01:23, 7 January 2008 (UTC)

Butyrylcholinesterase and the Nicotinic ACh receptor

Butyrylcholinesterase and pseudocholinesterase are the same thing, but butyrylcholinesterase is 'more' correct (more recent) and actually has a wiki page.

The ACh Nicotinic receptor is a ligand gated Sodium Channel. I agree some potassium probably leaks through but it is not widely accepted, nor labeled as a Sodium/Potassium Channel. If you are going to attempt to change it back please provide a reference. Maniaccs2 (talk) 14:18, 7 February 2008 (UTC)

Side Effects

I would argue Suxamethonium is never given to conscious patients, even in emergency situations. It is simple enough to provide even mild sedation and amnesia with concurrent agents. (But I haven't changed this statement on the wiki). Maniaccs2 (talk) 14:23, 7 February 2008 (UTC)

Suxamethonium is preffered in emergency situations because of it's low latency in effect. — Preceding unsigned comment added by 95.175.139.171 (talk) 07:04, 8 May 2012 (UTC)

Sux is, in fact, given to awake patients both in house and prehospital. This is decidedly poor form, and has physiologic adverse consequences. However, any argument that it is not done has no basis in reality. DrC 2013 — Preceding unsigned comment added by 184.1.224.18 (talk) 17:16, 21 July 2013 (UTC)

Atropine

Atropine can only antagonize acetylcholine at muscarinic receptors, not at nicotinic receptors of neuromuscular junction. It does have a role in poisoning of organophosphorus, but not the way described in this article. Almazi (talk) 20:27, 16 May 2010 (UTC)

Organophosphorus poisoning

The paragraph about Organophosphorus poisoning has no relationship at all to Suxamethonium chloride, why is it there? --80.171.14.147 (talk) 11:22, 13 November 2010 (UTC)

You are correct. Accordingly, I have deleted the entire section. DiverDave (talk) 03:05, 18 November 2010 (UTC)

Organophosphate AChEi block butylcholinesterase as well, resulting in prolonged paralysis. Having some mention is germane. — Preceding unsigned comment added by 184.1.224.18 (talk) 17:19, 21 July 2013 (UTC)

Use in aversion therapy

A short section on the past use of this drug in aversion therapy would be worth adding. This chiefly took place during the 1960s, in which this compound, when administered without anesthesia, produced full paralysis, including a 60-second paralysis of breathing, while the person was conscious. The terrifying experience found its way into aversion therapy, initially on alcoholics, and later prisoners at Atascadero and Vacaville prisons. The latter proved particularly controversial and received a great deal of attention during the 1970s. This use of the drug has been long since discontinued. Peter G Werner (talk) 19:03, 1 April 2011 (UTC)

Phases I and II

So the current explanation for Phase II is just horrible. I looked back through it's edit history, and it looks like it has been changed a number of times and there seems to be general confusion about what is what, and more importantly, what the principal paralytic effect is. Could someone with some pharmacology background or even a pharmacology textbook please edit? I understand from my own (very limited source) that Phase I is a prolonged depolarization and that it cannot be reversed by cholinesterase inhibitors while Phase II is repolarized but blocked and can be reversed with cholinesterase inhibitors. I could use some help with the mechanism, however.

From my understanding, Phase I is marked by fasciculations. How long do these fasciculations last? Clinically, I would not think that fasciculations would be desirable for tracheal intubation, so it makes most sense to me that Phase II would have the principal paralytic effect. — Preceding unsigned comment added by Hosime (talk • contribs) 06:51, 7 September 2011 (UTC)

Fasciculations don't last very long, and you wait for them to stop before attempting instrumentation. I feel for me with my left hand little finger under the mandible if I am holding a mask, or right hand if the left already holds the scope. I don't think there is much phase II effect at the dose I use (1.5 mg/kg). You may see it at higher doses, but usually phase II happens if you continue to administer sux before the paralytic effect wears off. Giving repeated doses of sux after recovery (where you will again cause phase I) is a bad idea and a good way to cause life-threatening effects. — Preceding unsigned comment added by 184.1.224.18 (talk) 17:29, 21 July 2013 (UTC)

