Second case of the use of intravenous fat emulsion therapy for propafenone toxicity

To the Editor:

We read the case of “Intravenous fat emulsion therapy for intentional propafenone intoxication” in the recent edition of Clinical Toxicology (2011; 49:701) with great interest.¹ We also had a case of propafenone intoxication who had resolution of his dysrhythmia associated with administration of intravenous fat emulsion (IFE).

A 59-year-old male with a history of atrial fibrillation, hypertension and hypercholesterolemia, presented 2 and 1/2 hours after a reported ingestion of 30 tablets of dabigatrin (150 mg), 6 tablets of sildenafil (100 mg), and an unknown dose of enalapril. His home medications also included propafenone and pravastatin. The patient presented pale, diaphoretic, somnolent with BP: 60/40 mmHg, HR: 65 bpm and the following EKG (Fig. 1) with QRS = 180 msec:

Fig. 1. EKG illustrating evidence of sodium channel blockade.

The patient continued to have deterioration in mental status, was subsequently intubated and received a total of 450 meq of sodium bicarbonate for QRS prolongation that was presumed to be from propafanone ingestion. He was also given 3 liters IVF and started on dopamine, norepinephrine, and epinephrine. Though his BP improved to 140/80 mmHg and HR decreased to 80 bpm with intravenous fluids and also high dose dopamine, norepinephrine, and epinephrine, his QRS remained at 180 msec after 450 meq of sodium bicarbonate. The patient subsequently received another 300 meq of sodium bicarbonate with no change in his QRS. Because of persistent evidence of sodium channel blockade, the patient was given 100 ml bolus of IFE 20% followed by a continuous infusion of 1050 ml/hour for 30 minutes. Within one hour of the start of the infusion, the QRS duration improved to 110 msec; norepinephrine and epinephrine were titrated off and only dopamine at 5 mcg/kg/min was left. By hospital day(HD) #2, the patient was off all pressors. He was extubated on HD #4 but had to be reintubated secondary to respiratory distress and pneumonia. The patient was unable to be weaned off the ventilator during his hospital stay, received a tracheostomy on HD #17 and was transferred to a rehabilitation facility.

We recognize that this case is limited by the lack of an explicit history of exposure and our inability to obtain serum propafanone concentrations. While we cannot absolutely document exposure to propafanone or exclude occult ingestion of another sodium channel antagonist, the presentation is highly suggestive of propafanone toxicity in a suicidal patient who had access to propafanone and not consistent with the reported ingestion of dabigatrin, sildenafil, and enalapril. The use of sodium bicarbonate, as administered in our case, has been proposed treatment for propafenone toxicity.² The temporal trend of his QRS shortening is consistent with reversal of propafanone cardiotoxicity by IFE. While we cannot exclude that the resolution was natural course of his disease, his lack of response to high doses of sodium bicarbonate suggest that he was severely toxic at the time of treatment. Propafanone is a highly lipid soluble sodium channel antagonist, and lipid infusion has been shown to reverse cardiotoxicity of other medications with increased lipophilicity.^3–6 Based on these animal experiments, the experience of Ten Tusscher et al. and our experience, we believe IFE is a reasonable rescue therapy for propafanone cardiotoxicity that does not respond to standard therapy.

Declaration of Interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this paper.