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Correspondence key clinical effects after smoke inhalation, or demonstrate that smoke constituents, such as methemoglobin-inducing NO2, mitigate the effects of cyanide.5,6 Moreover, animal models of smoke inhalation, with their tightly controlled environments and limited smoke composition, are poor comparisons to real-life human exposures, in which a complex array of factors contribute. Any number of toxins, hydrogen sulfide being one, could play a critical, even more important, role than cyanide, but may go unstudied or unrecognized in the laboratory. So, while animal data suggest that cyanide could contribute to adverse effects in certain clinical settings, they do not prove that it actually does in most cases. Borron and Baud dismiss the apparent underreporting of skin discoloration in their study by noting that this particular adverse event was simply “not queried for” in the case report forms.4 But this is precisely my concern, because it suggests a significant and more systemic methodological limitation to the safety data collection in their trial. Were only those events which could be predicted and “queried for” on forms actually collected? What other adverse events, especially potentially serious events, might have been overlooked or simply discounted as related to the underlying poisoning? Without rigorous and unsolicited reporting of all adverse events in a trial, we should be cautious about extrapolating the safety information. Lastly, and most importantly, the comments by Borron and Baud ignore the main point of my editorial, which was to argue that there is, as yet, insufficient evidence to demonstrate either the safety or clinical efficacy of hydroxocobalamin when administered in the post-inhalational exposure setting (keeping in mind that cyanide is rapidly absorbed and distributed, and essentially acts immediately). Is hydroxocobalamin simply a costly placebo in this setting, or worse, a drug with unintended adverse consequences? The published animal data using intravenous single-agent cyanide, and limited human data with historical controls are, in my view, inadequate to make this assessment. Until rigorous, well-controlled clinical data is published, I believe emergency physicians and their patients would be best served by limiting the administration of hydroxocobalamin only to the most severely affected patients, in whom potential risks are (hopefully) more likely to be outweighed by a potential for benefit. Andrew R. Erdman, MD Genentech Pharmaceutical San Francisco, California doi:10.1016/j.annemergmed.2007.08.025

Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article, that might create any potential conflict of interest. The author has stated that no such relationships exist. See the Manuscript Submission Agreement in this issue for examples of specific conflicts covered by this statement. 1. Gill JR, Goldfeder LB, Stajic M. The happy land homicides: 87 deaths due to smoke inhalation. J Forensic Sci. 2003;48:161-163.

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2. Barillo DJ, Goode R, Esch V. Cyanide poisoning in victims of fire: analysis of 364 cases and review of the literature. J Burn Care Rehabil. 1994;15:46-57. 3. Erdman AR. Is hydroxocobalamin safe and effective for smoke inhalation? Searching for guidance in the haze. Ann Emerg Med. 2007;49:814-816. 4. Borron SW, Baud FJ, Barriot P, et al. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med. 2007;49:794-801. 5. Chaturvedi AK, Sanders DC, Endecott BR, et al. Exposures to carbon monoxide, hydrogen cyanide and their mixtures: interrelationship between gas exposure concentration, time to incapacitation, carboxyhemoglobin and blood cyanide in rats. J Appl Toxicol. 1995;15:357-63. 6. Levin BC. New research avenues in toxicology: 7-gas N-Gas Model, toxicant suppressants, and genetic toxicology. Toxicology. 1996;115:89-106.

