Post Your Cases > A rescue using CELEPID 20% (Claris Lifesciences)
Thanks for posting so quickly. Very interesting case. I know this sounds anathema but I have some very good data indicating that epinephrine impairs efficacy of lipid rescue. This is in addition to the data showing that lipid (alone) compared with either epi (alone; see Anesthesiology 2008) or vasopressin (alone; see Critical Care Medicine March 2009)is far more effective than either of those in a rodent model of bupivacaine toxicity. The paper showing that adding epi to lipid really ruins outcomes has been submitted but we've not yet heard if it is accepted for publication. Can you clarify when the patient's blood pressure and ECG normalized? Did you get the sense whether it was concomitant with the delivery of the lipid or the epi? or wasn't it possible to discriminate.
Thanks again,
Guy
Thanks again,
Guy
March 2, 2009 |
[Guy Weinberg]
[Guy Weinberg]
Hi Guy,
The epi was given according to standard resuscitation protocols and epi infusion started to try and raise and maintain blood pressure as patient was getting persistent hypotension. We took about 5 mins to get the lipid from pharmacy (sent a med student running for it) as we did not have it in theatre (that will change from today). ECG was also showing various abnormal rhythms. After the 100ml lipid bolus and about 10 min into the lipid infusion his blood pressure stabilized and ECG reverted to sinus tachycardia. At that point his epi infusion was stopped completely. Everybody present felt that the lipid infusion was what did the trick as he was still getting hypotensive despite having had about 3mg epi via infusion over 10 mins.
The epi was given according to standard resuscitation protocols and epi infusion started to try and raise and maintain blood pressure as patient was getting persistent hypotension. We took about 5 mins to get the lipid from pharmacy (sent a med student running for it) as we did not have it in theatre (that will change from today). ECG was also showing various abnormal rhythms. After the 100ml lipid bolus and about 10 min into the lipid infusion his blood pressure stabilized and ECG reverted to sinus tachycardia. At that point his epi infusion was stopped completely. Everybody present felt that the lipid infusion was what did the trick as he was still getting hypotensive despite having had about 3mg epi via infusion over 10 mins.
March 2, 2009 |
Dr Peng Ewe
Dr Peng Ewe
thanks for the follow up dr. ewe,
the 'abnormal rhythm' is more consistent with bupivacaine effect if it were largely bradycardia or wide complex. narrow complex tachycardia wtih our without ectopy would be more consistent with epi effect. do you have any of the strips? what is your recollection about the worst pre-lipid ECG pattern?
guy
the 'abnormal rhythm' is more consistent with bupivacaine effect if it were largely bradycardia or wide complex. narrow complex tachycardia wtih our without ectopy would be more consistent with epi effect. do you have any of the strips? what is your recollection about the worst pre-lipid ECG pattern?
guy
March 3, 2009 |
[Guy Weinberg]
[Guy Weinberg]
It was mainly wide complex rhythms....his heart rate was not very high initially despite the epi...which I found strange. When he got the lipid infusion and his blood pressure raised then his heart rate increased significantly.
Unfortunately this gentleman had an asystolic arrest in the high dependency unit about 13 hours later. He was high risk on 5 antihypertensive agents, chronic renal failure with history of episodes of hypertensive crisis and flash pulmonary oedema.
Unfortunately this gentleman had an asystolic arrest in the high dependency unit about 13 hours later. He was high risk on 5 antihypertensive agents, chronic renal failure with history of episodes of hypertensive crisis and flash pulmonary oedema.
March 7, 2009 |
Dr Peng Ewe
Dr Peng Ewe
so sorry to hear of the patient's outcome. the wide complex is very consistent with LA toxicity (QRS duration is probably a good surrogate for myocardial tissue LA content).
you obviously gave him a good chance of survival with the rapid resuscitation. but co-morbidities often trump our best efforts in such cases.
guy
you obviously gave him a good chance of survival with the rapid resuscitation. but co-morbidities often trump our best efforts in such cases.
guy
March 9, 2009 |
[Guy Weinberg]
[Guy Weinberg]
Hi Guy,
One question that has been floeating around in our Dept is - Could the chronic renal failure contribute to some bupivicaine still hanging around in his system and after the lipid was metabolized causing cardiac toxicity again? I know that may seem a stretch of the imagination....Thanks
One question that has been floeating around in our Dept is - Could the chronic renal failure contribute to some bupivicaine still hanging around in his system and after the lipid was metabolized causing cardiac toxicity again? I know that may seem a stretch of the imagination....Thanks
March 16, 2009 |
Dr Peng Aun Ewe
Dr Peng Aun Ewe
Not to be trite at all....
but I think you've identified a valid line of inquiry. Now, design some experiments!
but I think you've identified a valid line of inquiry. Now, design some experiments!
March 17, 2009 |
[Guy Weinberg]
[Guy Weinberg]
Nearly 96% of Bupivacaine is metabolized by the liver into 2 inactive metabolites Pipecoloxylidine and Desbutylbupivacaine. Very little drug is actually excreted unchanged through the kidney.
May 15, 2009 |
Anu Sidhu
Anu Sidhu
26 year old gentleman with end stage renal failure (from yet undetermined cause - but has no other known medical problems) was scheduled for the creation of an arterio-venous fistula for haemodialysis.
A supraclavicular brachial plexus block was performed using a nerve stimulator by a colleague and approximately 10 minutes after the patient started to complain of dizziness. He was then noted to be sweating and complained of being very light headed. His ECG trace on the monitor showed him to be in Ventricular tachycardia and then suddenly became asystolic. He was immediately intubated and CPR commenced with adrenaline, atropine. Spontaneous circulation returned but was still hypotensive requiring a high dose adrenaline infusion. He also started having generalized tonic-clonic seizures with no prior history of seizures. Local anaesthetic toxicity from bupivicaine was suspected as the cause.
In our hospital, we do not have Intralipid 20% but we stock Celepid 20% manufactured by Claris Lifesciences. Celepid 20% (500ml bottle) was administered - 50ml bolus x 2, and the balance of 400ml given over 20mins via a central vein.
His blood pressure stabilized as the bottle was nearing completion and the adrenaline infusion was stopped. A second bottle was started to go over 4-6 hours and patient transfered to the intensie care unit. There he maintained his blood pressure without need for ionotropes and started to wake up with no further episodes of seizures. He was extubated about 3 hours after the arrest and is cardiovascularly stable with no evidence of any seizure of neurological deficit.