Predictors for delayed encephalopathy following acute carbon monoxide poisoning

Abstract

BackgroundIn Japan, many carbon monoxide (CO) poisoning cases are transported to emergency settings, making treatment and prognostic assessment an urgent task. However, there is currently no reliable means to predict whether “delayed neuropsychiatric sequelae (DNS)” will develop after acute CO poisoning. This study is intended to find out risk factors for the development of DNS and to characterize the clinical course following the development of DNS in acute CO poisoning cases.MethodsThis is a retrospective cohort study of 79 consecutive patients treated at a single institution for CO poisoning. This study included 79 cases of acute CO poisoning admitted to our emergency department after attempted suicide, who were divided into two groups consisting of 13 cases who developed DNS and 66 cases who did not. The two groups were compared and analyzed in terms of clinical symptoms, laboratory findings, etc.ResultsPredictors for the development of DNS following acute CO poisoning included: serious consciousness disturbance at emergency admission; head CT findings indicating hypoxic encephalopathy; hematology findings including high creatine kinase, creatine kinase-MB and lactate dehydrogenase levels; and low Global Assessment Scale scores. The clinical course of the DNS-developing cases was characterized by prolonged hospital stay and a larger number of hyperbaric oxygen (HBO) therapy sessions.ConclusionIn patients with the characteristics identified in this study, administration of HBO therapy should be proactively considered after informing their family, at initial stage, of the risk of developing DNS, and at least 5 weeks’ follow-up to watch for the development of DNS is considered necessary.

Acute carbon monoxide poisoning in a regional hospital in Hong Kong: historical cohort study

“…We identified the following prognostic factors associated with DNS development in patients with severe CO poisoning: LOC, lower GCS score, GCS score of 3, intubation requirement, elevated Tn level, and higher levels of Tn and CK. Other investigational prognostic markers reported worldwide include S100B protein, 24 low Mini-Mental State Examination score, 25 positive computed tomography of brain, 25,26 and plasma copeptin. 27 The results of this study reveal that severe DNS did not develop in any patient with severe CO poisoning who was treated with HBOT at PYNEH between 2008 and 2013.…”

Delayed Neuropsychiatric Sequelae of Carbon Monoxide Poisoning: A Case Report

“…Pepe et al reported that 24.1% incidence of DNS at 30 days from hospital discharge [5]. The risk factors that have been associated with the development of DNS include advanced age group, longer duration of exposure to carbon monoxide, delayed time in seeking treatment, duration of loss of consciousness, coma, early changes on head computed tomography (CT) or magnetic resonance (MRI) and grossly elevated CK, CKMB and LDH levels on blood investigations and severe metabolic acidosis [3,5,[8][9][10][11]. In this patient, the risk factors to develop DNS were prolonged exposure to carbon monoxide, presented in coma and had severe metabolic acidosis.…”

Delayed neurological sequelae in carbon monoxide poisoning – a case report and present state of knowledge

“…Previous associated diseases do not hasten the development of sequelae [7,8,9]. Possible prognostic factors for the development of DNS in patients with severe CO poisoning are serious disorders of consciousness or loss of consciousness at emergency admission, low Glasgow Coma Scale (GCS) score, head CT findings indicating hypoxic encephalopathy, haematology findings including high troponin, creatine phosphokinase, creatine kinase-MB and lactate dehydrogenase levels, low Global Assessment Scale scores, and intubation requirement [22,23]. Other factors that may be associated with increased risk of DNS development are: CO exposure duration >6 hours, GCS score <9, seizures, systolic blood pressure <90 mmHg and leukocytosis, but in the multivariate analysis the independent factors were only the GCS <9 (OR 7.15; CI 95%: 1.04-48.8) and leukocytosis (OR 3.31; CI 95%: 1.02-10.71) [24].…”