Post Your Cases > Intralipid treatment of bupivicaine toxicity in interscalene block
Nice job! While it's hard to for someone not there to have confidence the patient wouldn't have stayed out of Vfib without the lipid, I'm glad you've been convinced the lipid made a difference. I consider it good policy to trust the eyes and sentiment of the person who was there -they know what they saw.
The persistence of malignant arrhythmias is typical for bupivacaine toxicity. See the recent article by Levsky 2005, Canadian Journal of Clinical Pharm. for another variant on the same theme. Their case had persistent hypotension and recurrent arrests. Re: your patient - I'm curious to know if the QRS was abnormal and if so, did that improve with lipid. Also, how was the BP with NSR prior to the second episode of Vfib. Annette, you might consider writing this as a letter to the editor. Thanks for the great case. Guy
The persistence of malignant arrhythmias is typical for bupivacaine toxicity. See the recent article by Levsky 2005, Canadian Journal of Clinical Pharm. for another variant on the same theme. Their case had persistent hypotension and recurrent arrests. Re: your patient - I'm curious to know if the QRS was abnormal and if so, did that improve with lipid. Also, how was the BP with NSR prior to the second episode of Vfib. Annette, you might consider writing this as a letter to the editor. Thanks for the great case. Guy
March 6, 2007 |
[Guy Weinberg]
[Guy Weinberg]
I do not know about the QRS after the lipid was given but what was striking was that
the patient stayed in sinus rhythm after the lipid was given. The BP was quite high prior to the second episode of v.fib. because of all of the pressors that were given.
Annette
the patient stayed in sinus rhythm after the lipid was given. The BP was quite high prior to the second episode of v.fib. because of all of the pressors that were given.
Annette
March 6, 2007 |
Annette Zwick M.D.
Annette Zwick M.D.
This might blow your mind, but in the rat expts we're doing now.....epi and epi+vasopressin is associated with poor outcomes in LA toxicity. All the rats get severe hypertension, then pulmonary edema. Good cardiac output and organ perfusion shouldn't be equated with high blood pressure in these scenarios. There is a significant literature on the downside of using large dose epi during cardiac arrest. However, I know that personally, it will be very difficult NOT to give the drug we've all been taught to rely on for a patient in cardiovascular collapse. It's just that LA toxicity is different...somehow intense vasoconstriction really makes it worse. More research needed. Thanks again for the post. Guy
March 6, 2007 |
[Guy Weinberg]
[Guy Weinberg]
If this is the case, what is the sequence of resuscitative measures that you would recommend
for a presumed LA toxicity? Would you try to hold off on the vasopressors until the Intralipid is in and the patient is defibrillated? How about amiodarone? How about
vasopressin as a single dose?
Annette
for a presumed LA toxicity? Would you try to hold off on the vasopressors until the Intralipid is in and the patient is defibrillated? How about amiodarone? How about
vasopressin as a single dose?
Annette
March 8, 2007 |
Annette Zwick
Annette Zwick
Good question and hopefully I'll have a more evidence-based answer for you when I finish the current experimental series (ongoing for almost a year). In rats, at least, the combination of vasopressin and epi is particularly bad. My hypothesis is that the intense vasoconstriction in the face of a poorly contracting (LA-toxic) but stiff (epi-induced) ventricle causes the gross/hemorrhagic pulmonary edema. ADH (vasopressin) alone doesn't help at all in the rodent model of bupivacaine toxicity I'm using.
There is a very well established resuscitation group that has published many articles showing a benefit, for a variety of causes of shock/arrest, of increasing coronary perfusion pressures with combined pressor therapy (epi/vasopressin). On the other hand, there are many clinical and lab studies suggesting that high dose epi in cardiac arrest is bad for outcomes. I think it will be difficult, lacking exceedingly convincing data to the contrary, to get people to hold back on giving epi while waiting for the lipid to be drawn up.
Right now, my un-tested and only partially-evidence-based opinions are to
1. make certain the patient is well oxygenated and ventilated THIS IS KEY!
2. if they are still awake and showing signs of CNS toxicity (agitation, or seizures) give benzodiazepine to prevent/suppress seizures.
3. if pulseless, you must deliver good chest compressions throughout..THIS IS ALSO KEY.
4 if you prefer to use epi...use the standard 1mg but hold off on repeated doses.
5. personally, i wouldn't use ADH.
6. lipid therapy.
I trust that the current experiments from our group and, presumably others, will help establish what combination of lipid and pressor is best. .....stay tuned. Lipid alone may be our recommendation; can't say for sure at this point.
There is a very well established resuscitation group that has published many articles showing a benefit, for a variety of causes of shock/arrest, of increasing coronary perfusion pressures with combined pressor therapy (epi/vasopressin). On the other hand, there are many clinical and lab studies suggesting that high dose epi in cardiac arrest is bad for outcomes. I think it will be difficult, lacking exceedingly convincing data to the contrary, to get people to hold back on giving epi while waiting for the lipid to be drawn up.
Right now, my un-tested and only partially-evidence-based opinions are to
1. make certain the patient is well oxygenated and ventilated THIS IS KEY!
2. if they are still awake and showing signs of CNS toxicity (agitation, or seizures) give benzodiazepine to prevent/suppress seizures.
3. if pulseless, you must deliver good chest compressions throughout..THIS IS ALSO KEY.
4 if you prefer to use epi...use the standard 1mg but hold off on repeated doses.
5. personally, i wouldn't use ADH.
6. lipid therapy.
I trust that the current experiments from our group and, presumably others, will help establish what combination of lipid and pressor is best. .....stay tuned. Lipid alone may be our recommendation; can't say for sure at this point.
March 9, 2007 |
[Guy Weinberg]
[Guy Weinberg]
hi annette,
could you pls email me:
guyw@uic.edu
thanks,
guy
could you pls email me:
guyw@uic.edu
thanks,
guy
March 27, 2007 |
[Guy Weinberg]
[Guy Weinberg]
block done and then patient became cyanotic and seized.
Patient was in asystole and then v. fib. CPR done with
defibrillation and sinus rhythm re-established but then
reverted to V. fib. 200 cc of 20% Intralipid given and
drip strarted at 20cc/hr. Rhythm and hemodynamics stabilized and never went back into v. fib. Pt. extubated within 2 hours and was alert and talking several hours later. Every facility where blocks are done should have Intralipid available.