Cyanide: an unreported cause of neurological complications following smoke inhalation

Abstract

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.

Figure 1

Serial non-contrast enhanced CT and MRI. (a) Day 2 after exposure. CT scan does not reveal any abnormality. Note cortical atrophy and ventricle enlargement. (b) – Day 7 after exposure. Axial T1 MR image reveals symmetrical sharply delimited and homogeneous hypointense lesions in the two putamini (long arrow), globi pallidi (short arrow) and caudate nuclei. (c) – Day 7 after exposure. Axial T2 MR image, at the same level, shows multiple punctuate foci of hyperintense signal in the same areas, most prominent on the antero-lateral part of the putamini (arrow). Note that (as on T1), especially on the right side, the globus pallidus interna and the globus pallidus externa are visualised as distinct structures, separated by a more hypointense zone. Cortical atrophy, ventricle enlargement and paraventricular and subcortical white matter patchy areas of hyperintensity are visible bilaterally. (d) – Day 17 after exposure. CT scan shows well-defined bilateral hyperdensity in the putamini, and at the posterior part of globus pallidi, (arrow), consistent with haemorrhage necrosis. Note more prominent cortical atrophy and ventricle enlargement. (e) – Day 60 after exposure. Axial T1 MR image reveals bilateral, homogeneous hypersignal intensity of both putamini (white arrow) and globi pallidi (black arrow).