Lipid rescue therapy for local anesthetic toxicity: is less more

2.5 out of 5 stars

Adverse events associated with a large dose of intravenous lipid emulsion for suspected local anesthetic toxicity. Corwin DJ et al. Clin Toxicol 2017 Jul;55:603-7.

Abstract

The key word in the title of this case report is “associated” — a.though the authors do not emphasize the point, it’s not at all clear that all of the adverse events described were actually caused by the IV lipid emulsion. Nonetheless, there are some important take-home lessons here.

CASE: An 11-year-old girl presented to hospital with confusion and somnolence 15 minutes after receiving local anesthesia with 54 mg mepivacaine for a dental procedure. She had facial twitching and 2 brief episodes of possible seizure activity that resolved spontaneously.

The local poison center was contacted and recommended that lipid emulsion therapy be given to treat local anesthetic toxicity:

The suggested dosing [20%] was to be given in three 1 mL/kg boluses spaced every five minutes, followed by an infusion of 0.25 mL/kg/min for one hour if symptoms persisted.

After the 3 bolus doses were given, the patient continued to have self-limited episodes of unresponsiveness and abnormal muscular activity, lasting seconds each. The 1-hour infusion dose was started. After transfer, the receiving hospital continued the infusion at 0.25 mL/kg/hr for an additional 4 hours. The reported total 20% lipid dose was 3670 mL (66 mL/kg) over 7 hours.

Neurological symptoms continued overnight after lipid infusion was stopped. Head CT was unremarkable; MRI showed enhanced signal in the dural venous sinuses, consisted with elevated serum lipid levels. EEG was consistent with presence of sedating medications but did not show seizure activity.

Not surprisingly, the patient’s serum was lipemic and her triglyceride level markedly elevated. Although she had episodes of tachycardia and tachypnea, workup did not reveal evidence of ARDS or fat emboli. Lipemia interfered with some laboratory tests.

On discharge after 3 days in hospital,  the patient’s neurological exam and laboratory results were normal.

DISCUSSION: Most of the “adverse events” associated with lipid rescue therapy have occurred after administration of relatively high doses. Although there have been no good studies demonstrating the maximum “safe” dose of intralipid for lipid rescue therapy, many authors recommended limiting the dose to that recommended by the FDA for nutritional support: 12.5 mL/kg (lean body mass) per day total. In specific cases it may be reasonable to consider extending the infusion beyond this, but such situations are likely rare. In this patient, who did not appear to have cardiovascular instability, it is not clear if the high dose administered was the result of careful consideration or lack of attention to total dose received as the patient was transferred and treated at a new hospital.

By the way, if the reader goes by Figure 1 in the paper, the total dose received would have been not 66 mL/kg but approximately 110 mL/kg. the authors do not explain the discrepancy.

To read my recent Emergency Medicine News column on lipid rescue therapy, click here.

Related posts:

Effect of lipid rescue therapy on laboratory tests

Excellent review of lipid rescue therapy

Lipid rescue therapy can interfere with critical lab values

 

 

Lipid rescue therapy for local anesthetic toxicity: is less more

2.5 out of 5 stars

Adverse events associated with a large dose of intravenous lipid emulsion for suspected local anesthetic toxicity. Corwin DJ et al. Clin Toxicol 2017 Jul;55:603-7.

Abstract

The key word in the title of this case report is “associated” — a.though the authors do not emphasize the point, it’s not at all clear that all of the adverse events described were actually caused by the IV lipid emulsion. Nonetheless, there are some important take-home lessons here.

CASE: An 11-year-old girl presented to hospital with confusion and somnolence 15 minutes after receiving local anesthesia with 54 mg mepivacaine for a dental procedure. She had facial twitching and 2 brief episodes of possible seizure activity that resolved spontaneously.

The local poison center was contacted and recommended that lipid emulsion therapy be given to treat local anesthetic toxicity:

The suggested dosing [20%] was to be given in three 1 mL/kg boluses spaced every five minutes, followed by an infusion of 0.25 mL/kg/min for one hour if symptoms persisted.

