local anesthetic class insensitivity

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Intubate

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This happened a while ago, but I just thought of it again...
I was called to see a laboring patient whose epidural wasn't working anymore. It had already been replaced once (by one of my partners). I dosed with 2% lidocaine--- no block. So I pulled it. Put in a new epidural, did a CSE with 15 mcg sufenta and 1 ml 0.25% bupivicaine. Excellent relief (I didn't check a level). Started the infusion and left. Called back an hour later. Hurting again. No sensory level. Bolused 2% lidocaine, no level. WTF. I had heard from a partner of a patient who was insensitive to amide local anesthetics, so I decided to try chloroprocaine. I bolused her with 10ml of 2% and she got comfortable right away with a T6 level. I ran an infusion of chloroprocaine for the rest of her labor and she did fine.

Has anyone seen this? Was this just a bizarre unrelated series of events that made it look like amides didnt work for her, or was it real? I can find no mention of this in the literature.

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I had a patient in residency. Labor, tall thin, red hair wanted epidural. She's totally healthy, but tells me that her last epidural never worked for her. Epidural goes in easily, all smooth and bolus with 10 cc of .2 % bupivicaine. 15 minutes later, she is still in pain, no level. Feels ice on her legs. 10 minutes later, she has her baby. I chalk it up to rapidly changing cervix and there is lots to do so I move on.

Later, I see her for a tubal. Epidural still in, so we bolus with 20cc of 2% lido. 30 minutes later, some numbness in the legs, maybe a T12 level. My attending doesn't want to give anymore through epidural, so we take it out and do a spinal with marcaine. T10 level. Sort of. She can still move her toes half hour after spinal goes in. She gets GETA. An hour later in recovery, she has no level. I did some lit searched, found nothing. I started cardio a few days later and forgot about it until today. So I don't know.
 
I had a pt in residency who claimed that local anesthetics didn't work for him. Of course we did not believe him and went ahead with a interscalene block for shoulder surgery. Good twitches 50ml of ropi 0.5% go in. 15 min later- nothing. My attending thought I moved while injecting so he went and did a second block with 30 ml of bupi 0.5% after getting good twitches. 10 min later-nothing. Pt started looking funny to us (we thought a seizure was coming) so we intubated him. In pacu about 2 hrs later he had no block at all.


OP, congratulations for trying chloroprocaine. Next time I'm in a similar situation I'll give it a try.
 
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I've had several patients over the last 14 years who seemed very "resistant" to the effects of local anesthetics even when the needles have obviously been placed in the proper locations.
 
This happened a while ago, but I just thought of it again...
I was called to see a laboring patient whose epidural wasn't working anymore. It had already been replaced once (by one of my partners). I dosed with 2% lidocaine--- no block. So I pulled it. Put in a new epidural, did a CSE with 15 mcg sufenta and 1 ml 0.25% bupivicaine. Excellent relief (I didn't check a level). Started the infusion and left. Called back an hour later. Hurting again. No sensory level. Bolused 2% lidocaine, no level. WTF. I had heard from a partner of a patient who was insensitive to amide local anesthetics, so I decided to try chloroprocaine. I bolused her with 10ml of 2% and she got comfortable right away with a T6 level. I ran an infusion of chloroprocaine for the rest of her labor and she did fine.

Has anyone seen this? Was this just a bizarre unrelated series of events that made it look like amides didnt work for her, or was it real? I can find no mention of this in the literature.

Have seen this once in eleven years of practice.

Of course it was on somebody I knew's wife.

Almost exactly the same scenerio except I did ropiv/sufenta CSE with no relief.

Then did it again.

Then replaced it again, this time normal epidural, lido 2%....nothing.

Chloroprocaine worked, huh?

Wish I wouldda tried it.

She delivered the old fashion way. :(
 
These are the cases it would be interesting to do actual pharmacokinetic studies on, but we're unable to do so. But, we have some interesting literature about local anesthetic distribution & metabolism for the CSF, mostly done in dogs & rabbits. Altho these studies do have their obvious limitations, we can extrapolate within certain parameters some of what may indeed go on in humans.

