Effect of hyperbaric oxygen therapy on whole blood cyanide concentrations in carbon monoxide intoxicated patients from fire accidents

Pia Lawson-Smith, Erik C Jansen, Linda Hilsted, Ole Hyldegaard, Pia Lawson-Smith, Erik C Jansen, Linda Hilsted, Ole Hyldegaard

Abstract

Background: Hydrogen cyanide (HCN) and carbon monoxide (CO) may be important components of smoke from fire accidents. Accordingly, patients admitted to hospital from fire accidents may have been exposed to both HCN and CO. Cyanide (CN) intoxication results in cytotoxic hypoxia leading to organ dysfunction and possibly death. While several reports support the use of hyperbaric oxygen therapy (HBO) for the treatment of severe CO poisoning, limited data exist on the effect of HBO during CN poisoning. HBO increases the elimination rate of CO haemoglobin in proportion to the increased oxygen partial pressure and animal experiments have shown that in rats exposed to CN intoxication, HBO can increase the concentration of CN in whole blood.

Objective: The purpose of the present study was to determine whole blood CN concentrations in fire victims before and after HBO treatment.

Materials and methods: The patients included were those admitted to the hospital because of CO intoxication, either as fire victims with smoke inhalation injuries or from other exposures to CO. In thirty-seven of these patients we measured CN concentrations in blood samples, using a Conway/microdiffusion technique, before and after HBO. The blood samples consisted of the remaining 2 mL from the arterial blood gas analysis. CN concentration in blood from fire victims was compared to 12 patients from non-fire accidents but otherwise also exposed to CO intoxication.

Results: The mean WB-CN concentration before patients received HBO did not differ significantly between the two groups of patients (p = 0.42). The difference between WB-CN before and after HBO did not differ significantly between the two groups of patients (p = 0.7). Lactate in plasma before and after did not differ significantly between the two groups of patients. Twelve of the 25 fire patients and one of the non-fire patients had been given a dose of hydroxycobalamin before HBO.

Discussion and conclusion: CN concentrations in blood from patients admitted to hospital with CO intoxication and smoke inhalation exposure did not differ significantly from controls. Accordingly, we were not able to detect any changes in CN concentrations in blood after treatment with HBO.

Trial registration: ClinicalTrials.gov identifier: NCT00280579.

