Delayed hyperbaric oxygen treatment after acute carbon monoxide poisoning

Abstract

Carbon monoxide (CO) is a colorless, odourless, highly toxic gas [1]. The diagnosis of CO-poisoning depends mainly on the history of exposure [2]. Carboxyhemoglobin reduces the oxygen-carrying capacity of blood, causing hypoxia [1–4]. After a period of apparent recovery, survivors of acute CO-poisoning can develop a potentially permanent neurologic deterioration (DNS) [1–3, 8]. DNS is a rare, poorly known encephalopathy with a 1–47% prevalence among CO-poisoned patients [5, 6]. Its symptoms and signs range from subtle abnormalities to severe dementia, parkinsonism, gait disturbances, mutism, and incontinence [1, 2]. Appropriate therapy for DNS is widely debated; particularly, the role of hyperbaric oxygen therapy (HBO2) is controversial. We describe a patient suffering from a striking neurologic decline after complete recovery from severe COpoisoning, who recovered after delayed HBO2 treatment. A 62 year old man was admitted to our hospital after having developed an akinetic-mute state with stereotyped movements, incontinence, gait-disturbances and cognitive deterioration over a period of 2 weeks. Twelve days before symptom’s onset, he was found unconscious in his smokefilled flat. He underwent intubation and high-flow oxygen therapy was provided. The cranial computerized tomography (TAC) which was immediately performed was normal, while after a few days it revealed symmetric hypodense globus pallidus (GP) lesions. He regained consciousness after 1 day. A week later he was asymptomatic and his neurological condition was unremarkable. Back home he returned to his normal activities. However, 12 days later he developed confusion and memory disturbances. His neurologic state began to deteriorate rapidly, progressing to akinetic mutism over the next week. He became totally unresponsive and incontinent. When he was referred to our hospital he showed a severe speechimpairment, with very poor expression and comprehension, dysarthria, and apraxia, also involving the cranial district. He was hypomimic, and he presented stereotyped movements, especially with his hands. His tone was markedly increased, standing and gait had become severely affected (Video Segment-1 of electronic supplementary material). Neuropsychological testing revealed severe dysfunction in all cognitive domains. Diffuse white matter (WM) hyperintensities, also involving the corpus callosum, were seen on T2-weighted MRI scans, accompanied by bilateral GP collapses (Fig. 1). A diagnosis of delayed encephalopathy after CO-intoxication was made. HBO2 therapy was carried out every day for 10 days at 2.5 absolute atmosphere (ATA), each session lasting 70 min, with gradual and progressive clinical improvement starting since the very first sessions of HBO2 therapy. After the treatment, the patient’s neurological state was unremarkable, with only Electronic supplementary material The online version of this article (doi:10.1007/s00415-011-5958-4) contains supplementary material, which is available to authorized users.