Multidimensional metabolic profiling in carbon monoxide poisoning: acid-base disturbances correlate with neurological severity.

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.