Delayed neurological sequelae in carbon monoxide poisoning – a case report and present state of knowledge

Dariusz Kotlęga, Barbara Peda, Monika Gołąb-Janowska, Przemysław Nowacki


Introduction: Carbon monoxide (CO) is one of the most common causes of fatal gas poisoning through the airways mainly due to central heating faults. Carbon monoxide inhibits oxygen transport by binding to haemoglobin and the formation of carboxyhaemoglobin. The neuropsychological symptoms of poisoning are defined as delayed neurological sequelae and usually occur after a lucid interval.

Case report: We present a patient with neurological symptoms that occurred 27 days after acute poisoning that had been treated with the use of hyperbaric oxygen therapy. On examination the patient was in a mutism-like state, had severe cognitive disorders, hypomimia, bilateral limb stiffness, increased deep tendon reflexes, bilateral Babinski sign and sphincter incontinence. The brain magnetic resonance imaging showed diffused bilateral 

hyperintensities in the white matter with additional lesions in semioval centres. She was treated with amantadine infusions, sertraline, levodopa and piracetam with gradual improvement. Besides neurological improvement the outcome was fatal. In our patient the initial Glasgow Coma Scale score was 7 points, and leukocytosis and troponin increase were detected. These results might be potentially used as prognostic factors in the course of the observed neurological symptoms.

Conclusions: Further studies should be performed for a better understanding of delayed neurological sequelae pathogenesis aiming at the prevention or effective treatment of this significantly disabling disorder.


delayed neurological sequelae; carbon monoxide; intoxication; encephalopathy; treatment

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