After the 3 bolus doses were given, the patient continued to have self-limited episodes of unresponsiveness and abnormal muscular activity, lasting seconds each. The 1-hour infusion dose was started. After transfer, the receiving hospital continued the infusion at 0.25 mL/kg/hr for an additional 4 hours. The reported total 20% lipid dose was 3670 mL (66 mL/kg) over 7 hours.

Neurological symptoms continued overnight after lipid infusion was stopped. Head CT was unremarkable; MRI showed enhanced signal in the dural venous sinuses, consisted with elevated serum lipid levels. EEG was consistent with presence of sedating medications but did not show seizure activity.

Not surprisingly, the patient’s serum was lipemic and her triglyceride level markedly elevated. Although she had episodes of tachycardia and tachypnea, workup did not reveal evidence of ARDS or fat emboli. Lipemia interfered with some laboratory tests.

On discharge after 3 days in hospital,  the patient’s neurological exam and laboratory results were normal.

DISCUSSION: Most of the “adverse events” associated with lipid rescue therapy have occurred after administration of relatively high doses. Although there have been no good studies demonstrating the maximum “safe” dose of intralipid for lipid rescue therapy, many authors recommended limiting the dose to that recommended by the FDA for nutritional support: 12.5 mL/kg (lean body mass) per day total. In specific cases it may be reasonable to consider extending the infusion beyond this, but such situations are likely rare. In this patient, who did not appear to have cardiovascular instability, it is not clear if the high dose administered was the result of careful consideration or lack of attention to total dose received as the patient was transferred and treated at a new hospital.

By the way, if the reader goes by Figure 1 in the paper, the total dose received would have been not 66 mL/kg but approximately 110 mL/kg. the authors do not explain the discrepancy.

To read my recent Emergency Medicine News column on lipid rescue therapy, click here.

Related posts:

Effect of lipid rescue therapy on laboratory tests

Excellent review of lipid rescue therapy

Lipid rescue therapy can interfere with critical lab values

 

 

Hemodialysis and the intubated salicylate-toxic patient

3.5 out of 5 stars

The association of hemodialysis and survival in intubated salicylate-poisoned patients. McCabe DJ, Lu JJ. Am J Emerg Med 2017 Apr 10 [Epub ahead of print]

Abstract

[Disclosure: the co-authors of this paper are members of the Toxikon Consortium in Chicago, as am I.]

This retrospective observational study looked at cases from the Illinois Poison Center over 12 years (2003 thru 2015) to identify intubated patients with recorded serum salicylate levels > 50 mg/dL. The goal was “to describe the impact of hemodialysis on survival rates of salicylate-intoxicated patients . . .”

The authors identified 64 patients. Eight patients were excluded because of “clear lack of association [of intubation] with salicylate intoxication.” The remaining 56 patients were analyzed. Of the 31 patients who received hemodialysis, 4 (13%) died; of the 25 patients who did not receive HD, 11 ( 44%) died. No patient required intubation after hemodialysis was initiated.

The authors’ conclusion: “In salicylate-poisoned patients who required mechanical ventilation emergent hemodialysis is associated with a mortality benefit.” They suggest that it is reasonable to recommend prompt hemodialysis for all intubated salicylate overdose patients.

We’ve discussed previously the problems inherent in analyzing computerized poison center data, including lack of complete clinical data, inability to establish causation rather than mere association, and the presence of multiple confounders,  The authors are aware of and discuss these limitations.

It seems to me the overall conclusion is generally one of common sense, but a tad overly broad. The phrase “salicylate-poisoned patients” is somewhat ambiguous especially if potential co-ingestions complicate the clinical picture. The authors most likely limited their analysis to patients with salicylate levels > 50 mg/dL to be as confident as possible that intubation was required because of complications of salicylate toxicity such as respiratory failure, acidosis, ARDS, and decreased mental status. I agree that in any case when the clinician decides salicylate toxicity is the sole or major factor leading to intubation, arrangements should be made for hemodialysis. If the clinicians decides that hemodialysis is not needed, or that intubation was due to effects of co-ingestant(s) or some other cause, the thinking behind that decision should be carefully documented.
Related post:

Recommendations for starting hemodialysis in salicylate toxicity