Delayed Postanoxic Encephalopathy Following Acute Carbon Monoxide Poisoning: A Case Report and Literature Review

Carbon monoxide (CO) poisoning is the leading cause of death from accidental poisoning worldwide. It is associated with significant mortality and morbidity. The mere notion of exposure to risk should lead to the diagnosis of CO poisoning in an emergency situation. Neurological (coma and delayed neuropsychological sequelae) and cardiac (ischemic changes with normal coronary arteries) clinical scenarios are explained by complex mechanisms: carboxyhemoglobin formation, cytochrome oxidase inhibition, oxidative stress, as well as ischemia-reperfusion phenomenon. Delayed neurological sequelae (DNS) or delayed encephalopathy is characterized by a neurological clinical picture that arises after acute CO intoxication and after a period of apparent recovery. The onset of DNS is unpredictable. The true prevalence of DNS is difficult to determine; the estimates range from 1% to 47% of patients after CO poisoning. The exact incidence rate is also unclear. Studies using rigorous methodologies, including neuropsychological testing, report the frequency to be as high as 67%. CO poisoning causes severe neurocognitive after-effects that are rarely studied in the literature. Here, we describe the case of a patient aged 18 years old with no known comorbidities, a victim of accidental CO poisoning, who initially presented with behavioral disorders. The evolution was marked by the occurrence of memory and attention disorders a few weeks later. Neuropsychological assessment revealed a dysfunction of several processes (executive, attentional, and memory). Brain MRI revealed restrictive bilateral occipital, frontal, and temporal lesions of hypoxic origin. The patient underwent three sessions of hyperbaric oxygen therapy and received symptomatic drug treatment and neurocognitive rehabilitation, with a more or less favorable evolution of her disorders.