The Poison Review

Diltiazem poisoning treated with hyperinsulinemic euglycemic therapy and intravenous lipid emulsion. Montiel V et al.  Eur J Emerg Med2010 Nov 17 [Epub ahead of print]

Abstract

A consistent feature of severe calcium channel blocker (CCB) toxicity is insulin resistance.  It is typical to see these patients present with elevated serum glucose levels which remained high even after treatment with high dose insulin.  Some research has suggested that serum glucose levels correlate with the severity of CCB poisoning. There has also been other research suggesting that intravenous lipid emulsion (ILE) therapy may improve clinical outcomes in overdose of lipophilic CCBs such as verapamil or diltiazem.

This interesting but inconclusive case report from Belgium describes an 18-year-old 50-kg woman who presented to hospital 8 hours after ingesting 3600 mg of sustained-release diltiazem.  On admission blood glucose level was 274 mg/dl and diltiazem level 7893 ng/ml (therapeutic 40-160 ng/ml).  She developed respiratory failure requiring mechanical ventilation and persistent hypotension, and was treated with hyperinsulinemia euglycemia therapy (HIE)  11 hours after admission (19 hours after ingestion).  Three hours later no significant hemodynamic improvement was noted. The blood glucose level had remained stable despite minimal supplementation.  At that point ILE was administered. Within one hour, the glucose level began to decrese at an accelerated rate and insulin infusion was tapered and discontinued.

One possible interpretaton of this narrative is that ILE provided a lipid sink, pulling diltiazem out of tissues and thus decreasing its toxic effects.   However, there was so much going on in this case and so many other treatment modalities were administered that it is impossible to draw any strong conclusions.  I agree with the  authors that the clinical course might have been different if HIE had been started earlier and/or using higher doses of insulin. 

Actually, a close inspection of figure 1 in the paper makes the e  the ILE on the glucose level less impressive than does the author’s narrative.  Although the glucose level had begun to fall long before ILE was administered, it does appear that the rate of decrease accelerated somewhat after ILE. An interesting observation, but no more.