[The relationship between lactate clearance rate and delayed encephalopathy after acute carbon monoxide poisoning]

To study the relationship between lactate clearance rate (LCR) and prognosis after acute carbon monoxide poisoning in patients with delayed encephalopathy (DEACMP).

Data from 354 patients with acute severe carbon monoxide poisoning (ASCOP) were retrospectively analyzed. The patients were divided into hyperlactacidemia group (arterial lactic acid > 2 mmol/L, n=263) and low lactic acidosis group (arterial lactate ≤2 mmol/L, n=91) according to the blood lactic acid level at admission. Arterial blood (1 mL) was collected from all patients before and 6, 24, 72 hours after treatment at ambient air, and arterial blood lactic acid was determined, and LCR was calculated. The initial level of blood lactic acid and LCR at 6, 24, 72 hours were compared between two groups. At the same time, the patients with hyperlactacidemia were divided into high LCR group (LCR more than 10%, n=101) and low LCR group (LCR less than or equal to 10%, n=162) according to 6-hour LCR, and the incidence of DEACMP was compared between two groups. The relationship between LCR and the incidence of DEACMP was analyzed with Spearman linear correlation analysis. The risk factors associated with DEACMP were analyzed with logistic regression analysis.

The initial level of blood lactic acid (2.73±0.57 mmol/L vs. 1.69±0.20 mmol/L, t=5.327, P=0.001) and LCR at 6, 24, 72 hours [6 hours: (9.0±2.4)% vs. (1.2±0.6)%, t=9.468, P=0.001; 24 hours: (8.6±3.7)% vs. (1.2±0.4)%, t=4.889, P=0.001; 72 hours: (14.0±3.9)% vs. (1.7±1.0)%, t=5.211, P=0.001] in hyperlactacidemia group were significantly higher than those in low lactic acidosis group. The initial level of blood lactic acid in high LCR group was significantly lower than that in low LCR group (2.41±0.23 mmol/L vs. 2.92±0.63 mmol/L, t=2.429, P=0.023), and LCR at 6 hours and 24 hours were significantly higher than those in low LCR group [6 hours: (11.0±1.2)% vs. (8.0±2.1)%, t=4.487, P=0.001; 24 hours: (12.2±3.0)% vs. (6.3±1.8)%, t=6.264, P=0.001]. But there was no difference in 72-hour LCR between high LCR group and low LCR group [(14.1±3.6)% vs. (13.9±4.1)%, t=0.182, P=0.857]. The incidence of DEACMP in high LCR group was significantly lower than that in low LCR group [15.8% (16/101) vs. 61.1% (99/162), χ(2)=51.814, P=0.001]. The blood LCR at early period (6, 24, 72 hours) in ASCOP patients with hyperlactacidemia was negatively correlated with the incidence of DEACMP (r1=-0.493, P1=0.011; r2=-0.408, P2=0.038; r3=-0.428, P3=0.029). Logistic regression analysis showed that LRC at 6 hours and 24 hours [odds ratio (OR) was 2.701, 1.070, P value was 0.035, 0.001], long-time coma (OR=1.537, P=0.068), contact carbon monoxide (CO) long time (OR=2.686, P=0.014), age (OR=1.464, P=0.017), acute carbon monoxide complications (OR=1.363, P=0.072) patients with ASCOP had an increased risk of DEACMP.

LCR is helpful for the assess of DEACMP patients severity, for the treatment guide and for prognosis judgement.