Likewise, we're becoming more & more aware of the CYP enzymes which metabolize these drugs. You wouldn't think that should influence what you put in the epidural space, but it does - depending on what is occuring within the distribution kinetics of that space.

We know that there are three competing uptake processes of epidural drug disposition: thru the meninges into the CSF, thru capillary vessels into the systemic circulation & into epidural fat. After studying individual drugs in animals, we've found that protein binding in the CSF & distribution into epidural fat, which we thought to be minimal is indeed not minimal at all & can be of tremendous variance. Likewise, the protein binding pattern of individual drugs, both amides & amines vary significantly. Altho in vitro, there is a 4 fold difference in the absorption rate constant between bupivacaine & lidocaine, this is not as predictable in humans due to the variance in the complexities in how each is handled in vivo between the epidural, intrathecal, fat & systemic circulations - each is a different "compartment" pharmacologically.

Actual human studies have found a biphasic elimination pattern of most local anesthetics administered epidurally, but the pattern of their distribution & elimination vary widely. Part of this is based on their lipophilicity, their diffusion coeffiecients into the epidural space, protein binding & many other variables. Generally, the bioavailability of lidocaine in humans is 20% & 10% for bupivacaine when administered epidurally.

So....long post, mostly irrelevant to all of you perhaps & certainly not complete, but why would one drug work when another doesn't? Many reasons, absorption, distribution, protein binding & sometimes just genetic variances in how the drug is actually eliminated after it reaches steady state with the general circulation.

Now after this long-winded post, none of this would change your practice, but it may give you some peace it was not your technique - rather it might have been just one of those abnormal ways that one particular individual might have processed the drug.

Out of curiousity - do any of you ever ask what the experience these pts have had with dental anesthesia (would give some insight into the liver metabolism)???? I'm not sure that would change your medical choices, but it may give you some insight into those who might be "difficult" persons to obtain adequate anesthesia at the outset.

It would be interesting to correlate that to decrease the variances - these studies are very, very hard to do in humans!
 
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Out of curiousity - do any of you ever ask what the experience these pts have had with dental anesthesia (would give some insight into the liver metabolism)???? I'm not sure that would change your medical choices, but it may give you some insight into those who might be "difficult" persons to obtain adequate anesthesia at the outset.

I do ask if their last epidural (if applicable) worked well. On occassion the patients tell me that the dentist had to re-dose them several times. I usually just tuck it in the back of my head because I have no idea what drug they used, ester vs amide.

If they say the last anesthesia guy didnt do a good job because the epidural never worked...I usually defend the previous technique and explain the limitations of an epidural. I think from now on I may consider using a different drug (chloroprocaine) if the patient paints a picture of a previously continuously failing epidural despite several adjustments. Thanks for the post Intubate.

Also, almost all of my laboring epidurals are a combined spinal epidural technique. I do notice a significant variance in the onset of action, depth and duration of the spinal dose (much easier to notice as compared to an epidural loading dose). This helps me determine the rate and concentration of the continuous infusion.....although it is still just a guess.

When patients ask if the epidural is going to work....I usually reply with "I have no idea....we will soon find out". :)
 
This happened a while ago, but I just thought of it again...

Has anyone seen this? Was this just a bizarre unrelated series of events that made it look like amides didnt work for her, or was it real? I can find no mention of this in the literature.

Write it up. This needs to be in the literature. And everyone else with posts and similar experiences should write these things up.
 
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"-Hypokalemic sensory overstimulation.
People with hypokalemic sensory overstimulation also have a reduced effectiveness of the local anesthetic lidocaine. This was first noted during minor surgery, in which one person was given lidocaine "in repeated injections totaling 15 mL because the patient reported continued sensation" but nevertheless he "could document the inadequacy of anesthesia by reporting accurately the location of forceps touches to the toe under conditions in which he could not see his toe."

