Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2025
Multidimensional metabolic profiling in carbon monoxide poisoning: acid-base disturbances correlate with neurological severity.
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Wang Weiguang, Huang Huihua, Xiong Xianwei, Ye Changsheng, Huang Jin, Ling Yong Ai
Аннотация
BACKGROUND: Acute carbon monoxide poisoning triggers complex metabolic derangements including acidosis and alkalosis, but their correlation with neurological injury severity remains insufficiently characterized clinically.
METHODS: Consecutive poisoning patients (age ≥14) admitted between January 2019 and February 2025 were classified by neurological impairment severity. Acid-base parameters were analysed using Kruskal-Wallis tests, Spearman's correlation, and principal component analysis with varimax rotation.
RESULTS: Among 940 patients (37.2% male), participants were categorized into three groups by neurological impairment severity: Mild (n = 597), moderate (n = 225), and severe (n = 118). Severe cases showed lower pH (7.39 vs. 7.41), reduced PaCO2 (34.5 vs. 38.2 mmHg), greater base excess deficit -3.3 vs. 0.4), and higher lactate (3.7 vs. 1.6 mmol/L) (all p < 0.001). Neurological severity positively correlated with lactate (rho = 0.338) and inversely with base excess (rho = -0.268). Principal component analysis identified two components: Factor Component 1 (FAC1) (metabolic compensation, 47-65% variance) and FAC2 (respiratory regulation, 26-41% variance), with FAC1 inversely correlating with severity (rho = -0.319, p < 0.001).
CONCLUSIONS: Neurological impairment severity shows dose-dependent correlation with metabolic dysfunction (lactate accumulation, mixed metabolic acidosis-respiratory alkalosis). FAC1 (metabolic compensation) is a strong prognostic biomarker in acute carbon monoxide poisoning.
METHODS: Consecutive poisoning patients (age ≥14) admitted between January 2019 and February 2025 were classified by neurological impairment severity. Acid-base parameters were analysed using Kruskal-Wallis tests, Spearman's correlation, and principal component analysis with varimax rotation.
RESULTS: Among 940 patients (37.2% male), participants were categorized into three groups by neurological impairment severity: Mild (n = 597), moderate (n = 225), and severe (n = 118). Severe cases showed lower pH (7.39 vs. 7.41), reduced PaCO2 (34.5 vs. 38.2 mmHg), greater base excess deficit -3.3 vs. 0.4), and higher lactate (3.7 vs. 1.6 mmol/L) (all p < 0.001). Neurological severity positively correlated with lactate (rho = 0.338) and inversely with base excess (rho = -0.268). Principal component analysis identified two components: Factor Component 1 (FAC1) (metabolic compensation, 47-65% variance) and FAC2 (respiratory regulation, 26-41% variance), with FAC1 inversely correlating with severity (rho = -0.319, p < 0.001).
CONCLUSIONS: Neurological impairment severity shows dose-dependent correlation with metabolic dysfunction (lactate accumulation, mixed metabolic acidosis-respiratory alkalosis). FAC1 (metabolic compensation) is a strong prognostic biomarker in acute carbon monoxide poisoning.