Tag Archives: ultrasound

Through the Looking Glass: Chirocaine vs Bupivicaine

I’ve seen a few paediatric femoral shaft fractures in the last couple of years, and while they always make my spidey-sense tingle for non-accidental injury, most (even the spiral fractures) have been explained away by plausible mechanisms of injury; they are usually late toddling age, have got their feet stuck, twisted and fallen over.

I’ve even seen a few which were pathological – undoubtedly the result of the vitamin d deficiency which stems from the miserable attempt at sunshine we have to put up with here in the North West.

The way I’ve managed these patients has changed with my experience and skill level; as an SHO I looked at them with sympathy while the oramorph, ibuprofen and paracetamol were absorbed slowly from their (no doubt static) GI tracts. As a registrar, they now get a squirt of intranasal diamorphine and an application of ametop over the ipsilateral groin, in anticipation of an ultrasound-guided femoral nerve block when they return from x-ray. I mix up a 50:50 solution of 1% lidocaine with 0.5% bupivacaine and, before ultrasound guidance, used 1mL per year of age. It works out as less than 2mg/kg of lidocaine (usually) and less than 1mg/kg bupivacaine – so relatively small doses. I’ve done it a few times, and it works pretty well, especially in combination with a Thomas splint. The great thing about ultrasound-guidance besides lower failure rates is that you can use even smaller drug volumes – it ends up more like 0.5mL per year of age.

So as I examined the two year old, who was refusing to weight bear, with little deformity to his leg but clear femoral tenderness, I reached for the trusty bupivacaine/lidocaine combination to make splint application less of an auditory assault. But shock! Horror! No bupivacaine!

Instead, there was chirocaine – which completely confused me, as I had no idea what it was (and there was apparently no bupivacaine to be had anywhere). I asked around – and no-one seemed to be entirely sure how the two drugs related to one another. So, after some research, I thought I’d share.

Chirocaine (levobupivacaine), as you may know (I didn’t), is “the pure S-enantiomer” of bupivacaine. The story is that some drugs exist in a 50:50 (racaemic) mixture of two stereo-isomers; molecules which are mirror images of one another. Where the mirror images cannot be superimposed, the molecules are said to be chiral, and the most common cause for this is an asymmetrical carbon atom. There is a right (dex-, or d-) and left (levo-, or l-) version of the molecules which cannot be made symmetrical no matter the orientation in the same way as your left foot just doesn’t fit in your right shoe [NB: an important differential in the non-weight bearing child]. Where drugs bind to receptors, one isomer may be able to bind, while the other cannot – or may generate alternative effects.

You probably knew this already, right? Every time you prescribe levothyroxine, esomeprazole, escitalopram or levofloxacin, you think proudly about how you are selecting out the correct isomer for your patient, yes? And how you are therefore giving half the dose, as they aren’t getting the 50% of isomers which don’t give a clinical effect? Well, it doesn’t quite work as predictably as that. In fact, in some cases the dose is significantly lower for the same clinical effect (notably escitalopram, 30 times more potent than citalopram) and in others confers no therapeutic advantage at equivalent doses (see esomeprazole) or may even be harmful (see thalidomide).

So what’s so special about chirocaine? It’s twice the price of standard bupivacaine per 10mL ampule, so it’s twice as good, isn’t it?

Well, no – it seems to be equivalent at providing analgesia in a variety of blocks (caudal, ilioinguinial, rectus sheath… The list goes on…), but every study is focussed on the reduction in adverse (cardiac) effects with levobupivacaine. It seems the rationale for selecting out this isomer is reducing cardiac toxicity. Where does this come from?

Most data comes from animal studies (in case you didn’t know, children are no more little adults than they are little rats, pigs, rabbits…).

You have to dig quite deep for original studies. All roads seem to lead back to this one paper. 14 healthy, adult, male subjects were injected with bupivacaine or levobupivacaine infusion and asked “do you have any symptoms?”. OK, let’s be fair, they’ve powered the study to detect a 10% difference in their primary outcome (stroke volume), but their bottom line conclusion is “that levobupivacaine may be a safer drug than rac-bupivacaine for procedures requiring high doses of local anaesthetic.” So not really our fractured femur toddlers, then.

Which brings us back to the beginning. Studies in children have suggested that levobupivacaine produces equivalent anaesthetic efficacy, but what they haven’t done is convince me that we should ditch bupivacaine when we are using such tiny doses. It’s cheaper, and with ultrasound guidance we can use a miniscule amount to achieve local anaesthesia long enough to reduce the fracture in a Thomas splint.

So the bottom line is this; use what you’ve got unless there’s specific cardiac risk for your paed patient, and using 50:50 with 0.5% chirocaine provides the same analgesia as bupivacaine (in our hospital the maximum dosing for ilioinguinal block is apparently 1.25mg/kg/side). Whatever you use, do the block; your patients will probably thank you (but we might have to wait to find out).

