Association between Glasgow Coma Scale in Early Carbon Monoxide Poisoning and Development of Delayed Neurological Sequelae: A Meta-Analysis

Abstract

A significant number of people experience delayed neurologic sequelae after acute carbon monoxide (CO) poisoning. The Glasgow Coma Scale (GCS) can be used to predict delayed neurologic sequelae occurrence efficiently and without any restrictions. Here, we investigated the association between a low GCS score observed in cases of early CO poisoning and delayed neurologic sequelae development through a meta-analysis. We systematically searched MEDLINE, EMBASE, and the Cochrane Library for studies on GCS as a predictor of delayed neurologic sequelae occurrence in patients with CO poisoning in June 2021. Two reviewers independently extracted study characteristics and pooled data. We also conducted subgroup analyses for the cutoff point for GCS. To assess the risk of bias of each included study, we used the quality in prognosis studies tool. We included 2328 patients from 10 studies. With regard to patients with acute CO poisoning, in the overall pooled odds ratio (OR) of delayed neurologic sequelae development, those with a low GCS score showed a significantly higher value and moderate heterogeneity (OR 2.98, 95% confidence interval (CI) 2.10–4.23, I2 = 33%). Additionally, in subgroup analyses according to the cutoff point of GCS, the development of delayed neurologic sequelae was still significantly higher in the GCS < 9 group (OR 2.80, 95% CI 1.91–4.12, I2 = 34%) than in the GCS < 10 or GCS < 11 groups (OR 4.24, 95% CI 1.55–11.56, I2 = 48%). An initial low GCS score in patients with early CO poisoning was associated with the occurrence of delayed neurologic sequelae. Additionally, GCS was quickly, easily, and accurately assessed. It is therefore possible to predict delayed neurologic sequelae and establish an active treatment strategy, such as hyperbaric oxygen therapy, to minimize neurological sequelae using GCS.

Predicting acute brain lesions on magnetic resonance imaging in acute carbon monoxide poisoning: a multicenter prospective observational study

“…Previous studies have suggested an association between a GCS score < 9 and the development of DNS and/or ABLs 22 , 23 , 32 . Results from our study were comparable.…”

An artificial intelligence algorithm for analyzing globus pallidus necrosis after carbon monoxide intoxication

“…39,40 Moreover, a meta-analysis including 2328 patients from 10 studies demonstrated that patients with initial low GCS score had higher risk for developing DNS compared to those with higher GCS score. 41 Future studies may explore the different contributions of each variable to GPN.…”

Clinical features and predictors of delayed neurological syndrome in carbon monoxide poisoning: the AMICO study

“…Este cuadro aparece entre 3 y 40 días después de la exposición inicial, y se manifiesta de forma plural y variable en forma de apatía, deterioro de la memoria, desorientación, mutismo, irritabilidad, incapacidad para concentrarse, cambios de personalidad, labilidad emocional, neuropatía, incontinencia, corea, apraxia, psicosis, demencia y parkinsonismo [9][10][11] . En la actualidad aún no están bien definidos los criterios de confirmación diagnóstica ni los mecanismos que ocasionan el SNT, aunque algunos autores han relacionado recientemente su aparición con puntuaciones bajas en la Escala del Coma de Glasgow (ECG) en la fase aguda de la intoxicación 12 . La detección de daños en la sustancia blanca y el hipocampo o fenómenos de desmielinización en las resonancias magnéticas de pacientes con SNT apoyarían esta teoría [12][13][14][15] .…”

“…En la actualidad aún no están bien definidos los criterios de confirmación diagnóstica ni los mecanismos que ocasionan el SNT, aunque algunos autores han relacionado recientemente su aparición con puntuaciones bajas en la Escala del Coma de Glasgow (ECG) en la fase aguda de la intoxicación 12 . La detección de daños en la sustancia blanca y el hipocampo o fenómenos de desmielinización en las resonancias magnéticas de pacientes con SNT apoyarían esta teoría [12][13][14][15] . Otras teorías propuestas relacionan su desarrollo con algunos factores predisponentes: edad avanzada, duración de la exposición, retraso en el inicio del tratamiento, el estrés oxidativo con incremento de las concentraciones de lactato o presencia de hipertermia, pero no existe un consenso claro 12,[16][17][18] .…”