"-Local anaesthetic failure in joint hypermobility syndrome
Alan J Hakim, Rodney Grahame, [...],

When taking biopsies to assess skin strength in Ehlers–Danlos syndrome type III (EDS–III), a Danish group noticed that the patients experienced much pain despite conventional local anaesthesia.1 When asked, all these patients reported previous experience of partial or complete failure of local anaesthesia in dental or obstetric procedures—for which reason some had been dismissed as hysterics. Pursuing this finding, Arendt-Nielsen et al.2 compared the effects of local anaesthesia in 8 patients with EDS–III and 8 controls. Although the patients did gain analgesia from intradermal lidocaine the duration of effect was much shorter than in controls. EDS–III (now known as EDS–hypermobility type) is regarded by many authorities as identical to joint hypermobility syndrome (JHS).3,4 We wish to draw attention to the possibility of resistance to local anaesthesia in individuals with this common and under-diagnosed condition."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1079398/
 
I had a patient in residency. Labor, tall thin, red hair wanted epidural. She's totally healthy, but tells me that her last epidural never worked for her. Epidural goes in easily, all smooth and bolus with 10 cc of .2 % bupivicaine. 15 minutes later, she is still in pain, no level. Feels ice on her legs. 10 minutes later, she has her baby. I chalk it up to rapidly changing cervix and there is lots to do so I move on.

Later, I see her for a tubal. Epidural still in, so we bolus with 20cc of 2% lido. 30 minutes later, some numbness in the legs, maybe a T12 level. My attending doesn't want to give anymore through epidural, so we take it out and do a spinal with marcaine. T10 level. Sort of. She can still move her toes half hour after spinal goes in. She gets GETA. An hour later in recovery, she has no level. I did some lit searched, found nothing. I started cardio a few days later and forgot about it until today. So I don't know.

be careful when doing this, high spinals are more likely. one of my partners had it happen to him a couple of weeks ago...
 
A patient has lived in their body and knows it better than your cursory examination reveals it to you. Were you aware that it has been documented that Persons with hyper mobility or Ehlers-danlos syndrome (both invisible disabilities) are immune to local anesthesia? Many doctors brand them as hysterics (how paternal) or drug seekers. Ask a few questions of the patient, are you double jointed? Have you dislocated anything? Do you bruise easily? How do you respond to dental anesthesia? FYI most hyper mobile people have no reaction to the caines. That's novocaine AND lidocaine. They are candidates for gas. With these patients you must also be aware of the fragile yet stretchy skin and carefully place your needles.

I have E-D and had horrible dental experiences as a kid, because my dentist didn't believe me when I said I wasn't numb. It's a common trait, because the four following dentists behaved the same way. If you've gone through a deep root planing on two quadrants with no pain prevention, you would also speak up when your colleagues blow their patients off.
 
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I sympathize, but you are barking up the wrong tree. Most anesthesiologists will believe a patient who says s/he's still uncomfortable, and will advocate for the patient, even if it's the surgeon who's giving the local. We really do want our patients to have an as good as it gets experience (and will be superprotective with an E-D patient, specifically). We will also welcome any literature about anesthesia in the context of the patient's rare syndrome.

The E-D patients are actually very rare in an anesthesia practice, and this thread is mainly about others, the patients with unexplainably high local anesthetic tolerance/metabolism. They are way more frequent. Anyway, when somebody does not respond to a drug, any smart doc will just switch to a different class, instead of debating the patient. That's exactly what happened above.

The same way some people never get drunk, some people have problems with other enzymes. The key is giving every patient the benefit of the doubt.
 
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I had a pt in residency who claimed that local anesthetics didn't work for him. Of course we did not believe him and went ahead with a ......
There are exceptions. My point is that if you have a doubt, ask more questions, the answer may reveal itself. Many people who are hyper mobile think that they are just really flexible, and are unaware of the complete nature of their condition.

A look at the patient's POV https://www.inspire.com/groups/ehle...cs-conscious-sedation-and-general-anesthesia/
 
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