Effect of ethanol in carbon monoxide poisoning and delayed neurologic sequelae: A prospective observational study

Abstract

Objectives: Carbon monoxide (CO) is one of the most common poisoning substances, which causes mortality and morbidity worldwide. Delayed neurologic sequelae (DNS) have been reported to occur from several days to months after exposure to CO. Thus, there is a need for prevention, recognition, and treatment of DNS. Patients with CO poisoning as a component of intentional suicide often also consume ethanol, but there is debate regarding its role in DNS. We explored whether ethanol has a neuroprotective effect in CO poisoning.

Methods: This prospective observational study included patients who visited the emergency department from August 2016 to August 2019 due to CO poisoning. After treatment of acute CO poisoning, patients were interviewed by telephone to ascertain whether DNS had occurred within 2 weeks, 1 month, and 3 months from the time of CO exposure.

Results: During the study period, 171 patients were enrolled. 28 patients (16.37%) developed DNS. The initial Glasgow Coma Scale (GCS) scores were 15 (10.5-15) for the non-DNS group and 10 (7-15) for the DNS group (p = 0.002). The ethanol levels were 11.01 ± 17.58 mg/dL and 1.49 ± 2.63 mg/dL for each group (p < 0.001). In multivariate logistic regression analysis, the GCS score had an odds ratio of 0.770 (p < 0.001) and the ethanol level had 0.882 (p < 0.030) for onset of DNS.

Conclusions: Higher ethanol level and higher initial GCS score were associated with lower incidence of DNS. Ethanol could have a neuroprotective effect on the occurrence of DNS in CO poisoning patients.

Fig 1. Study population.

Fig 2. Receiver operating characteristic curve.