Carbon Monoxide-Induced Cortical Visual Loss: Treatment with Hyperbaric Oxygen Four Years Later

Abstract

Objective: We present a patient who developed visual loss after carbon monoxide (CO) poisoning and was treated with hyperbaric oxygen. Clinical Presentation and Intervention: A 21-year-old woman poisoned with CO (with coma lasting 4 h and carboxyhemoglobin level 46%) developed seizures and cortical blindness 3 days after poisoning. Four years later, her visual acuity was 0.2 in both eyes. An ¹⁸F-fluorodeoxyglucose positron emission tomography (PET) scan showed reduced metabolism in the bilateral posterior temporal and occipital lobes. The patient received a total of 50 hyperbaric oxygen sessions over 3 months for visual loss and the visual acuity improved to 0.5 in both eyes. In addition, increased metabolism was detected in the brain in post-treatment PET scans. Conclusion: PET documented brain hypoperfusion 4 years after CO poisoning and hyperbaric oxygen therapy improved visual acuity. However, we cannot endorse routine use of hyperbaric oxygen for such patients, until results of further clinical trials demonstrate efficacy of hyperbaric oxygen in CO-induced chronic brain injury.

Neuroimaging Studies in Carbon Monoxide Intoxication

“…The lucid interval after acute CO poisoning, on average, is around 20 days, varying from one to 240 days (Choi 1983;Lee and Marsden 1994;Ernst and Zibrak 1998;Pavese, Napolitano et al 1999;Hsiao, Kuo et al 2004), with a prevalence of 0.2-40% (Hsiao, Kuo et al 2004;Otubo, Shirakawa et al 2007). Delayed neuropsychiatric sequelae include parkinsonism (Lee and Marsden 1994), chorea (Park and Choi 2004), akinetic mutism (Lee and Marsden 1994), increased irritability, verbal aggressiveness, violence, impulsiveness (Meredith and Vale 1988), mood disorders (Weaver 2009), dementia (Meredith and Vale 1988;Ernst and Zibrak 1998;Weaver 2009), psychosis (Ernst and Zibrak 1998), sleep disturbances (Weaver 2009), cortical blindness (Quattrocolo, Leotta et al 1987;Senol, Yildiz et al 2009) and incontinence (Ernst and Zibrak 1998). The cognitive deficits are often very diverse (Hurley, Hopkins et al 2001;Parkinson, Hopkins et al 2002;Raub and Benignus 2002) including impairment in verbal or visual episodic memory, language, visuospatial ability, executive function and calculation (Chang, Chang et al 2010).…”

“…In a comparison between those with delayed neuropsychiatric sequelae and those without sequelae, significant hypoperfusion was noted over bilateral frontal lobes, bilateral insula and right temporal lobe in patients with delayed neuropsychiatric sequelae, whilst only bilateral frontal lobe hypoperfusion was noted in those without neuropsychiatric sequelae (Watanabe, Nohara et al 2002). To date, there have only been a limited number of reports on [ 18 F] FDG-PET in the evaluation of metabolic dysfunction in the cortical areas of patients with CO intoxication (Tengvar, Johansson et al 2004;Senol, Yildiz et al 2009). One case report of a middle-aged man revealed hypometabolism of bilateral frontal lobes and anterior cingulate cortices (Tengvar, Johansson et al 2004), and his neurological deficit of akinetic mutism was regarded as the consequence of the hypometabolism state of the involved regions (Tengvar, Johansson et al 2004).…”

“…In another case report on a 21-year-old woman who had coma, seizure and cortical blindness within three days after CO poisoning, the neurological deficit of cortical blindness remained. A subsequent [ 18 F] FDG-PET four years later still showed hypometabolism of bilateral posterior temporal and occipital lobes (Senol, Yildiz et al 2009). One month after CO intoxication, a patient's (age: 30) PET revealed reduced uptake of FDG in bilateral temporal and occipital lobes (11A, arrows), while the brain CT (11B) did not detect any hypodense lesions over the corresponding areas.…”

Delayed hyperbaric oxygen treatment after acute carbon monoxide poisoning

“…CO-effects are not confined to the time immediately following exposure [1,8], given that all poisoned patients are at risk of developing DNS. The clinical picture of our patient included delayed cognitive and motor disturbances after a lucid interval from intoxication, compatible with this syndrome.…”

“…Carboxyhemoglobin reduces the oxygen-carrying capacity of blood, causing hypoxia [1][2][3][4]. After a period of apparent recovery, survivors of acute CO-poisoning can develop a potentially permanent neurologic deterioration (DNS) [1][2][3]8]. DNS is a rare, poorly known encephalopathy with a 1-47% prevalence among CO-poisoned patients [5,6].…”