Abstract

Objective: This study aimed to investigate whether the serum N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin I levels at emergency department (ED) presentation predict long-term neurologic outcomes after acute charcoal-burning carbon monoxide (CO) poisoning.Methods: This retrospective study included 220 patients suffering from charcoal-burning CO poisoning. The demographics, serum NT-proBNP and troponin I levels at ED presentation, treatment, clinical course during hospitalization, and long-term neurologic outcomes were collected.Results: The median serum NT-proBNP level at presentation was 48.8 (16.5–259) pg/mL, and 78 patients (35.5%) had elevated troponin I (>0.04 ng/mL) after acute charcoal-burning CO poisoning. The upper NT-proBNP and elevated troponin I groups had higher prevalences of respiratory failure, hypotension, and myocardial injury during hospitalization and altered mentality (GCS ≤14) at discharge than the lower NT-proBNP and normal troponin I groups. The incidence of persistent severe neurologic sequelae at 25 months after acute CO poisoning was 10.9%. The upper NT-proBNP and elevated troponin I groups had a higher incidence of poor long-term neurologic outcome than the counterpart groups. Log-transformed NT-proBNP and elevated troponin I were associated with poor long-term neurologic outcome in the univariate analysis, but only the adjusted log-transformed NT-proBNP remained an independent factor in the multivariate analysis. Compared with a predictive model including previously proposed predictors, the addition of log NT-proBNP improved the diagnostic accuracy for predicting poor long-term neurologic outcome. The serum NT-proBNP values for predicting poor long-term neurologic outcome were 74.6 and 32.7 pg/mL at fixed sensitivities of 95 and 99%, respectively.Conclusions: Elevated serum NT-proBNP at ED presentation is correlated with a risk of poor long-term neurologic outcome after discharge in cases of acute charcoal-burning CO poisoning. NT-proBNP could significantly improve the risk stratification of patients who will experience poor long-term neurologic outcome after CO poisoning. This potentially valuable marker should be further validated.

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