The effects of hyperbaric oxygen dosing on the delayed neuropsychiatric sequalae of carbon monoxide poisoning.

Abstract

A paucity of evidence exists as to the comparative effectiveness of various hyperbaric oxygen regimens in preventing delayed neuropsychiatric sequelae. We aimed to compare the effect of four such treatment regimens: (1)O= 2.0for 90 min once; (2)O= 2.0for 90 min thrice; (3)O= 2.8for 90 min once; and (4)O= 2.8for 90 min once followed by two sessions of 2.0. We retrospectively reviewed the records of all patients treated in a large regional hyperbaric referral facility over the past 30 years, and identified patients displaying any new cognitive, motor or psychiatric symptoms within 2-40 days from exposure to carbon monoxide - any of which was defined as delayed neuropsychiatric sequelae. Excluded were patients not complying with the full prescribed treatment course or those lacking a full medical record for at least a year following exposure. Of 312 patients included in the final analysis, the incidence of delayed neuropsychiatric sequelae was 31/87 (36%), 20/54 (37%), 20/102 (20%) and 13/69 (19%) in the 2.0once, 2.0thrice, 2.8once and 2.8thrice treatment groups, respectively ( = 0.011). Patients treated with the lower-pressure regimen (2.0once and thrice) had a significantly higher delayed neuropsychiatric sequelae rate compared to those treated with higherO(2.8once and thrice) - 36.2% versus 19.3% respectively ( = 0.0013). In a multivariate logistic regression model adjusting for age, carboxyhemoglobin levels, and presenting symptoms, the higher-pressure protocol was independently associated with a 55% reduction in the odds of developing delayed neuropsychiatric sequelae (adjusted odds ratio = 0.45; 95% confidence interval: 0.26-0.77; = 0.004). Increasing the frequency of sessions from one to three was not associated with a statistically significant benefit ( = 0.9). The presence of seizures on admission was the strongest predictor of poor outcome (adjusted odds ratio = 4.27; = 0.023). The observed 55% reduction in the odds of developing delayed neuropsychiatric sequelae with the 2.8protocol suggests that achieving a higher initial partial pressure of oxygen is critical to effectively interrupting the inflammatory cascades associated with carbon monoxide toxicity. Because additional sessions did not confer a statistically significant benefit, meeting this initial therapeutic threshold appears more impactful than treatment frequency. Notably, the neuroprotective benefits of the higher-pressure regimen were sustained even among high-risk patients presenting with seizures. AOof 2.8rather than 2.0in the initial hyperbaric oxygen session, is associated with superior neuroprotective outcomes, while the overall number of sessions is not.