Natalie May


  • A comparison of the cardiovascular effects of levobupivicane and rac-bupivicane following intravenous administration to healthy volunteers. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1873676/pdf/bcp0046-0245.pdf
  • EPG data sheet on Chirocaine http://www.epgonline.org/drugs/chirocaine/
  • Regional anaesthesia for kids with femoral fractures at BestBets http://www.bestbets.org/bets/bet.php?id=130

The time bomb of doom: What I think about when I’m tending broad beans


When I have downtime and I’m riding my bike or indeed tending to my Dads “prize winning” broad beans on the allotment; my mind unfortunately often wanders to recent cases in the ED that have gone bad.

I start to reflect on things I could have done better, or wonder if I could have affected patient outcomes for the better….

It’s the curse of the Emergency Physician.

This last week I have been pondering the dissecting thoracic aortic aneurysm (really type A dissections). Perhaps I’m practicing an area of unknown high incidence but I have come across 2 cases in recent months (normal incidence – by the way – 3/100,000) that have ended badly. Now, we all know that it’s a diagnosis that we find scary – the time bomb of doom – 1-2% of patients will die for each hour after onset of symptoms untreated. We know that symptoms aren’t reliable and you’ve gotta have a high index of suspicion (it is the “most undiagnosed serious condition” with up to 30% of diagnosis made at autopsy!).


I don’t claim to be a normal person, but I am always wary of patients (not intentionally, but, their “truths” can vary, they hide things, they’re never classic….) and my index of suspicion is always high….

BUT when you need some diagnostic imaging for your crazy, paranoid  hypotheses – it not always that easy to get a timely solution from our friendly radiologists.

What are the conventional options?

The Chest x-ray whilst much loved is awful as a rule-in or rule-out for dissecting thoracic aneurysm.  It will be completely normal in 20% of your patients and if your looking for mediastinal widening then you’ll only see that in 15%….as for the other myriad of “classic” signs we might as well get our euro millions lottery ticket.

The contrast CT, 79-100% sensitive, 87-99% specific – great, but not as “readily available” at the district hospital (where most EP’s) work as we might hope. The radiologist will argue that there is a high dose of radiation and no-one ever likes to use contrast. Meanwhile as we are debating and waiting for a slot in the scanner the time bomb is ticking.

And, Yes, there are also MR scan, transoesophageal echo and retrograde angiography, but I’m not convinced these diagnostics are available in many centres.

SO… what do I want in an ideal world? I would like bedside diagnostics that I can perform to help me expedite treatment rapidly…..So my big idea has been to use the ED ultrasound to perform Transthoracic echo (TTE) and measure the aortic root and get views of the arch to look for intimal flaps combined with standard descending aorta views. The question is – How confident can I be to use my ultrasound as a rule-out or rule-in for dissecting type A aneurysm?

Allow me to look over the literature:

The European Society of Cardiology have recommendations for aortic disease. They say that “TTE is an excellent modality for imaging aortic root dilatation…..not the ideal tool for visualizing all aortic segments”. In a related article from the Society they quote the “Literature of the past” i.e .1980’s and 1990’s, suggesting that for type A dissection TTE has a sensitivity of 78-100%, but as low as 57% in some series! They do point out that there have been no recent studies…. and certainly they would not use TTE as a rule-out. All very opinion based………

Luckily, to the rescue of evidence based practitioners, comes a diagnostic study published this year by an Italian team headed by Moreno Cecconi. They have asked a question similar to my own – “what is the current diagnostic value and the possible role of TTE in the management of patients with suspected aortic arch syndrome?”

270 patients (retrospectively collected data!?! And selection criteria not explained) all assessed by TTE as first line investigation and subsequently imaged by either CT/MR or transoesophageal echo…..Quoting: Sensitivity 87%, Specificity 91%, PPV 75%, NPV 95%.

In all honesty there are lots of problems with the methodology, and it’s from a dedicated cardiac centre  – not really generalisable for the average EP ultrasound operator – but it’s the only data we have using the latest generation of ultrasound technology. The authors are confident with their results and even go as far to say bedside TTE is “useful in establishing or excluding the differential diagnosis in the acutely unwell patient, particularly in the absence of aortic root dilatation”.

What conclusions can I draw from the limited evidence? Well, as with FAST and FASH etc, bedside TTE is another diagnostic modality in our armoury…. Its highly operator dependent but its quick and safe and can definitely guide your management. Would I rely on it to completely exclude a diagnosis of type A aortic dissection? Probably not… But I would measure the aortic root diameter and think hard about my next move…

Rare conditions with serious outcomes – its like being a goalkeeper facing a penalty in soccer – make a save and you’re a hero, drop the ball and you feel like a villian with the weight of the world on your shoulders… but the odds were always stacked against you. The magic wand of ultrasound – when used wisely – can be a significant arrow in your quiver of imaging diagnostics, but when the incidence is low and the risks are high, think hard before using TTE as a lone rule-out investigation…Its not an ideal world in the world of diagnostics…….

And that is what I think about when I’m tending broad beans.