Post Your Cases > Intralipid use in TCA overdose
Congratulations on an interesting case.
We have seen haematuria in the lab in the past with lipid treated animals. A necropsy has shown a haemorrhagic cystitis. We haven't histologically examined either the GU tract or kidneys tho looking for other causes.
Re: the issue with bloods one research solution used in the past has been to spin the blood, freeze it and then scrape off the lipid phase. A lot of work and time for the clinical situation though.
We have seen haematuria in the lab in the past with lipid treated animals. A necropsy has shown a haemorrhagic cystitis. We haven't histologically examined either the GU tract or kidneys tho looking for other causes.
Re: the issue with bloods one research solution used in the past has been to spin the blood, freeze it and then scrape off the lipid phase. A lot of work and time for the clinical situation though.
May 29, 2009 |
Grant Cave
Many thanks for reporting your case.
Our experience with intentional overdoses with significant obtundation has been that of ingestion of more than one drug occasionally supplemented with alcohol (similar to your account). Recovery following intralipid administration has been consistent in situations where all the drugs ingested have been lipid soluble.
Our biochemistry department has also reported interference (due to lipaemia) with routine analysis when more than 1000cc intralipid has been infused rapidly.
I would be interested to learn how quickly your patient's level of consciousness was restored and how long she remained intubated and ventilated.
Our experience with intentional overdoses with significant obtundation has been that of ingestion of more than one drug occasionally supplemented with alcohol (similar to your account). Recovery following intralipid administration has been consistent in situations where all the drugs ingested have been lipid soluble.
Our biochemistry department has also reported interference (due to lipaemia) with routine analysis when more than 1000cc intralipid has been infused rapidly.
I would be interested to learn how quickly your patient's level of consciousness was restored and how long she remained intubated and ventilated.
May 31, 2009 |
David Uncles
Sorry for the long delay in replying to this interesting post. First, note the excellent comments by Drs. Cave and Uncles who are leaders in the field. Dr. Cave has published extensived data from animal models of lipid infusion and Dr. Uncles has probably more experience than any other physician with lipid rescue for non-local anesthetic overdoses. Now to the post:
Two main issues emerge in this report, effects of high lipid volumes and the patient's clinical course. First are the laboratory and clinical effects of high-dose lipid infusion. Laboratory results, particularly blood chemistries will unquestionably be thrown off by extremely lipemic serum, and I'm a bit surrprised there hasn't been more in the literature on this effect - it's certainly approachable in animal models. Anyone interested in doing these studies?? I wonder if you could have measured a hematocrit in this patient as an alternative to Hb concentration? I also wonder if ultracentrifuging the plasma then popping the lipid cap off would allow you to measure chemistries in the remaining plasma (we do this in the lab). The other concern of course has to do with the very large lipid load given this patient. The safety profile of acute lipid infusion isn't known. The typical doses administered to patients in cardiac arrest (bolus plus infusion) are on the order of 4mL/kg over 30 minutes. This would generally mean less much than a liter for an adult. I'm unsure where the maximal safe dose is, but wouldn't feel comfortable giving much more than a liter. Interesting to hear of Dr. Caves experience with cystitis and makes one wonder if that was the case here.
Second, I would echo Dr. Uncles query about the rate of resolution of GCS. Is it clear the improvement correlated temporally with the lipid infusion? Perhaps you could plot out the GCS vs time and note where the lipid was infused....just trying to be objective. Was there any other ECG alteration besides QRS? How about QT? See our paper in Ann Int Medicine this May.
Interesting case, but we'd love to know more.
Guy
Two main issues emerge in this report, effects of high lipid volumes and the patient's clinical course. First are the laboratory and clinical effects of high-dose lipid infusion. Laboratory results, particularly blood chemistries will unquestionably be thrown off by extremely lipemic serum, and I'm a bit surrprised there hasn't been more in the literature on this effect - it's certainly approachable in animal models. Anyone interested in doing these studies?? I wonder if you could have measured a hematocrit in this patient as an alternative to Hb concentration? I also wonder if ultracentrifuging the plasma then popping the lipid cap off would allow you to measure chemistries in the remaining plasma (we do this in the lab). The other concern of course has to do with the very large lipid load given this patient. The safety profile of acute lipid infusion isn't known. The typical doses administered to patients in cardiac arrest (bolus plus infusion) are on the order of 4mL/kg over 30 minutes. This would generally mean less much than a liter for an adult. I'm unsure where the maximal safe dose is, but wouldn't feel comfortable giving much more than a liter. Interesting to hear of Dr. Caves experience with cystitis and makes one wonder if that was the case here.
Second, I would echo Dr. Uncles query about the rate of resolution of GCS. Is it clear the improvement correlated temporally with the lipid infusion? Perhaps you could plot out the GCS vs time and note where the lipid was infused....just trying to be objective. Was there any other ECG alteration besides QRS? How about QT? See our paper in Ann Int Medicine this May.
Interesting case, but we'd love to know more.
Guy
June 2, 2009 |
[Guy Weinberg]
GCS deteriorated enroute to hospital, with GCS 3 on arrival. Patient was intubated and transfered to the ICU. QRS on arrival was 114ms Patient was tachycardic, but had a preserved blood pressure.
Intralipid was started 3 hours after arrival in hospital and 1 hour after arrival into the ICU. Patient was given 1.5ml/Kg of 20% intralipid bolus over 1 minute, followed by an infusion of 0.25ml/kg/min for the following 2 hours. Total dose received was 1900cc of 20% intralipid. QRS duration decreased to 100ms 4 hours after arrival and remained under 100ms during her brief stay in the ICU of 48 hours. She remained hemodynamically satble throughout her ICU stay.
Surpirisingly patient developed macroscopic hematuria 4-5 hours into her ICU stay. Attempts to verify her hemoglobin level even 24 hours after her intralipid infusion were not possible owing to the lipid content found in her arterial blood sample. Attempts to wash the sample with saline in the core lab did not resolve this issue. I'm not clear on whether this is an expected complication, but it may have hampered our efforts had her hematuria persisted beyond the first 12 hours of her hospitalization. Perhaps this remains a dosing problem.