Post Your Cases > dr
Hi Beverly,
Very interesting case. Hope you've recovered. A few thoughts:
Propofol almost certainly did NOT help prevent progression: there's not enough lipid in the formulation to provide any protection at standard (safe) rates of infusion or even with bolus dose. Propofol itself is cardiodepressant. If there is any advantage, it is in the prevention or suppression of seizures and the resulting acidosis/hypoxia (read on).
Low cardiac output did not protect the patient. The slower circulation time delays onset but worsens the cardiac toxicity. This is due to the fact that the drug is diluted in a smaller volume of blood, much as the peak of temperature change when doing thermodilution measures of cardiac output are much greater when the cardiac output is low.
OK, how was the patient saved?
I believe three elements contributed:
1. Rapid recognition of the problem
2. Rapid intervention to support ventilation and oxygenation (possibly the most important factor in saving this patient).
3. Interpatient variability in sensitivity to LA toxicity. Some patients will exhibit extreme negative inotropism with small doses of LA while others are apparently resistant. Note that myocardial ischemia and conduction abnormalities definitely predispose to toxiciity. Your patient was apparently in the 'resistant' category.
One can also theorize that luck had a part, or perhaps having the lipid right there scared off the evil spirits of LA toxicity. But I prefer to commend you for being prepared and acting quickly.
Guy
Very interesting case. Hope you've recovered. A few thoughts:
Propofol almost certainly did NOT help prevent progression: there's not enough lipid in the formulation to provide any protection at standard (safe) rates of infusion or even with bolus dose. Propofol itself is cardiodepressant. If there is any advantage, it is in the prevention or suppression of seizures and the resulting acidosis/hypoxia (read on).
Low cardiac output did not protect the patient. The slower circulation time delays onset but worsens the cardiac toxicity. This is due to the fact that the drug is diluted in a smaller volume of blood, much as the peak of temperature change when doing thermodilution measures of cardiac output are much greater when the cardiac output is low.
OK, how was the patient saved?
I believe three elements contributed:
1. Rapid recognition of the problem
2. Rapid intervention to support ventilation and oxygenation (possibly the most important factor in saving this patient).
3. Interpatient variability in sensitivity to LA toxicity. Some patients will exhibit extreme negative inotropism with small doses of LA while others are apparently resistant. Note that myocardial ischemia and conduction abnormalities definitely predispose to toxiciity. Your patient was apparently in the 'resistant' category.
One can also theorize that luck had a part, or perhaps having the lipid right there scared off the evil spirits of LA toxicity. But I prefer to commend you for being prepared and acting quickly.
Guy
April 1, 2008 |
[Guy Weinberg]
[Guy Weinberg]
Did the propofol act as an intralipid infusion, or did his poor circulation avoid a rapid bolus of bupivacaine to his heart? Any comments appreciated.