Tag Archives: analgesia

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

Ref

  • 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

NICE faces the sickle

New guidance out on sickle disease from NICE in the BMJ

I must admit to having a bit of an interest in sickle cell disease and the ED. There are two reasons for this.

Firstly, and most importantly, it is a really important disease to manage well. It’s a proper disease that we have learnt about since the very first weeks of med school, one for which the pathology, pathophysiology and treatment is well described and understood.

Secondly, I am constantly intrigued to see new docs arrive in the ED with preconceptions about the disease and it’s sufferers that I cannot understand or explain.
So, back to basics. Sickle cell anaemia is a ‘proper disease’, it can kill you, and shortens your life expectancy which is bad, very bad indeed. Living with sickle disease can be tough and patients suffer painful vaso-occlusive crises that may require them to come to our EDs for help. If you work in a multi-ethnic practice like Virchester then you will meet many patients with Sickle disease so it’s important that we understand how to help them. In our ED that means that we have a really good working relationship with our haematologists and in particular a specialist nurse in sickle disease who knows our local population really well and who has encouraged the development of personalised treatment plans. These are shared with the ED (the pink file), the patients, and with the haematology team. If not then we have a great pathway for the treatment of ‘unknown’ patients with sickle disease. It’s safe, evidence based and it works. Many of our local patients manage their disease very well at home and only come to see us when home management has failed. With few exceptions they only come to us when they really need help.

So, in Virchester everything is rosy. Except it’s not because I still occasionally come up against ideas which I find difficult to explain and understand, and this is almost always around the use of analgesia in vaso-occlusive crises.

So, let’s think about analgesia. In many ways I think that sickle disease is the poster boy for good analgesia management in the ED. Get this right and you probably have an ED that manages most pain well (there is a poster girl as well – but that’s for another day).

Why is it the poster boy? Well, because the management of sickle disease is one where analgesia is a cornerstone of management, where there are few physical signs, but where I see clinicians manage patients in very different ways. Such variation is not just an issue in my practice, but also in past studies and papers where the experiences of patients attending EDs is far from optimal. Take this quote from a 1999 paper in the BMJ

“The experiences of patients with sickle cell disease of hospital care are characterised by mistrust, stigmatisation, control, and neglect”

Now that was a long time ago (1999) and I like think we have made fantastic progress locally, but I am not convinced that this is the case everywhere because I still see suspicion and concern amongst some junior docs rotating in from St Elsewhere. Why is this I wonder? Where and how did they learn it? Why is it that we have a disease that causes pain, suffering, shortens lives but for which I sometimes see docs and nurses ‘not believe’ that the patient is genuinely in pain and as a result their analgesic management is suboptimal.

Why then? Is it the disease itself? Well perhaps as there are often few physical signs in sickle disease that ‘justify’ the pain to the physician. There is no bleeding, deformity and often few physiological signs. I hear odd comments such as ‘nobody in that much pain has a pulse less than 110’……! Really, do you want me to demonstrate whilst I take your pulse….? Until we have a pain-ometer that can quantify pain then we have to presume that the patient is telling the truth unless we know otherwise. In law we are innocent until proven guilty and the same should apply here. Similarly, on a general approach to pain then we must decide whether analgesia is something that we should freely offer, or should it be something that is earned? What do I mean by this? Well, its that I believe that analgesia is one of the most important things that we can do to improve the patient experience of illness and injury. We should be seeking out pain and treating it, not waiting for our patients to beg for it to be taken away.

This cannot be right and we cannot accept it, but how can we make it better.

I would suggest the following.

  • 1. Speak to your local haematologists and devise a protocol for the management of sickle pain. Why not use something like that advised by NICE and abstracted in this weeks BMJ
  • 2. Use sickle as a teaching tool for analgesia. Ask your colleagues about their attitudes towards sickle disease and the patients. Challenge, argue and question any attitudes that trouble you.
  • 3. Role model the care of sickle patients in the ED. As a senior these are great cases to see with a junior doc. Great for the patient as they get great care. Great for you as it tells you a lot about their attitude towards the disease and analgesia in general. Ask them how they ‘measure pain’, you might be surprised at the results…
  • 4. Talk to your local haematologists. Establish a mechanism for them to tell you about difficult or complex patients.
  • 5. Train the whole team. Analgesia is something often prescribed by docs but prioritised by the nurses. If you only train one of the tribes then you will fail.
  • 6. Listen to Dr Gentile.

When the patient is comfortable ask them what they felt about their experiences in your ED. It’s highly unlikely that this will be their first attendance at the ED. Ask them how you did, ask them about good and bad experiences in the past. In general they will tell you.

Lastly, another plug for the unbelievably fantastic podcast from Dr Gentile on pain management in the ED. Whilst not strictly about sickle disease you just know that if you did have sickle disease (or anything else painful) you would want Dr Gentile to look after you.

I am told that my posts might be too thought provoking where some people just want the answers. I think not. I’d rather write about things that we all find challenging. Where there are answers we can give them, but so much of our practice is dependent not just on the evidence but also on ourselves. We should never stop questioning the evidence, we should never stop questioning ourselves.

vb

Simon C

PS. This is our current management protocol for ‘unknown’ sickle patients. Time for a review I think, but even so this works pretty well at the moment. Advice on changes welcome.

EDP_2003-22_Sickle_Cell_Crisis