Propofol-Induced Movement Disorders To the Editor: In the August 2007 issue of Annals, Miner and Burton ably present a clinical practice advisory for the use of propofol in the emergency department (ED).1 They cover many aspects of propofol use, including potential adverse effects, and suggest future research ideas. I compliment the authors for their work on this important topic but would like to mention that movement disorders (eg, dystonia) are another, though uncommon, adverse effect associated with propofol. I was recently reminded of this after witnessing propofolinduced dystonia in an animal “model.” My dog received 10mg/kg of propofol intramuscularly and then intubated for a procedure. During recovery he developed significant (disconjugate!) opsoclonus, torticollis and myoclonus (including repeated extension and deviation of his tongue). The veterinary staff reported seeing this “sometimes” in animals recovering from propofol, but that Wilson’s case was “impressive.” This experience compelled me to review the human literature. Propofol has been implicated in causing movement disorders for 20 years.2-6 Others have reported movement disorders or agitation after administering propofol with other medications.7-13 Typically these effects are encountered in “unique” scenarios and outside of the ED (ie, at higher doses used for generalized anesthesia, in patients with underlying movement disorders or during specialized procedures).14 The mechanism for these movement disorders has not been identified but may involve the rapid change in the cerebral concentration of propofol.15,16 Interestingly, propofol has also been used to treat refractory movement disorders (ie, seizures and dystonia).17,18 Propofol’s ability to both cause and treat movement disorders suggests a complex, central-mediated effect and remains an area for future research. Daniel E. Brooks, MD Banner Poison Center Department of Medical Toxicology Banner Samaritan Regional Medical Center Annals of Emergency Medicine 111

Correspondence Phoenix, AZ doi:10.1016/j.annemergmed.2007.08.023

Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article, that might create any potential conflict of interest. The author has stated that no such relationships exist. See the Manuscript Submission Agreement in this issue for examples of specific conflicts covered by this statement. 1. Miner JR, Burton JH. Clinical practice advisory: emergency department procedural sedation with propofol. Ann Emerg Med. 2007;50:182-187. 2. Dingwall AE. Oculogyric crisis after day case anaesthesia. Anaesth. 1987;42:565. 3. Cameron AE. Opisthotonos again. Anaesth. 1987;42:1124. 4. Bendiksen A, Larsen LM. Convulsions ataxia and hallucinations following propofol. Acta Anaesth Scand. 1998;42:739-741. 5. Zabani I, Vaghadia H. Refractory dystonia during propofol anaesthesia in a patient with torticollis-dystonia disorder. Can J Anaesth. 1996;43:1062-1064. 6. Stark RD, Binks SM, Dutka VN, et al. A review of the safety and tolerance of propofol (diprivan). Postgrad Med J. 1985;61(Suppl 3):152-156. 7. Asai T, Eguchi Y, Shingu K. Masseter spasm during induction of anaesthesia using propofol and fentanyl. Eur J Anaesthsiol. 1998; 15:614-615.

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8. Bragonier R, Bartle D, Langton-Hewer S. Acute dystonia in a 14-yrold following propofol and fentanyl anaesthesia. Br J Anaesth. 2000;84:828-829. 9. Schramm BM, Orser BA. Dystonic reaction to propofol attenuated by benztropine (cogentin). Anesth Analg. 2002;94: 1237-1240. 10. Snow KA, Clements EA, Eppert AJ, et al. Antimuscarinic syndrome after propofol administration in the emergency department. J Emerg Med. 2007;33:29-32. 11. Steele RG, Ajayoglu B. Novel management of propofol induced dystonia in the post anaesthesia care unit. Anaesth Intensive Care. 2007;35:138. 12. McManus KF. Convulsion after propofol/enflurane. Anaesth Intensive Care. 1992;20:245. 13. Collier C, Kelly K. Propofol and convulsions – the evidence mounts. Anaesth Intensive Care. 1991;19:573-575. 14. Mikuni N, Takayama M, Satow T, et al. Evaluation of adverse effects in intracarotid propofol injection for wada test. Neurology. 2005;65:1813-1816. 15. Walder B, Tramer MR, Seeck M. Seizure-like phenomena and propofol: a systematic review. Neurology. 2002;58:13271332. 16. Steigerwald F, Hinz L, Pinsker MO, et al. Effects of propofol anesthesia on pallidal neuronal discharges in generalized dystonia. Neurosci Lett. 2005;386:156-159. 17. Teive HA, Munhoz RP, Souza MM, et al. Status dystonicus: study of five cases. Arq Neuropsiquiatr. 2005;63:26-29. 18. Rossetti AO, Reichhart MD, Schaller MD, et al. Propofol treatment of refractory status epilepticus: a study of 31 episodes. Epilepsia. 2004;45:757-763.

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