References

    1. Alarie Y. Toxicity of fire smoke. Crit Rev Toxicol. 2002;32:259–289. doi: 10.1080/20024091064246.
    1. Eckstein M, Maniscalco PM. Focus on smoke inhalation--the most common cause of acute cyanide poisoning. Prehosp Disaster Med. 2006;21:s49–s55.
    1. Jones J, McMullen MJ, Dougherty J. Toxic smoke inhalation: cyanide poisoning in fire victims. Am J Emerg Med. 1987;5:317–321. doi: 10.1016/0735-6757(87)90360-3.
    1. Baud FJ, Barriot P, Toffis V, Riou B, Vicaut E, Lecarpentier Y, Bourdon R, Astier A, Bismuth C. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991;325:1761–1766.
    1. Walsh DW. Hydrogen cyanide in fire smoke:an unrecognized threat to the american firefighter. Smoke, perceptions, myths, and misunderstandings. 2008. pp. 4–8.
    1. Ikegaya H, Iwase H, Hatanaka K, Sakurada K, Yoshida K, Takatori T. Diagnosis of cyanide intoxication by measurement of cytochrome c oxidase activity. Toxicol Lett. 2001;119:117–123. doi: 10.1016/S0378-4274(00)00297-6.
    1. Gorman DF, Clayton D, Gilligan JE, Webb RK. A longitudinal study of 100 consecutive admissions for carbon monoxide poisoning to the Royal Adelaide Hospital. Anaesth Intensive Care. 1992;20:311–316.
    1. Raphael JC, Elkharrat D, Jars-Guincestre MC, Chastang C, Chasles V, Vercken JB, Gajdos P. Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet. 1989;2:414–419. doi: 10.1016/S0140-6736(89)90592-8.
    1. Weaver LK. Carbon monoxide poisoning. Crit Care Clin. 1999;15:297–317. doi: 10.1016/S0749-0704(05)70056-7. viii.
    1. Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002;347:1057–1067. doi: 10.1056/NEJMoa013121.
    1. Baud FJ. Cyanide: critical issues in diagnosis and treatment. Hum Exp Toxicol. 2007;26:191–201. doi: 10.1177/0960327107070566.
    1. Borron SW, Baud FJ, Megarbane B, Bismuth C. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Am J Emerg Med. 2007;25:551–558. doi: 10.1016/j.ajem.2006.10.010.
    1. Hall AH, Rumack BH. Hydroxycobalamin/sodium thiosulfate as a cyanide antidote. J Emerg Med. 1987;5:115–121. doi: 10.1016/0736-4679(87)90074-6.
    1. Megarbane B, Delahaye A, Goldgran-Toledano D, Baud FJ. Antidotal treatment of cyanide poisoning. J Chin Med Assoc. 2003;66:193–203.
    1. Astier A, Baud FJ. Complexation of intracellular cyanide by hydroxocobalamin using a human cellular model. Hum Exp Toxicol. 1996;15:19–25. doi: 10.1177/096032719601500104.
    1. Hall AH, Rumack BH. Clinical toxicology of cyanide. Ann Emerg Med. 1986;15:1067–1074. doi: 10.1016/S0196-0644(86)80131-7.
    1. Thom SR, Keim LW. Carbon monoxide poisoning: a review epidemiology, pathophysiology, clinical findings, and treatment options including hyperbaric oxygen therapy. J Toxicol Clin Toxicol. 1989;27:141–156. doi: 10.3109/15563658909038578.
    1. Way JL, End E, Sheehy MH, De MP, Feitknecht UF, Bachand R, Gibbon SL, Burrows GE. Effect of oxygen on cyanide intoxication. IV. Hyperbaric oxygen. Toxicol Appl Pharmacol. 1972;22:415–421. doi: 10.1016/0041-008X(72)90247-5.
    1. Gill AL, Bell CN. Hyperbaric oxygen: its uses, mechanisms of action and outcomes. QJM. 2004;97:385–395. doi: 10.1093/qjmed/hch074.
    1. Lawson-Smith P. Treatment of Cyanide Poisoning with HBO. UHMS. 2008;35:303–304.
    1. Laforge M, Buneaux F, Houeto P, Bourgeois F, Bourdon R, Levillain P. A rapid spectrophotometric blood cyanide determination applicable to emergency toxicology. J Anal Toxicol. 1994;18:173–175.
    1. Meyhoff CS. Rapid detection of blood cyanide concentration in victims of smoke inhalation. Rune Frandsen AHJLHaECJ. 2008;107:A1974. Anesthesiology 2007.
    1. Schulz V. Clinical pharmacokinetics of nitroprusside, cyanide, thiosulphate and thiocyanate. Clin Pharmacokinet. 1984;9:239–251. doi: 10.2165/00003088-198409030-00005.
    1. Baud FJ, Borron SW, Megarbane B, Trout H, Lapostolle F, Vicaut E, Debray M, Bismuth C. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med. 2002;30:2044–2050. doi: 10.1097/00003246-200209000-00015.
    1. Kales SN, Christiani DC. Acute chemical emergencies. N Engl J Med. 2004;350:800–808. doi: 10.1056/NEJMra030370.
    1. Williams HL, Johnson DJ, McNeil JS, Wright DG. Studies of cobalamin as a vehicle for the renal excretion of cyanide anion. J Lab Clin Med. 1990;116:37–44.
    1. Rachinger J, Fellner FA, Stieglbauer K, Trenkler J. MR changes after acute cyanide intoxication. AJNR Am J Neuroradiol. 2002;23:1398–1401.
    1. Rosenow F, Herholz K, Lanfermann H, Weuthen G, Ebner R, Kessler J, Ghaemi M, Heiss WD. Neurological sequelae of cyanide intoxication--the patterns of clinical, magnetic resonance imaging, and positron emission tomography findings. Ann Neurol. 1995;38:825–828. doi: 10.1002/ana.410380518.

Source: PubMed

Sponsorer og samarbeidspartnere

Medisinsk tilstand

Legemiddelintervensjoner

3
Abonnere