If it ain’t broke… Etomidate for paediatric sedation.

@dralangrayson and I have been itching to talk about this paper since I spotted it in my monthly email digest of Pediatric Emergency Care when it landed in my inbox.

Procedural sedation – of any patients – remains a hot topic in the ED. Barely a day goes by without someone on twitter or the more exclusive St Emlyn’s ED forums bringing a new angle to the subject; be it reducing shoulders without any sedation at all or the endless cycle of arguments for and against ketofol…

In kids, procedural sedation has all sorts of uses. Keeping a small patient still long enough to suture a wound or remove a foreign body can be tricky, and since I first worked in an Emergency Department back in 2006 the approach to these patients has shifted dramatically from “nil-by-mouth, stick-them-in-an-ambulance-to the-children’s-hospital” to “could we do this with a bit of ketamine?” EM is a rapidly evolving (mutating?) specialty and our willingness to diversify and refine our practice is, I believe, one of our great strengths.

So should we now be moving away from ketamine into the dark, mysterious and historical world of etomidate for paediatric sedation? Let’s find out..!





Why have the authors even undertaken this study?

They tell us it’s because etomidate is commonly used for procedural sedation in adults, but its use in children has not been extensively evaluated. Etomidate is of interest, they say, because of its rapid onset/offset time and minimal haemodynamic and respiratory effects.

Well, I’m not sure that this assertion about adults is true – at least in the UK. I for one have NEVER used etomidate for ANY patient (including a total of 6 months list and emergency anaesthesia and 12 months in intensive care settings). Why? Because there are better agents. For predictable sedation with quick onset and offset, there’s propofol. For deeper anaesthesia and RSI, there’s thiopentone. For painful procedures where airway reflexes and respiratory drive should be preserved, there’s ketamine. I simply haven’t found myself in need of anything else, so  the rationale of the study immediately sits uncomfortably.

But I shouldn’t be so judgemental – what if etomidate is a wonder drug, offering all your sedation needs (rapid onset, short duration of action, minimal side effects) and more (patient, doctor, nurse and parental satisfaction) – shouldn’t we know about it?

OK then. I’ll read on. But I’m already suspicious (must be all that child protection training).



What are the authors trying to investigate? They tell us that they want to identify the etomidate dose associated with optimal procedural sedation and few adverse events for ED procedures and to identify the type of procedure for which etomidate may be most effective.

Personally, I would prefer a dose at which there were no adverse events. Call me picky. But OK, let’s go along with it and see what happens.



Who are we talking about here? Apparently:

A convenience sample of ASA grade I or II patients aged 4-18 years, requiring a procedure projected to be of short duration for which procedural sedation was necessary.

Examples of these procedures included closed fracture reduction, joint reduction and incision and drainage of abscesses (although this was later excluded as etomidate proved inadequate for sedating for I&D).

Patients were excluded if they had adverse reactions to etomidate or fentanyl, any suggestion of adrenal insufficiency or suppression, multiple or non-acute injuries, altered pain threshold or impaired mental status.

In practice this translated into 61 actual patients enrolled over the 4 year study period. No, it’s not a typo – 61 patients over 4 years. And then one was excluded because he was given “too much” etomidate. Hmmmm, I hear you say, that’s not very many patients. I agree – apparently there were only 79 eligible for inclusion, and the majority of those who didn’t participate were non-consenting (we learn from their neat consort diagram).

So it’s not an enormous RCT – instead  a rather small prospective  cohort. Sometimes the best things, I’m told, come in small packages. Maybe it’s a neat, well designed study with some impressive results which could be up-scaled into a multicentre RCT. We can hope…



What actually happened to the patients?

So there was no randomising, placebos, standard therapy or anything fancy. They gave some etomidate  to their patients and measured what happened, and then drew conclusions about it. Let’s look in more detail.

Their primary outcome was achievement of adequate sedation as demonstrated by Wisconsin Sedation Score and successful completion of a painful procedure after standard dose fentanyl and study dose etomidate.

The patients received at 1µg/kg IV fentanyl (unless they’d already had opioids, in which case they got 0.5µg/kg fentanyl), then within 1-2 mins they received an etomidate bolus of 0.1mg/kg (in the first 10 patients in the study – this proved to be inadequate, so subsequently they increased the etomidate  bolus to 0.2mg/kg). If they weren’t quite sedated enough, they could then have 0.1mg/kg more etomidate to maximum 0.3mg/kg.

Hmmmm, that dose sounds familiar. Haven’t I read that somewhere? Ah, yes – here:

Hang on – doesn’t that excerpt from the BNF say “induction of anaesthesia”? With the same dose? Yes, it does. More on that later…

Patients were monitored with vital signs, pulse oximetry, Bispectral Index Scoring (BIS – measure of sedation, although in 8 patients it wouldn’t trace accurately), and ETCO2 monitoring (as a proxy for evidence of respiratory depression – controversial in itself).

Sedation was assessed using BIS and the Wisconsin sedation scale (subjectively scored by someone – they don’t tell us who). Satisfaction scoring was completed by the ED physician, the ED nurse, the provider of the procedure and the parent. Adverse events were  recorded by trained observer nursing staff.



What happened to the subjects?

The procedure was a success in 59/60 patients. Median sedation time (etomidate to discharge-ready) was 21 minutes. That’s pretty impressive compared with ketamine but hang on – the range was 8-100 minutes. 100 minutes?! I’d be a little concerned by a child sedated for 100 minutes in my ED…

The authors give mean and median sedation scores by etomidate dose, which are pretty modest in themselves, but again the ranges are interesting. For the 0.2mg/kg patients, the median sedation score ranged from 1-5 (almost anaesthesia to barely sedated). In the 0.3mg/kg patients, the median sedation score ranged from 3-6 (conscious sedation to not sedated at all). Doesn’t this make etomidate seem a little… well… unpredictable.





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5 thoughts on “If it ain’t broke… Etomidate for paediatric sedation.”

  1. So, I’m guessing that you’re not going for etomidate then?

    Any thoughts on adrenal suppression in kids? That’s one of the concerns in big children (adults).

    In adults I very, very, very rarely use it. Maybe once a year? This year in one patient with hypotension and VT who was SICK and needed some VIRWEB to make better


    VIRWEB – Virchester West Electricity Board aka Defibrillation.

    1. Seem to recollect less evidence of adrenal suppression in kids but this being used as one (of many) reasons not to introduce etomidate in several institutions I’ve worked in. Congrats to Natalie on a great deconstruction of this – IMHO paed sedation drug options are really straightforward: nitrous oxide (+ LAT where necessary) and ketamine. Everything else is simply showing off.

    1. Interesting! I’ve no experience with nebulised opiates. Intranasal spray yes, but nebulised, through a mask nebuliser then not something I’ve done.

      Since ket has such great analgesic properties what’s the advantage of adding another analgesic???

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