Recent rat studies show different tissue distributions of vitamin B12 (B12), administered orally as hydroxo-B12 (HO-B12) (predominant in food) and cyano-B12 (CN-B12) (common in supplements). Here we examine male Wistar rats kept on a low-B12 diet for 4 weeks followed by a 2-week period on diets with HO-B12 (n 9) or CN-B12 (n 9), or maintained on a low-B12 diet (n 9). Plasma B12 was analysed before, during and after the study. The content of B12 and its variants (HO-B12, glutathionyl-B12, CN-B12, 5'-deoxyadenosyl-B12 (ADO-B12), and methyl-B12 (CH3-B12)) were assessed in the tissues at the end of the study. A period of 4 weeks on the low-B12 diet reduced plasma B12 by 58 % (from median 1323 (range 602–1791) to 562 (range 267–865) pmol/l, n 27). After 2 weeks on a high-B12 diet (week 6 v. week 4), plasma B12 increased by 68 % (HO-B12) and 131 % (CN-B12). Total B12 in the tissues accumulated differently: HO-B12>CN-B12 (liver, spleen), HO-B12<CN-B12 (kidneys), and HO-B12≈CN-B12 (brain, heart). Notably, more than half of the administered CN-B12 remained in this form in the kidneys, whereas HO-B12 was largely converted to the bioactive ADO-B12. Only <10 % of the other cofactor, CH3-B12, were found in the tissues. In conclusion, dietary CN-B12 caused a higher increase in plasma and total kidney B12 but provided less than half of the active coenzymes in comparison to dietary HO-B12. These data argue that HO-B12 may provide a better tissue supply of B12 than CN-B12, thereby underscoring the lack of a direct relation between plasma B12 and tissue B12.

Enclosed-space smoke inhalation is the fifth most common cause of all unintentional injury deaths in the United States. Increasingly, cyanide has been recognized as a significant toxicant in many cases of smoke inhalation. However, it cannot be emergently verified. Failure to recognize the possibility of cyanide toxicity may result in inadequate treatment. Findings suggestive cyanide toxicity include: (1) a history of an enclosed-space fire scene in which smoke inhalation was likely; (2) the presence of oropharyngeal soot or carbonaceous expectorations; (3) any alteration of the level of consciousness, and particularly, otherwise inexplicable hypotension (systolic blood pressure ≤90 mmHg in adults). Prehospital studies have demonstrated the feasibility and safety of empiric treatment with hydroxocobalamin for patients with suspected smoke inhalation cyanide toxicity. Although United States Food and Drug Administration (FDA)-approved since 2006, the lack of efficacy data has stymied the routine use of this potentially lifesaving antidote. Based on a literature review and on-site observation of the Paris Fire Brigade, emergency management protocols to guide empiric and early hydroxocobalamin administration in smoke inhalation victims with high-risk presentations are proposed.

Effective management of cyanide poisoning from chemical terrorism, inhalation of fire smoke, and other causes constitutes a critical challenge for the pre-hospital care provider. The ability to meet the challenge of managing cyanide poisoning in the prehospital setting may be enhanced by the availability of the cyanide antidote hydroxocobalamin, currently under development for potential introduction in the United States. This paper discusses the causes, recognition, and management of acute cyanide poisoning in the prehospital setting with emphasis on the emerging profile of hydroxocobalamin, an antidote that may have a risk:benefit ratio suitable for empiric, out-of-hospital treatment of the range of causes of cyanide poisoning. If introduced in the US, hydroxocobalamin may enhance the role of the US prehospital responder in providing emergency care in a cyanide incident.