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renders it approximately three times more lipid soluble [3]. Drug lipid solubilities, expressed as their log P values, have been used to determine the ability of lipid emulsion to suppress the toxic effects of nitrates in vitro [4]. Log P values are determined when the drug is presented as the unionised species. However, when pH values outside the normal physiological range are considered, expression of lipid solubility by its log D value at a specified pH may be more appropriate, as this takes into account both the ionised and unionised species [5]. Therefore, log D values may be a more precise measure of lipid solubility for guiding clinical treatment using lipid emulsion. In this case, at pH 6.8 and pH 7.2 the log D values would have been more appropriate, with distribution coefficient values approximating 0.3 and 0.9, respectively (implying that cocaine is more lipid soluble at pH 7.2) [3]. Secondly, street cocaine in the UK may contain adulterants, such as the local anaesthetic benzocaine. This replicates the numbing effect of cocaine and gives the user a false assurance of quality [6]. Several case reports have described cocaine-associated methaemoglobinaemia, not directly attributable to cocaine or its metabolites, but rather due to benzocaine [7]. However, in this case the patient is known to have possessed a normal methaemoglobin concentration of 1.5% as determined by cooximetry (personal communication from authors). Nevertheless, benzocaine is unionised throughout the pH range 6–8 and hence possesses identical log P and log D values (both 1.50) [3]. This implies that a patient’s acidaemia would not affect the lipid solubility of benzocaine. Thus, bearing in mind that benzocaine may complicate cocaine overdose, the lipid sink effect would be sustained (in contrast to cocaine) at the low pH values described (< 6.8). Therefore, it is important to note that lipid emulsion may reduce the amount of methaemoglobin formed through sequestering benzocaine and contribute further to the improvement in a patients’ clinical condition even without correction of acidaemia. Finally, the authors should be commended on their implementation of well-recognised and established interventions in the treatment of a lipophilic drug overdose. There is an increasing need to determine which lipophilic drug toxidromes are amenable to treatment with lipid emulsion, since many overdoses include combinations of lipid soluble and ⁄ or insoluble drugs. Lipid emulsion is fast becoming a useful adjunct in the treatment of lipophilic drug toxicity, and we endorse the authors regarding its use in the treatment of cocaine overdose with life-threatening cardiovascular arrhythmias and collapse. Recognising the requirement to treat acidaemia and awareness of other drugs that could potentially be present in a cocaine overdose will further improve the appropriateness of lipid emulsion for this clinical scenario. We would encourage clinicians who have deployed intravenous lipid emulsions for treatment of lipid soluble drug toxidromes to report their cases to the Lipid Registry (http://www.lipidregistry.org) and consider posting their experiences on the Lipid Rescue website (http:// www.lipidrescue.org). T. L. Samuels A. Papadopoulou J. W. Willers D. R. Uncles Worthing Hospital Worthing, UK Email: dr.tsamuels@gmail.com