"fatal allergy" is incorrect

Sux can be dangerous in some individuals and ethnic groups because those individuals/groups have a genetic trait that leads to a lack of plasma (or butyl) cholinesterases that normally break down the molecule rapidly. These patients have suxamethonium, or scoline, apnoea (lack of breathing). Death only results if anaesthetists or recovery staff fail to recognise this happening AND allow the patient to become hypoxic. It is not an allergy, in that no part of the immune system is involved and the molecule is not doing anything, or triggering any reaction, that it is not supposed to do. Recovery will eventually occur. If given to a patient with the enzyme deficiency, supportive care for a number of hours may be required (ventilation and sedation) but no harm is actually done. — Preceding unsigned comment added by 121.45.27.165 (talk) 07:19, 13 March 2012 (UTC)

anaphylaxis is rare

Assertion that sux allergy is common is wrong. It is a small, rapidly hydrolyzed molecule and mounting an immune response would be very unlikely. Need citations which address reports of anaphylaxis and understanding that the only reason case reports ever get published is due to exceptional rarity or discovery of something novel. "Common" reactions make consistent appearances in clinical research.

DrC 2013 — Preceding unsigned comment added by 184.1.224.18 (talk) 17:56, 21 July 2013 (UTC)

Sux does not cause V-Tach or V-fib

I edited the adverse effect section removing the statement that sux causes V-fib. You can see V-fib as the result of other problem (e.g. hypoxia), but sux causes bradycardic problems, both due to direct agonist effect on the SA and AV node resulting in (potentially profound in children) sinus bradycardia. Due to hyperkalemia you can see conduction system related bradycardia a with wide QRS and brady-a systolic PEA. Asystole isn't really a rhythm, but that happens, with arrest in diastole.

Anyone who thinks that any sort of tachydysrythmia occurs needs to provide sufficient references (and a case report does Not count), as this is both physiologically implausible, and has not been described in the modern (post-WW II) medical literature.

DrC 2013 — Preceding unsigned comment added by 184.1.224.18 (talk) 17:42, 21 July 2013 (UTC)

SuccinylCholine as a poison

Someone before mentioned Tom Clancy, however Sux has been often cited in Literature, Television shows, and movies as a poison; as well as having been used to poison people in real life. As used, Sux is metabolised in the victim leading to being undetectable post mortem. Shjacks45 (talk) 10:48, 26 February 2014 (UTC)

Reference 20 Link Incorrect

Hi,

I just noticed the link and doi (URL) address are wrong. Oddly, this paper also appears not to be on Pubmed. Anyway, here's a proposed, revised citation for Reference #20 below. I'm new here so don't want to change the wiki myself, to

Appiah-Ankam J, Hunter JM. Pharmacology of neuromuscular blocking drugs, Continuing Education in Anaesthesia Critical Care & Pain, Volume 4, Issue 1, February 2004, Pages 2–7, https://doi.org/10.1093/bjaceaccp/mkh002

https://academic.oup.com/bjaed/article/4/1/2/356873 GebienD (talk) 19:02, 4 March 2023 (UTC)

From Old:

Appiah-Ankam J, Hunter JM (February 2004). "Pharmacology of neuromuscular blocking drugs". Continuing Education in Anaesthesia Critical Care & Pain. 4 (1): 29–30. doi:10.1093/bjaceaccp/mkh010

GebienD (talk) 19:05, 4 March 2023 (UTC)

I went ahead and changed it in the edit where it is described: "/* Phase 1 block */ Fixing citation DOI and pages as per GebienD suggestion on talk page. I looked as well and agree. If I formatted it wrong please fix." 24.21.80.230 (talk) 22:01, 30 September 2023 (UTC)

Attempted to fix Phase 2 section

I attempted to fix the phase 2 section. It still needs more sources or perhaps to use Katzung, Bertram G. (2011). Basic and Clinical Pharmacology (8 ed.). Lange Medical Books/McGraw-Hill. pp. 446–461. ISBN 9780071179683. As a source, which is the one used in the https://en.wikipedia.org/wiki/Neuromuscular-blocking_drug page. I don't have access to this book but it seems likely to be a good source for the claims that still need citation. It may also allow the removal of "may" to be able to make the stronger assertion that the earlier version of the article had. Since the article cited only refers to it as a possibility, I was forced to use that "may" to lessen the strength of the assertion. I am inexperienced with wiki work so I apologize if I screwed anything up. 24.21.80.230 (talk) 21:50, 30 September 2023 (UTC)