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  1. Re:Acute cyanide poisoning from apricot kernels

    Dear Collegues,

    We were very glad to reply your letter posted online on the emj website in october, 6 2011. We read very carefully your concerns regarding the verifiability of cyanide as the poisoning agent. Certainly You can agree with us that, in a brief report with a fixed length, it is very difficult to give all the information and in some case you have to choose what you consider more important . In this case we thank you for giving us the opportunity to clarify some points that obviously were not so clear in the original paper.

    First of all, the patient was uncooperative but not unresponsive; so we asked her if she had effectively chewed and swallowed the apricot seeds and she confirmed it, enjoying the bittersweet taste. We also visualized many fragments of seeds on gastric lavage, so we were sure that she had masticated and swallowed the seeds.

    For your second objection, unfortunately we are not able to measure cyanide levels in our emergency department, so we consider the possibility that the metabolic acidosis with increased anion gap was due to an abnormal lactate production, as we can see in cyanide poisoning [1].

    Moreover the anamnesis of the patient was negative for inappropriate ingestion of drugs of any kind, and she confirmed to us that she did not ingest any other substance. She did not take medications at home and she has no access to medications of her parents. Finally, we reported that the patient was dyspnoic, hypotensive and she developed metabolic acidosis with increased anion gap [2].

    These symptoms, according with the anamnesis of recent ingestion of cyanide-releasing substance, suggested us the diagnosis of cyanide poisoning [3]. In addition the quick response of the patient to the antidotal therapy for cyanide poisoning indirectly confirm the cyanide intoxication.

    Thank you again and best regards

    Cigolini Davide, MD Ricci Giorgio, MD

    References

    [1] Beasley DM, Glass WI. Cyanide poisoning : phatophysiology and treatment reccomendations. Occup Med (Lond) 1998;48:427-31

    [2] Cigolini D, Ricci G, Zannoni M et al. Hydroxocobalamin treatment of acute cyanide poisoning from apricot kernels. Emerg Med J. Sep 2011;28(9):804-05

    [3] Vogel SN, Sultan TR, Ten Eyck RP. Cyanide poisoning. Clin Toxicol 1981;18:367-83

    Conflict of Interest:

    None declared

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  2. Acute cyanide poisoning from apricot kernels

    We congratulate Cigolini and colleagues on their case report of apparent cyanide poisoning from apricot kernels[1]. However, we have several concerns regarding the verifiability of cyanide as the poisoning agent. These concerns were not addressed in the case description or in a limitations section.

    First, while the patient was surrounded by apricot kernels, ingestion of the kernels was not verified visually (on lavage), on questioning of the patient, or radiographically. In addition, to release hydrogen cyanide, the kernels must be masticated, which was not described in the case[2,3].

    Second, cyanide exposure was not documented. A cyanide level was not reported. A lactate acidosis is common, but a serum lactate level was not reported after the patient became symptomatic, which would support a diagnosis of cyanide toxicity[4]. In addition, a "mentally ill" and "uncooperative" patient could have ingested almost any chemical, object, or medication (including her own, which were not mentioned). Confirmatory drug or chemical urine and blood testing with gas chromatography mass spectrometry or thin layer chromatography was not reported.

    Finally, cyanide toxic patients typically develop significant sedation, apnea, and lactic acidosis before developing hypotension5. None of these symptoms was reported. The patient's tachycardia and hypotension could have been from antipsychotic medications, tricyclic antidepressants, or dihydropyridine calcium channel blocker as from cyanide. Hydroxocobalamin increased the patient's blood pressure; however, with its nitric oxide scavenging effects, it increased blood pressure even in healthy volunteers.

    In summary, as written the case description does not confirm this patient was exposed to and intoxicated by cyanide.

    Vikhyat Bebarta, MD Shawn M. Varney, MD

    References

    1. Cigolini D, Ricci G, Zannoni M, et al. Hydroxocobalamin treatment of acute cyanide poisoning from apricot kernels. Emerg Med J. Sep 2011;28(9):804-805.

    2. Kerns W, Isom G, Kirk MK. Cyanide and Hydrogen Sulfide. In: Goldfrank LR, ed. Goldfrank's toxicologic emergencies. 7th ed ed. New York :: McGraw-Hill, Medical Pub. Division; 2002:1498-1510.

    3. Suchard JR, Wallace KL, Gerkin RD. Acute cyanide toxicity caused by apricot kernel ingestion. Ann Emerg Med. Dec 1998;32(6):742-744.

    4. Baud FJ, Borron SW, Megarbane B, et al. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med. 2002;30(9):2044-2050.

    5. Bebarta VS, Tanen DA, Lairet J, Dixon PS, Valtier S, Bush A. Hydroxocobalamin and sodium thiosulfate versus sodium nitrite and sodium thiosulfate in the treatment of acute cyanide toxicity in a swine (Sus scrofa) model. Ann Emerg Med. Apr 2010;55(4):345-351.

    Conflict of Interest:

    None declared

    Submit response
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