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agement: we feel it is unnecessary, unhelpful and should be changed. M. Stott M. Davies Royal Liverpool & Broadgreen University Hospitals NHS Trust Liverpool, UK Email:
[email protected] No external funding and no competing interests declared. Previously posted at the Anaesthesia Correspondence website: http://www.anaesthesia correspondence.com.
Reference 1. Lu Y, Jiang H, Zhu YS. Airtraq laryngoscope versus conventional Macintosh laryngoscope: a systematic review and metaanalysis. Anaesthesia 2011; 66: 1160–7. doi: 10.1111/j.1365-2044.2012.07070.x
Care is never withdrawn I read with interest the editorial by Gordon and Hartle regarding the practicalities of donation after circulatory death (DCD) and the implications for anaesthetists [1]. The authors raise a number of questions related to re-intubation of the trachea during DCD, to reduce the risk of aspiration if lung donation is intended. Whilst I agree that the issues of who will perform this potentially time-critical and technically challenging task remain unresolved, I would suggest that they represent only a small barrier to successful organ transplantation. Data from NHS Blood and Transplant indicate that only 26 lung donations occurred after circulatory death during the year 01 ⁄ 04 ⁄ 2010– 31 ⁄ 03 ⁄ 2011 [2]. This compares with a total of 1010 deceased
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donors during this time period, of which 373 were DCD. Additionally, given that practices during withdrawal of treatment vary widely, it is uncertain how many of the 26 DCD lung donations required reintubation of their tracheas after confirmation of circulatory death. A greater barrier to higher rates of deceased donor transplantation is the high rate of family refusal for organ donation. In an analysis of potential deceased donors in UK intensive care units and emergency departments, 1043 families refused consent for organ donation during a 12-month period in 2010-2011, representing a 43% refusal rate [2]. Whilst the reasons for families’ refusal are numerous, one factor may be poor communication by those approaching the families [3, 4]. Unfortunately, Gordon and Hartle provide an example of potentially poor communication in their editorial; they use the expression ‘how care is withdrawn’. Whilst treatment and life-sustaining therapy are withdrawn and limited, care is never withdrawn [5]. Though the terms ‘treatment’, ‘therapy’ and ‘care’ are frequently used interchangeably, it is vital in all cases of end-of-life care, but particularly in the context of organ donation, that the care of the patient, and the perception of it by their families, continues following the withdrawal of treatment and during the donation process. Accordingly, I would caution care and sensitivity with regard to the terminology used when discussing limitation and withdrawal of treatment.
Anaesthesia ª 2012 The Association of Anaesthetists of Great Britain and Ireland
T. Husain Northwick Park Hospital London, UK Email:
[email protected]
References 1. Gordon AC, Hartle AJ. Donation after circulatory death – a new role for the anaesthetist? Anaesthesia 2011; 66: 761–4. 2. NHS Blood and Transplant. Transplant activity in the UK. Activity report 2010 ⁄ 11. http://www.uktransplant.org.uk/ukt/ statistics/transplant_activity_report/current_ activity_reports/ukt/activity_report_2010_ 11.pdf (accessed 04 ⁄ 12 ⁄ 2011). 3. Siminoff LA, Marshall HM, Dumenci L, Bowen G, Swaminathan A, Gordon N. Communicating effectively about donation: an educational intervention to increase consent to donation. Progress in Transplantation 2009; 19: 35–43. 4. Siminoff LA, Traino HM, Gordon N. Determinants of family consent to tissue donation. Journal of Trauma Injury, Infection and Critical Care 2010; 69: 956–63. 5. Faber-Langendoen K, Lanken PN. Dying patients in the intensive care unit: forgoing treatment, maintaining care. Annals of Internal Medicine 2000; 133: 886–93. doi: 10.1111/j.1365-2044.2012.07063.x
Logging the delivery of intravenous lipid emulsion for cocaine and other lipophilic drug overdoses We read with interest the case report by Jakkala-Saibaba and colleagues describing the successful treatment of cocaine overdose with lipid emulsion [1]. Theirs is a welcome contribution to the body of published reports [2], and raises some interesting discussion points. The authors initiated correction of the profound acidosis using intravenous bicarbonate and invasive ventilation. In doing so, it is likely they indirectly increased the capacity for lipid emulsion to bind cocaine, as an 437
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increase from pH less than 6.8 to 7.2 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 438
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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:
[email protected]
References 1. Jakkala-Saibaba R, Morgan PG, Morton GL. Treatment of cocaine overdose with lipid emulsion. Anaesthesia 2011; 66: 1168– 70. 2. Jamaty C, Bailey B, Larocque A, Notebaert E, Sanogo K, Chauny JM. Lipid emulsions in the treatment of acute poisoning: a systematic review of human and animal studies. Clinical Toxicology 2010; 48: 1–27. 3. Chemicalize. Physiochemical properties for Cocaine. http://www.chemicalize. org/structure/#!mol=CN1[C%40H]2CC [C%40%40H]1[C%40H]%28[C%40H]% 28C2%29OC%28%3DO%29c3ccccc3% 29C%28%3DO%29OC&source=fp (accessed 03 ⁄ 12 ⁄ 2011). 4. Samuels TL, Willers JW, Uncles DR, Monteiro R, Halloran C, Dai H. In vitro suppression of drug-induced methaemoglobin formation by Intralipid in whole human blood: observations relevant to the ‘lipid sink theory’. Anaesthesia 2011; 67: 23–32. 5. Uncles DR, Willers JW, Samuels TL, Papadopoulou A, Short S, Short G. Investigating the effect of ionisation on the behaviour of lipophilic drugs in an intravenous lipid emulsion in vitro. Anaesthesia 2011; 67: 197. 6. Hunter L, Gordge L, Dargan PI, Wood DM. Methaemoglobinaemia associated with the use of cocaine and volatile nitrites as recreational drugs: a review. British Journal of Clinical Pharmacology 2011; 72: 18–26. 7. Chakladar A, Willers JW, Pereskokova E, Beaumont PO, Uncles DR. White powder, blue patient: methaemoglobinaemia associated with benzocaine-adulterated cocaine. Resuscitation 2010; 81: 138–9. doi: 10.1111/j.1365-2044.2012.07097.x
Smartphones, Twitter and new learning opportunities at anaesthetic conferences Smartphones and their apps are extremely popular with anaesthetists [1]. Smartphones were originally
Anaesthesia ª 2012 The Association of Anaesthetists of Great Britain and Ireland
