RT Journal Article
SR Electronic
T1 Cyanide: an unreported cause of neurological complications following smoke inhalation
JF BMJ Case Reports
FD BMJ Publishing Group Ltd
SP bcr0920114881
DO 10.1136/bcr.09.2011.4881
VO 2011
A1 Frédéric Baud
A1 Monique Boukobza
A1 Stephen W Borron
YR 2011
UL http://casereports.bmj.com/content/2011/bcr.09.2011.4881.abstract
AB Although the combustion of natural and synthetic products can yield cyanide, its toxic role in residential fires is unclear. This case concerns a woman aged over 50 years who presented comatose, pulseless and apnoeic after a domestic fire. Cardiopulmonary resuscitation and on-site administration of 2.5 g hydroxocobalamin as an antidote to cyanide resulted in a return of spontaneous circulation. On admission to the intensive care unit, the patient was treated with hyperbaric oxygen for suspected carbon monoxide poisoning. In a blood specimen collected at the scene before hydroxocobalamin administration, blood cyanide and carbon monoxide levels were 68 µmol/l and 10.9%. On admission to hospital, plasma lactate was at 4.6 mmol/l. Brain scans revealed lesions which were confirmed 2 months later, consistent with the haemorrhagic necrosis often seen after poisoning by cyanide. These data suggest that smoke inhalation in a residential fire may cause cyanide poisoning. This case provides clinical, biological, analytical and brain imaging data supporting the hypothesis of the toxic role of smoke-induced cyanide poisoning which may result in neurological sequelae.